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Aug.5.2020
Jul.20.2020

Elsevier Drug Monographs

Dexamethasone

Indications/Dosage

Labeled

  • acne rosacea
  • acute lymphocytic leukemia (ALL)
  • Addison's disease
  • adrenocortical insufficiency
  • adrenogenital syndrome
  • allergic conjunctivitis
  • allergic rhinitis
  • alopecia
  • anaphylactic shock
  • anaphylaxis
  • angioedema
  • ankylosing spondylitis
  • anterior segment inflammation
  • asthma exacerbation
  • atopic dermatitis
  • berylliosis
  • bursitis
  • cerebral edema
  • chronic obstructive pulmonary disease (COPD)
  • congenital adrenal hyperplasia
  • contact dermatitis
  • corneal abrasion
  • corneal ulcer
  • Crohn's disease
  • cutaneous T-cell lymphoma (CTCL)
  • cyclitis
  • dermatitis
  • dermatitis herpetiformis
  • dermatomyositis
  • diabetic macular edema
  • discoid lupus erythematosus
  • epicondylitis
  • erythema multiforme
  • erythroblastopenia
  • exfoliative dermatitis
  • food allergy
  • gouty arthritis
  • graft-versus-host disease (GVHD)
  • granuloma annulare
  • hemolytic anemia
  • herpes zoster ocular infection
  • Hodgkin lymphoma
  • hypercalcemia
  • hypoplastic anemia
  • hypothalamic-pituitary-adrenal (HPA) suppression diagnosis
  • immune thrombocytopenic purpura (ITP)
  • iritis
  • juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA)
  • keloids
  • keratitis
  • kidney transplant rejection
  • lichen planus
  • lichen simplex
  • Loeffler's syndrome
  • macular edema following retinal vein occlusion
  • multiple myeloma
  • multiple sclerosis
  • myasthenia gravis
  • mycosis fungoides
  • necrobiosis lipoidica diabeticorum
  • nephrotic syndrome
  • non-Hodgkin's lymphoma (NHL)
  • ocular pain
  • osteoarthritis
  • otitis externa
  • pemphigus
  • perennial allergies
  • pneumonitis
  • polymorphous light eruption
  • polymyositis
  • postoperative ocular inflammation
  • proteinuria
  • pruritus
  • psoriasis
  • psoriatic arthritis
  • rheumatic carditis
  • rheumatoid arthritis
  • Rhus dermatitis
  • sarcoidosis
  • seasonal allergies
  • seborrheic dermatitis
  • serum sickness
  • Stevens-Johnson syndrome
  • systemic lupus erythematosus (SLE)
  • temporal arteritis
  • tenosynovitis
  • thrombocytopenia
  • thyroiditis
  • trichinosis
  • tuberculosis infection
  • ulcerative colitis
  • urticaria
  • uveitis
  • vernal keratoconjunctivitis
  • viral conjunctivitis

Off-Label

  • acute respiratory distress syndrome (ARDS)
  • altitude sickness
  • altitude sickness prophylaxis
  • amyloidosis
  • bronchiolitis
  • chemotherapy-induced nausea/vomiting
  • chemotherapy-induced nausea/vomiting prophylaxis
  • chronic lung disease (CLD)
  • Churg-Strauss syndrome
  • coronavirus disease 2019 (COVID-19)
  • infertility
  • laryngeal edema prophylaxis
  • laryngotracheobronchitis (croup)
  • macroglobulinemia
  • meningitis
  • mixed connective tissue disease
  • neonatal respiratory distress syndrome prophylaxis
  • polyarteritis nodosa
  • polychondritis
  • post-operative nausea/vomiting (PONV)
  • post-operative nausea/vomiting (PONV) prophylaxis
  • pulmonary edema
  • severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection
  • spinal cord compression
  • Wegener's granulomatosis
† Off-label indication

For the treatment of adrenocortical function abnormalities, such as adrenocortical insufficiency, congenital adrenal hyperplasia, chronic primary (Addison's disease) or secondary adrenocortical insufficiency, or adrenogenital syndrome

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. NOTE: Parenteral therapy may be needed in acute insufficiency. Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.

Infants, Children, and Adolescents

0.15 to 0.375 mg/m2/day PO once daily has been recommended for patients with congenital adrenal hyperplasia.[54489] [54490] Although most experts recommend hydrocortisone as first-line treatment of adrenal insufficiency in pediatric patients whose linear growth is incomplete due to a lower incidence of growth suppression, other authors have stated that dexamethasone may be used safely with close monitoring and individualization of dose based on growth, bone age, and hormone levels. Liquid formulations of dexamethasone are recommended for more precise titration of doses.[54123] [54155] 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Parenteral therapy may be needed in acute insufficiency.

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)

Adults

Initially, 0.5 to 9 mg/day IV or IM, divided every 6 to 12 hours. Adjust according to patient response. NOTE: Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.

Infants, Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

INVESTIGATIONAL USE: For adjunctive use in the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection†, the virus that causes coronavirus disease 2019 (COVID-19)†

Oral dosage

Adults

6 mg PO once daily for up to 10 days is recommended by the National Institutes of Health (NIH) COVID-19 treatment guidelines for use in mechanically ventilated patients and patients who require supplemental oxygen but are not on a mechanical ventilator. This recommendation also applies to pregnant women, as the potential benefit of decreased maternal mortality justifies the low risk of fetal adverse effects with the short course of therapy. The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting dexamethasone.[65314]

Children and Adolescents

Data are limited. The National Institutes of Health (NIH) COVID-19 treatment guidelines state that dexamethasone may be beneficial to pediatric patients who are on mechanical ventilation. For pediatric patients who require other forms of supplemental oxygen, consideration for the use of dexamethasone should be made on a case-by-case basis; but the use is generally not recommended in those who require low levels of oxygen support (i.e., nasal cannula only).[65314]

Intravenous dosage

Adults

6 mg IV once daily for up to 10 days is recommended by the National Institutes of Health (NIH) COVID-19 treatment guidelines for use in mechanically ventilated patients and patients who require supplemental oxygen but are not on a mechanical ventilator. This recommendation also applies to pregnant women, as the potential benefit of decreased maternal mortality justifies the low risk of fetal adverse effects with the short course of therapy. The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting dexamethasone.[65314]

Children and Adolescents

Data are limited. The National Institutes of Health (NIH) COVID-19 treatment guidelines state that dexamethasone may be beneficial to pediatric patients who are on mechanical ventilation. For pediatric patients who require other forms of supplemental oxygen, consideration for the use of dexamethasone should be made on a case-by-case basis; but the use is generally not recommended in those who require low levels of oxygen support (i.e., nasal cannula only).[65314]

For hypothalamic-pituitary-adrenal (HPA) suppression diagnosis (e.g., dexamethasone suppression tests)

For the prevention of extubation failure in pediatric patients at increased risk for laryngeal edema (i.e., laryngeal edema prophylaxis†)

Intravenous dosage (dexamethasone sodium phosphate)

Infants, Children, and Adolescents

0.5 mg/kg/dose IV (Maximum: 10 mg/dose IV) every 6 hours for 6 doses with the first dose given 6 to 12 hours prior to extubation has been studied with mixed results.[54396] [54507] One prospective, randomized study (n = 153) found no significant difference in the risk of postextubation stridor, the average number of racemic epinephrine treatments, or the number of patients requiring reintubation in patients receiving dexamethasone compared to those receiving placebo.[54396] Another prospective, randomized study (n = 66) found that dexamethasone-treated patients had a significantly lower rate of postextubation stridor at 10 minutes, 6 hours, and 12 hours but not 24 hours and fewer patients requiring epinephrine or reintubation compared to placebo-treated patients.[54507] A systematic review of clinical trials of dexamethasone for the prevention of postextubation stridor concluded that therapy may be beneficial in high-risk patients, such as those with underlying airway anomalies or multiple airway manipulations.[54508]

Neonates

Various regimens have been used. 0.25 mg/kg/dose IV every 8 hours for 3 doses with the first dose given approximately 4 hours prior to scheduled extubation was studied in a prospective, randomized trial in 50 premature neonates (mean gestational age, 27.7 to 28.7 weeks) who were at high risk for airway edema. The rate of postextubation stridor and reintubation was significantly lower in the dexamethasone group compared to the placebo group.[24997] A systematic review of clinical trials of dexamethasone for the prevention of extubation failure recommends therapy be reserved for use in high risk neonates, such as those with repeated or prolonged intubations, due to a lack of benefit in low risk neonates and the risk of adverse effects.[54509] Use preservative-free products for administration to neonates when possible.

For the treatment of cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection)

Adults

10 mg IV or IM as a single dose, followed by 4 mg IV or IM every 6 hours, until symptoms subside, then reduce dosage. A response should be seen within 12 to 24 hours, and a gradual dose reduction begun after 2 to 4 days, reducing over another 5 to 7 days. Replace with oral dosage as soon as possible. For palliative maintenance therapy when oral therapy is not feasible, 2 mg IM or IV can be given 2 to 3 times per day, if needed. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.[60760]

Oral dosage (dexamethasone)

Adults

For cerebral edema, 1 to 3 mg PO three times daily, can follow parenteral therapy; then, taper off over a period of 5 to 7 days.[60760] For palliative management of recurrent or inoperable brain tumors, maintenance with 2 mg PO given 2 or 3 times daily may be effective.[30011]

For use as an adjunct in the management of extradural malignant spinal cord compression† (MSCC†) associated with metastatic disease

Oral dosage (dexamethasone) or Intravenous dosage (dexamethasone sodium phosphate)

Adults

A bolus of 8 to 10 mg dexamethasone (or equivalent) PO or IV, followed by 16 mg/day PO (usually in twice-daily to four-times-daily doses for tolerance) is a typical dose; doses are adjusted to patient condition and are either maintained or tapered over a few weeks dependent on radiation therapy cycles and/or anticipated surgery. A broad dosage range of 16 to 100 mg/day has been used depending on the presence of paraparesis, etc. Higher quality data are needed to establish the benefits vs. risks and optimal dose and duration of therapy. Experts generally agree that patients who have neurologic deficits should receive dexamethasone; many patients with MSCC require corticosteroids to help preserve neurologic function, such as ambulation.[24582] [51639]

For the adjunctive treatment of bacterial meningitis† (non-tuberculous)

Intravenous dosage

Adults

0.15 mg/kg/dose IV every 6 hours for 2 to 4 days; the first dose should be given 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The Infectious Diseases Society of America (IDSA) recommends dexamethasone for the treatment of proven or suspected pneumococcal meningitis due to S. pneumoniae. The IDSA suggests dexamethasone in these patients may reduce neuronal injury mediated by proinflammatory cytokine expression. Adjunctive dexamethasone should not be administered to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA does not routinely recommend dexamethasone as adjunctive therapy for meningitis caused by any other bacterial pathogens. For the treatment of tuberculous (TB) meningitis, use doses for adjunctive treatment of TB.[32690]

Infants, Children, and Adolescents

0.15 mg/kg/dose IV every 6 hours for 2 to 4 days is recommended by the Infectious Diseases Society of America (IDSA) for the treatment of meningitis due to H. influenzae type B; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The IDSA suggests dexamethasone in these patients may reduce hearing impairment and neuronal injury mediated by proinflammatory cytokine expression. Do not administer adjunctive dexamethasone to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA and the American Academy of Pediatrics (AAP) do not recommend routine dexamethasone as adjunctive therapy for meningitis caused by bacterial pathogens other than H. influenzae type B in pediatric patients. The use of dexamethasone in pneumococcal meningitis (S. pneumoniae) is controversial and may be considered in patients older than 6 weeks of age after weighing the possible benefits and risks.[32690]

Neonates

The Infectious Diseases Society of America (IDSA) does not recommend adjunctive steroid therapy for neonates with bacterial meningitis due to insufficient data.[32690]

Oral dosage

Adults

0.15 mg/kg/dose PO every 6 hours for 2 to 4 days; the first dose should be given 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The Infectious Diseases Society of America (IDSA) recommends dexamethasone for the treatment of proven or suspected pneumococcal meningitis due to S. pneumoniae. The IDSA suggests dexamethasone in these patients may reduce neuronal injury mediated by proinflammatory cytokine expression. Adjunctive dexamethasone should not be administered to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA does not routinely recommend dexamethasone as adjunctive therapy for meningitis caused by any other bacterial pathogens. For the treatment of tuberculous (TB) meningitis, use doses for adjunctive treatment of TB.[32690]

Infants, Children, and Adolescents

0.15 mg/kg/dose PO every 6 hours for 2 to 4 days is recommended by the Infectious Diseases Society of America (IDSA) for the treatment of meningitis due to H. influenzae type B; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The IDSA suggests dexamethasone in these patients may reduce hearing impairment and neuronal injury mediated by proinflammatory cytokine expression. Do not administer adjunctive dexamethasone to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA and the American Academy of Pediatrics (AAP) do not recommend routine dexamethasone as adjunctive therapy for meningitis caused by bacterial pathogens other than H. influenzae type B in pediatric patients. The use of dexamethasone in pneumococcal meningitis (S. pneumoniae) is controversial and may be considered in patients older than 6 weeks of age after weighing the possible benefits and risks.[32690]

Neonates

The Infectious Diseases Society of America (IDSA) does not recommend adjunctive steroid therapy for neonates with bacterial meningitis due to insufficient data.[32690]

For the treatment of complicated or disseminated pulmonary tuberculosis infection (i.e., tuberculous meningitis and pericarditis) as adjunctive therapy in combination with antituberculous therapy

Oral dosage (dexamethasone)

Adults

The FDA-labeled initial dose is 0.75 to 9 mg/day PO depending on the disease severity.[54286] Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis. For meningitis, the Infectious Diseases Society of America (IDSA) recommends 12 mg/day PO for the initial 3 weeks, with doses tapered during the next 3 weeks.[33275] Alternatively for CNS infections in HIV patients, a dose of 0.3 to 0.4 mg/kg/day PO for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day PO, then reduce to 4 mg/day PO and taper by 1 mg/week for a total duration of approximately 12 weeks.[34362] Initial doses in clinical trials for tuberculosis in general have ranged from 2.25 to 16 mg/day IV or IM for 4 to 8 weeks; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of corticosteroids.[55862] A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis which may be influenced by genetic variation at the LTA4H gene.[55862]

Children and Adolescents weighing at least 25 kg

12 mg/day PO for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA).[33275] The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses.[53387] 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286]

Children and Adolescents weighing less than 25 kg

8 mg/day PO for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA).[33275] The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses.[53387] 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286]

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)

Adults

The FDA-labeled initial dose is 0.5 to 9 mg/day IV or IM depending on disease severity.[54557] Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis. For meningitis, the Infectious Diseases Society of America (IDSA) recommends 12 mg/day IV or IM for the initial 3 weeks, with doses tapered during the next 3 weeks.[33275] Alternatively for CNS infections in HIV patients, a dose of 0.3 to 0.4 mg/kg/day IV or IM for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day PO, then 4 mg/day PO and taper by 1 mg/week for a total duration of approximately 12 weeks.[34362] Initial doses in clinical trials for tuberculosis in general have ranged from 2.25 to 16 mg/day IV or IM for 4 to 8 weeks; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of corticosteroids.[55862] A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis which may be influenced by genetic variation at the LTA4H gene.[55862]

Children and Adolescents weighing at least 25 kg

12 mg/day IV or IM for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA).[33275] The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses.[53387] 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286]

Children and Adolescents weighing less than 25 kg

8 mg/day IV or IM for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA).[33275] The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses.[53387] 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286]

For the treatment of kidney transplant rejection in conjunction with other immunosuppressants or for the treatment of acute graft-versus-host disease (GVHD)

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate solution for injection)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in divided doses. Adjust according to patient response. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection.[51730] [51731]

Children and Adolescents

0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IM or IV in divided doses every 6 to 12 hours. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection.[51730] [51731]

For the reduction of edema and inflammation associated with selected cases of otitis externa

Otic dosage (using dexamethasone sodium phosphate ophthalmic solution)

Adults, Adolescents, and Children

Instill 3 or 4 drops (ophthalmic solution) into the aural canal 2 to 3 times per day. When a favorable response is obtained, reduce dosage gradually and eventually discontinue. If preferred, the aural canal may be packed with a gauze wick saturated with solution. Keep the wick moist with solution and remove from the ear after 12 to 24 hours. May repeat as needed at the discretion of the prescriber. There is no specific otic solution preparation; use ophthalmic solution. Used for steroid responsive inflammatory conditions of the external auditory meatus, such as allergic otitis externa, selected purulent and nonpurulent infective otitis externa when the hazard of steroid use is accepted to decrease edema and inflammation.[54348]

For the treatment of chemotherapy-induced nausea/vomiting† (CINV†) and for chemotherapy-induced nausea/vomiting prophylaxis†

Intravenous (dexamethasone sodium phosphate injection solution) or Oral dosage (dexamethasone)

Adults

American Society of Clinical Oncology (ASCO) guideline-based dosage regimens are stratified according to patient risk. HIGHLY EMETOGENIC CHEMOTHERAPY: 12 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 to 3 or days 2 to 4. If aprepitant is not included in the anti-emetic regimen, increase to dexamethasone 20 mg PO or IV prior to chemotherapy, then 16 mg PO or IV on days 2 to 3 or days 2 to 4. MODERATELY EMETOGENIC CHEMOTHERAPY: 8 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 and 3. LOW EMOTOGENIC RISK CHEMOTHERAPY: 8 mg PO or IV as a single dose prior to chemotherapy.[49434] (NOTE: Other regimens have been used historically during chemotherapy - e.g., 10 to 20 mg IV before administration of chemotherapy, with additional, lower doses given for 24 to 72 hours, as needed).

Children and Adolescents

10 to 14 mg/m2/dose IV is usually used prior to chemotherapy. A 5-HT3 antagonist is usually given along with dexamethasone for highly-emetogenic chemotherapy. An example regimen: dexamethasone 10 mg/m2/dose IV once daily, along with ondansetron. Some patients receive repeat dexamethasone every 12 hours, either IV or PO, but optimal regimens for repeat dosing are not established. For chemotherapy that is less emetogenic, doses as low as 6 mg/m2/dose PO have been given. The optimal dose of steroids for chemotherapy-induced nausea/vomiting (CINV) in children is not determined, and there are safety considerations.[49435] [54434]

For the treatment of pruritus and inflammatory effects of corticosteroid-responsive dermatologic disorders, including dermatitis, alopecia areata, atopic dermatitis, bullous dermatitis herpetiformis, contact dermatitis (including Rhus dermatitis due to poison ivy, poison oak, poison sumac), discoid lupus erythematosus, eczema, exfoliative dermatitis, granuloma annulare, keloids, lichen planus, lichen simplex chronicus or neurodermatitis, necrobiosis lipoidica diabeticorum, pemphigus, polymorphous light eruption, plaque psoriasis, cutaneous T-cell lymphoma (CTCL) or mycosis fungoides, severe seborrheic dermatitis, and erythema multiforme or Stevens-Johnson syndrome

For adjunctive therapy in the treatment of rheumatic disorders including acute gouty arthritis, ankylosing spondylitis, rheumatoid arthritis, juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), post-traumatic osteoarthritis, synovitis of osteoarthritis, and for psoriatic arthritis; or for the treatment of acute episodes or exacerbation of nonrheumatic inflammatory conditions including acute and subacute bursitis, epicondylitis, acute non-specific tenosynovitis, and cystic tumors of an aponeurosis tendon (ganglia)

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.[30011]

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response.

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection solution)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust maintenance dosage according to patient response.[60760]

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

Intra-Articular or Intrasynovial injection dosage (dexamethasone sodium phosphate injection solution)

Adults

Dosage ranges from 2 to 4 mg for large joints and 0.8 to 1 mg for small joints. Injection into intervertebral joints should not be attempted at any time and hip joint injection cannot be recommended as an office procedure. Intrasynovial should be employed only when affected areas are limited to 1 or 2 sites. May repeat from once every 3 to 5 days to once every 2 to 3 weeks.[60760]

Intralesional or Soft Tissue dosage (dexamethasone sodium phosphate injection solution)

Adults

The 4 mg/mL injection strength may be used for intralesional and soft tissue administration. Doses range from 0.2 mg to 4 mg injected as a single dose at the appropriate site. For soft tissue and bursal injections a dose of 2 to 4 mg is recommended. Ganglia require a dose of 1 to 2 mg. A dose of 0.4 to 1 mg is used for injection into tendon sheaths. Usually employed when condition to be treated is limited to 1 or 2 sites. Dosage dependent upon degree of inflammation, size, disease state, and location of affected area. Repeat doses may be given from once every 3 to 5 days to once every 2 to 3 weeks.[60760]

For the treatment of hematologic disorders such as secondary thrombocytopenia in adults, autoimmune hemolytic anemia, erythroblastopenia, congenital hypoplastic anemia, and thrombocytopenia associated with immune thrombocytopenic purpura (ITP)

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response. In an open study of 10 patients with ITP, pulse dosing produced a sustained improvement in platelet count with a total daily dose of 40 mg/day PO for 4 consecutive days out of each 28 day cycle for 6 consecutive cycles.[24390]

Infants, Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response.

Intramuscular or Intravenous dosage (dexamethasone sodium phosphate)

Adults

Initially, 0.5 to 9 mg/day IV or IM, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

For the treatment of respiratory conditions including aspiration pneumonitis, berylliosis, chronic obstructive pulmonary disease (COPD), Loeffler's syndrome, or noncardiogenic pulmonary edema†

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.

Infants, Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.[54557]

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.

For the treatment of acute respiratory distress syndrome (ARDS)†

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

Children and Adolescents

0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IV or IM, in divided doses every 6 to 12 hours.

For asthma exacerbation

Oral dosage

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.[54286] Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Use parenteral dexamethasone dosage for severe respiratory conditions or those compromising the airway.[64807]

Infants, Children, and Adolescents

0.6 mg/kg/dose PO as a single dose or once daily for 2 days. Max: 16 mg/dose.[54531] [54533] [59736] [59737] [64934] Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway. Single or 2-day regimens of dexamethasone have shown similar efficacy, less vomiting, and improved compliance when compared to a 5-day course of oral prednisone or prednisolone.[54531] [54533] [59736] [59737] Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects.[64807] Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.[33558] Of note, 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved initial dosage range for dexamethasone; however, this is significantly lower than the range used in clinical practice.[54286]

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate solution injection)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.[54285] Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects.[64807]

Infants, Children, and Adolescents

0.6 mg/kg/dose IV or IM as a single dose or once daily for 2 days. Max: 16 mg/dose.[54357] [59738] [64934] Single-dose regimens ranging from 0.3 to 1.7 mg/kg/dose have been reported. Max: 36 mg/dose.[59736] In a study of young children with moderate exacerbations, a single day regimen of parenteral dexamethasone resulted in similar efficacy as a 5-day course of oral prednisolone.[59738] Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects.[64807] Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.[33558] Of note, 0.5 to 9 mg per day IV or IM is the FDA-approved initial dosage range depending on the condition being treated; however, higher doses are sometimes used in clinical practice.[54285] [54286]

For the treatment of laryngotracheobronchitis (croup)†

Oral, Intravenous, or Intramuscular dosage

Infants, Children, and Adolescents

0.6 mg/kg/dose PO, IV, or IM (Max: 8 to 20 mg/dose depending on study) as a single dose is the most commonly used regimen; however, lower doses of 0.15 mg/kg/dose PO, IV, or IM (Max: 3 mg/dose) have been shown to have similar efficacy.[44772] [54351] [54542] [54543] [54544]

For fetal lung maturation and neonatal respiratory distress syndrome prophylaxis† in patients at risk for preterm delivery

Intramuscular dosage (dexamethasone sodium phosphate)

Pregnant females

6 mg IM every 12 hours for 4 doses in all pregnant women between 24 and 34 weeks gestation who are at risk for preterm delivery within 7 days. A single course of corticosteroids may also be considered starting at 23 weeks gestation for pregnant women who are at risk of preterm delivery within 7 days, regardless of membrane status. If labor is impending and further doses are unlikely, the first dose of dexamethasone should still be given because treatment with corticosteroids for less than 24 hours is still associated with a significant reduction in neonatal morbidity/mortality. However, no additional benefit has been demonstrated for courses of antenatal steroids with shorter dosage intervals than those recommended, often referred to as accelerated dosing, even when delivery is imminent. A repeat or rescue course of corticosteroids may be considered in women who are less than 34 weeks gestation, who are at risk of preterm delivery within the next 7 days, and whose prior course of antenatal corticosteroids was administered more than 14 days previously. Rescue course corticosteroids could be provided as early as 7 days from the prior dose if indicated by the clinical situation.[64435] Dexamethasone is comparable to betamethasone in preventing adverse outcomes and reducing neonatal intensive care unit (NICU) stays.[60414]

For the prevention of chronic lung disease (CLD)† in mechanically ventilated neonates

Intravenous dosage (dexamethasone sodium phosphate)

Preterm Neonates

Numerous dosing schedules have been studied. The Dexamethasone: A Randomized Trial (DART) study (n = 70, median gestational age 25 weeks) used the following tapering dose schedule over 10 days: 0.075 mg/kg/dose IV twice daily for 3 days, 0.05 mg/kg/dose IV twice daily for 3 days, 0.025 mg/kg/dose IV twice daily for 2 days, and 0.01 mg/kg/dose IV twice daily for 2 days. This dosing regimen facilitated extubation by day 10 but did not significantly improve mortality or oxygen dependence at 36 weeks; follow-up at 2 years of age did not indicate any significant adverse neurodevelopmental outcomes in patients treated with dexamethasone.[54555] [54556] Use is somewhat controversial, and most experts suggest using low doses and careful patient selection. The American Academy of Pediatrics (AAP) recommends against the use of high-dose dexamethasone (greater than 0.5 mg/kg/day) due to the risk of short- and long-term adverse effects, including neurodevelopmental effects.[54338] Late corticosteroid therapy (initiated after 7 days of age) may be preferred over early therapy (initiated at less than 7 days of age). Late therapy may reduce neonatal mortality without significantly increasing potential adverse long-term neurodevelopmental outcomes.[64673] [64674]

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust to patient response.[30011]

For the treatment of nephrotic syndrome to induce diuresis or decrease proteinuria

Oral dosage

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response until urine is protein-free, then slowly taper as indicated. Some patients may require long-term dosing.

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response.

Intravenous or Intramuscular dosage

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

For therapy in selected cases of acute rheumatic carditis, systemic dermatomyositis (polymyositis), systemic lupus erythematosus (SLE), temporal arteritis, Churg-Strauss syndrome†, mixed connective tissue disease†, polyarteritis nodosa†, relapsing polychondritis†, polymyalgia rheumatica†, symptomatic sarcoidosis, vasculitis†, or Wegener's granulomatosis†; also for the treatment of neurologic or myocardial involvement associated with trichinosis

Oral dosage

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosing can be quite variable, depending on the patient's condition. Adjust according to patient response.

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response.

Intramuscular or Intravenous dosage (dexamethasone sodium phosphate)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

For the treatment of Hodgkin lymphoma

Oral dosage

Adults and Children

Dosages vary depending upon the chemotherapy protocol. Common doses include 1.5 to 6 mg/m2/day PO for 8 to 21 days or 8 mg PO every 8 hours for 10 days.

For the treatment of non-Hodgkin's lymphoma (NHL)

For the treatment of acute lymphocytic leukemia (ALL)

Oral dosage

Adults

6 to 10 mg/m2/day PO for 14 days as part of induction, consolidation, or intensification combination regimens.

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range [54286]; however, doses may vary according to the specific protocol used.

Intravenous or Intramuscular dosage

Adults

Initially, 0.5 to 9 mg IV or IM daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate response. Taper dexamethasone gradually in patients receiving parenteral therapy for more than a few days; do not abruptly stop treatment.[60760]

Adolescents, Children, and Infants

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range [54285] [54286]; however, doses may vary according to the specific protocol used.

For the treatment of multiple myeloma

For the treatment of acute exacerbations of multiple sclerosis

Oral dosage

Adults

30 mg/day PO for 7 days, followed by doses of 4 to 12 mg PO every other day for 1 month have been shown to be effective. Controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations, they do not show that they affect the ultimate outcome or natural history of the disease.[30011]

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response.

Intravenous† or Intramuscular dosage†

Infants, Children, and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

For the treatment of a critical period of regional gastroenteritis (Crohn's disease) or ulcerative colitis

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.[30011] Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.[64393] [64397]

Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.[64393] [64397]

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection solution)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.[60760] Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.[64393] [64397]

Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.[64393] [64397]

For the treatment of steroid-responsive inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment inflammation of the globe, such as allergic conjunctivitis, eyelid acne rosacea, superficial punctate keratitis, herpes zoster ocular infection associated keratitis, iritis, cyclitis, vernal keratoconjunctivitis, selected infective viral conjunctivitis or postoperative ocular inflammation when the inherent hazard of steroid use is accepted to obtain an advisable diminution in edema and inflammation; corneal abrasion, corneal ulcer, or corneal injury from chemical or thermal burns, or penetration of foreign bodies; systemic treatment may be indicated for uveitis, sympathetic ophthalmia, and ocular inflammatory conditions unresponsive to topical corticosteroids

Ophthalmic dosage (ophthalmic solution)

Adults, Adolescents, and Children

Instill 1 or 2 drops of 0.1% ophthalmic solution in the affected eye(s) every hour during the day and every 2 hours at night; reduce application to every 4 hours (while awake) once a favorable response occurs. Later, further reduction in dosage to 1 drop 3 or 4 times daily may suffice to control symptoms.[54348] The duration of treatment will vary with the type of lesion and may extend from a few days to several weeks, according to therapeutic response. Relapses, more common in chronic active lesions than in self-limited conditions, usually respond to treatment.

Ophthalmic dosage (ophthalmic suspension)

Adults, Adolescents, and Children

Instill 1 or 2 drops of 0.1% ophthalmic suspension in the affected eye(s). In severe disease, drops may be used hourly, being tapered to discontinuation as the inflammation subsides. In mild disease, drops may be used up to 4 to 6 times daily.[61633]

Oral dosage (dexamethasone)

Adults

Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.[54286]

Infants, Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.[54286] Adjust according to patient response.

Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)

Adults

Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.[54285] [54286]

Infants, Children and Adolescents

0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.[54285] [54286] Adjust according to patient response.

For the treatment of diabetic macular edema

Intravitreal implant dosage (Ozurdex dexamethasone intravitreal implant only)

Adults

Inject the implant (containing 0.7 mg dexamethasone in a solid polymer delivery system) intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis.[41921] According to the American Diabetes Association (ADA), intravitreous steroid injections are considered second-line alternative treatment options for central-involved diabetic macular edema (CIDME). These drugs are rarely used as first-line treatment options, because when compared against intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents, steroid therapies are associated with inferior visual acuity outcomes and increased rate of cataracts and glaucoma.[61821]

For the treatment of macular edema following retinal vein occlusion, including branch retinal vein occlusion (BRVO) or central retinal vein occlusion (CRVO)

Intravitreal implant dosage (Ozurdex dexamethasone intravitreal implant only)

Adults

Inject the implant (containing 0.7 mg dexamethasone in a solid polymer delivery system) intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis.[41921]

For the treatment of acute altitude sickness†, including the treatment of high altitude cerebral edema

Oral (dexamethasone) or Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)

Adults

4 mg PO, IV, or IM every 6 hours for the treatment of acute altitude sickness without high altitude cerebral edema (HACE) or 8 mg PO, IV, or IM once followed by 4 mg PO, IV, or IM every 6 hours for the treatment of HACE is recommended by clinical practice guidelines.[56782] [56794] Descent is the preferred initial treatment. When descent is not possible or effective, symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including dexamethasone, should be considered. Dexamethasone is more reliably effective than acetazolamide for acute altitude sickness of any degree, especially moderate to severe illness. Consideration can be given to adding acetazolamide for persons with HACE. Continue treatment until symptoms resolve. Of note, dexamethasone does not facilitate acclimatization.[56782]

Infants, Children, and Adolescents

0.15 mg/kg/dose PO, IV, or IM every 6 hours (Max: 4 mg/dose).[56782] [56794] Descent is the preferred initial treatment, particularly for younger children and infants. When descent is not effective or not possible, dexamethasone is the preferred pharmacologic therapy, especially for moderate to severe disease. Symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including acetazolamide, should also be considered. Dexamethasone does not facilitate acclimatization; advise patients to delay further ascent until they are asymptomatic off medication. If the drug is discontinued at altitude before acclimatization, rebound can occur.[56398] [56782]

For altitude sickness prophylaxis, including prevention of high altitude cerebral edema

Oral dosage

Adults

2 mg PO every 6 hours or 4 mg PO every 12 hours is recommended by clinical practice guidelines.[56782] [56794] 4 mg PO every 6 hours may be considered for very high risk situations necessitating immediate physical performance after being airlifted to high altitudes (e.g., military or search and rescue operations).[56782] Prophylactic medications should be considered in addition to slow ascent for moderate- to high-risk situations, and acetazolamide is preferred. Dexamethasone may be used in individuals with a history of intolerance or allergy to acetazolamide, or in emergency circumstances that require very rapid ascent, dexamethasone may be considered for concomitant use with acetazolamide. Start prophylaxis with dexamethasone the day of the ascent and continue prophylaxis for 2 to 3 days after reaching the target altitude or until descent is initiated. Duration of use should not exceed 10 days to prevent glucocorticoid toxicity or adrenal suppression.[56782]

For the adjunctive treatment of infertility† in combination with clomiphene therapy

Oral dosage

Adult females

0.5 mg PO once daily at bedtime, administered on cycle days 3 to 12, days 5 to 9, or starting on day 5 and continuing through conception, in combination with clomiphene (doses ranging from 50 to 200 mg/day) has been studied.[32778] [32779] [32781] Alternatively, dexamethasone 2 mg PO once daily on cycle days 5 to 14 in combination with clomiphene 200 mg/day or dexamethasone 1 mg PO twice daily on cycle days 3 to 12 in combination with clomiphene 100 mg/day PO has also been studied; HCG was administered to augment ovulation.[32780] [32782] Optimal timing and dose of dexamethasone is not clear and has varied from study to study. Combination therapy has been shown to increase ovulation rates (range, 75% to 100%) and pregnancy rates (range, 38% to 74%) in women with both normal and elevated DHEA-S concentrations and in those women with or without polycystic ovary syndrome (PCOS). A Cochrane's review indicates that dexamethasone-clomiphene combination is one of the few adjunctive therapies for infertility that has been shown to improve pregnancy rates (fixed OR 11.3, 95% CI 5.3 to 24; NNT 2.7, 95% CI 2.1 to 3.6) [32783]; the 2 studies in this review used differing doses of 0.5 mg PO at bedtime on days 5 to 9 or 2 mg PO/day on days 5 to 14.[32778] [32782] Several theories on the mechanism of dexamethasone in infertility exist. One theory is that dexamethasone enhances folliculogenesis by suppressing adrenal androgen hypersecretion, which should augment the actions of clomiphene. Dexamethasone may increase FSH concentrations thereby facilitating folliculogenesis. Finally, dexamethasone may decrease the elevated LH concentrations in patients with PCOS.

For the treatment of post-operative nausea/vomiting (PONV)†

Intravenous dosage (dexamethasone sodium phosphate injection)

Adults

2 to 4 mg IV once for established post-operative nausea/vomiting (PONV), per treatment guidelines; readministration of longer-acting drugs, such as dexamethasone, is not recommended.[57398] If PONV prophylaxis was either inadequate or not initially given, dexamethasone is an appropriate rescue treatment option if not initially used for PONV prophylaxis. Of note, the 5-HT3 antagonists are the only class of drugs that have been adequately studied for the treatment of established PONV.[57398]

For post-operative nausea/vomiting (PONV) prophylaxis†

Intravenous dosage (dexamethasone sodium phosphate injection solution)

Adults

4 to 5 mg IV at anesthesia induction is recommended by treatment guidelines for patients at an increased risk for post-operative nausea and vomiting (PONV); administration at induction rather than at the end of surgery is preferred. Some studies suggest that 8 mg IV is associated with a dose-dependent increase in quality of recovery, including reduced fatigue, postoperative pain, and need for opioid analgesia; however, further confirmation is necessary before larger doses are universally recommend. Safety data regarding the perioperative use of dexamethasone point to a possible increased risk of wound infection and/or increased blood glucose in some patients. A single dexamethasone dose (4 to 8 mg IV) is, however, considered safe for PONV prophylaxis. For patients with labile glucose control, dexamethasone use is relatively contraindicated.[57398]

Children and Adolescents

0.15 to 1 mg/kg/dose IV (Max: 8 to 25 mg/dose IV) given as a single intraoperative dose reduces the incidence of postoperative nausea/vomiting in the first 24 hours, improves postoperative pain control, and decreases the time to resumption of soft/solid diet without adverse effects and is recommended in patients undergoing tonsillectomy.[54553] [54554] A lower dose of 0.015 mg/kg/dose (Max: 5 mg/dose) in combination with ondansetron 0.1 mg/kg/dose (Max: 4 mg) is recommended first-line for postoperative vomiting prophylaxis in children by the Society for Ambulatory Anesthesiology.[57398]

For the treatment of bronchiolitis†

Oral dosage

Infants

Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting.[58442] However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients.[54551] One randomized trial of 800 infants seen in the emergency department used 1 mg/kg PO once (Max: 10 mg/dose) followed by 0.6 mg/kg/dose PO once daily (Max: 10 mg/dose) for 5 days. Dexamethasone in combination with nebulized epinephrine was effective in reducing hospital admissions by day 7 of illness compared to treatment with dexamethasone alone, epinephrine alone, or placebo.[39327] In a study of 200 infants (median age 3.5 months) with an asthma risk, as determined by eczema or a family history of asthma in a first-degree relative, dexamethasone 1 mg/kg (single dose) PO then 0.6 mg/kg/dose PO once daily for 4 more days was administered with salbutamol. In infants receiving dexamethasone with salbutamol, the time to readiness for discharge was 18.6 hours vs. 27.1 hours in patients not receiving dexamethasone (p = 0.015).[56911] In contrast, 1 mg/kg/dose PO (Max: 12 mg/dose) given as a single dose did not reduce hospitalization rates, Respiratory Assessment Change Scores (RACS), length of hospitalization for those patients who required admission, or subsequent hospitalizations within 7 days compared to placebo in another large, randomized trial (n = 600).[33394]

Intravenous dosage (dexamethasone sodium phosphate injection solution)

Infants

Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting.[58442] However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients.[54551] 0.15 mg/kg/dose IV every 6 hours for 48 hours with the first dose administered within 24 hours of mechanical ventilation was used in patients with respiratory syncytial virus. In a post hoc analysis of patients with bronchiolitis (n = 39), the mean duration of mechanical ventilation and of supplemental oxygen were significantly shorter in patients receiving dexamethasone compared to those receiving placebo (4.9 and 7.7 days vs. 9.2 and 11.3 days, respectively); no differences were seen in the length of intensive care unit or hospital stay.[54547]

For the treatment of Waldenstrom macroglobulinemia†

For the treatment of amyloidosis†

Therapeutic Drug Monitoring

Maximum Dosage Limits

    Patients with Hepatic Impairment Dosing

    Systemic dosage may need adjustment depending on the degree of hepatic insufficiency, but quantitative recommendations are not available.

    Patients with Renal Impairment Dosing

    Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

    † Off-label indication
    Revision Date: 07/20/2020, 09:01:10 AM

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Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.54338 - American Academy of Pediatrics Committee on Fetus and Newborn. Postnatal corticosteroids to prevent or treat bronchopulmonary dysplasia. Pediatrics 2010;126:800-8.54348 - Dexamethasone sodium phosphate ophthalmic solution package insert. Bridgewater, NJ: Bausch and Lomb Inc.; 2016 June.54351 - Bjornson CL, Klassen TP, Williamson J, et al. A randomized trial of a single dose of oral dexamethasone for mild croup. N Engl J Med 2004;351:1306-1313.54357 - Ebrahimi S, Sarkari B. Comparative efficacy of dexamethasone versus hydrocortisone in severe acute pediatric asthma. Iran J Allergy Asthma Immunol 2007;6:159-60.54396 - Tellez DW, Galvis AG, Storgion SA, et al. Dexamethasone in the prevention of stridor in children. J Pediatr 1991;118:289-94.54434 - Holdsworth MT, Raisch DW, Frost J. Acute and delayed nausea and emesis control in pediatric oncology patients. Cancer. 2006;106:931-940.54489 - Rivkees SA. Dexamethasone therapy of congenital adrenal hyperplasia and the myth of the "growth toxic" glucocorticoid. Int J Pediatr Endocrinol 2010:1-7.54490 - Joint LWPES/ESPE CAH Working Group. Consensus statement on 21-hydroxylase deficiency from the Lawson Wilkins Pediatric Endocrine Society and the European Society for Paediatric Endocrinology. J Clin Endocrinol Metab 2002;87:4048-53.54499 - White PC. Cushing syndrome. In: Kliegman RM, Stanton BF, St. Geme JW, et al., eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia: Elsevier;2011:1939-41.54501 - Batista DL, Riar J, Keil M, et al. Diagnostic tests for children who are referred for the investigation of Cushing syndrome. Pediatrics 2007;120:575-86.54507 - Anene O, Meert KL, Uy H, et al. Dexamethasone for the prevention of postextubation airway obstruction: a prospective, randomized, double-blind, placebo-controlled trial. Crit Care Med 1996;24:1666-9.54508 - Khemani RG, Randolph A, Markovitz B. Corticosteroids for the prevention and treatment of post-extubation stridor in neonates, children and adults. Cochrane Database Syst Rev 2009;3:CD001000.54509 - Davis PG, Henderson-Smart DJ. Intravenous dexamethasone for extubation of newborn infants. Cochrane Database Syst Rev 2001;4:CD000308.54512 - Pfenninger J, Kaiser G, Lutschg J, et al. Treatment and outcome of the severely head injured child. Intensive Care Med 1983;9:13-6.54531 - Greenberg RA, Kerby G, Roosevely GE. A comparison of oral dexamethasone with oral prednisone in pediatric asthma exacerbations treated in the emergency department. Clin Pediatr (Phila) 2008;47:817-23.54533 - Qureshi F, Zaritsky A, Poirier MP. Comparative efficacy of oral dexamethasone versus oral prednisone in acute pediatric asthma. J Pediatr 2001;139:20-6.54542 - Rittichier KK, Ledwith CA. Outpatient treatment of moderate croup with dexamethasone: intramuscular versus oral dosing. Pediatrics 2000;106:1344-8.54543 - Geelhoed GC, Macdonald WB. Oral dexamethasone in the treatment of croup: 0.15mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Pediatr Pulmonol 1995;20:362-8.54544 - Chub-Uppakarn S, Sangsupawanich P. A randomized comparison of dexamethasone 0.15 mg/kg versus 0.6 mg/kg for the treatment of moderate to severe croup. Int J Pediatr Otorhinolaryngol 2007;71:473-7.54547 - van Woensel JB, van Aalderen WM, de Weerd W, et al. Dexamethasone for treatment of patients mechanically ventilated for lower respiratory tract infection caused by respiratory syncytial virus. Thorax 2003;58:383-7.54551 - de Benedictis FM, Bush A. Corticosteroids in respiratory diseases in children. Am J Respir Crit Care Med 2012;185:12-232.54553 - Baugh RF, Archer SM, Mitchell RB. Clinical practice guideline: tonsillectomy in children. Otolaryngol Head Neck Surg 2011;144:S1-30.54554 - Steward DL, Grisel J, Meinzen-Derr J. Steroids for improving recovery following tonsillectomy in children. Cochrane Database Syst Rev 2011;8:CD003997.54555 - Doyle LW, Davis PG, Morley CJ, et al. Low-dose dexamethasone facilitates extubation among chronically ventilator-dependent infants: a multicenter, international, randomized, controlled trial. Pediatrics 2006;117:75–83.54556 - Doyle LW, Davis PG, Morley CJ, et al. Outcome at 2 years of age of infants from the DART study: a multicenter, international, randomized, controlled trial of low-dose dexamethasone. Pediatrics 2007;119:716–21.54557 - Dexamethasone sodium phosphate injection package insert. Schaumburg IL: APP Pharmaceuticals; 2008 Jan.55862 - Critchley JA, Young F, Orton L, et al. Corticosteroids for prevention of mortality in people with tuberculosis: a systematic review and meta-analysis. Lancet Infect Dis 2013;13:223-37.56398 - Pollard AJ, Niermeyer S, Barry P, et al. Children at high altitude: an international consensus statement by an ad hoc committee of the international society for mountain medicine, March 12, 2001. High Alt Med Biol 2001;2:389-403.56782 - Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med 2010;21:146-55.56794 - Centers for Disease Control and Prevention (CDC). Travelers' Health. Chapter 2: The Pre-Travel Consultation. Retrieved March 4, 2014. Available on the World Wide Web at: http://wwwnc.cdc.gov/travel/yellowbook/2014/chapter-2-the-pre-travel-consultation/altitude-illness56911 - Alansari K, Sakran M, Davidson BL, et al. Oral dexamethasone for bronchiolitis: a randomized trial. Pediatrics. 2013; 132: e810-e816.57398 - Gan TJ, Diemunsch P, Habib AS, et al. Consensus guidelines for the management of postoperative nausea and vomiting. Anesth Analg 2014;118:85-113.58442 - Ralson SL, Lieberthal AS, Meissner HC. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics 2014;134:e1474-1502.58806 - Revlimid (lenalidomide) tablets package insert. Summit, NJ: Celgene Corporation; 2019 May.58821 - Farydak (panobinostat) capsules package insert. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2016 June.58822 - San-Miguel JF, Hungria VT, Yoon SS, et al. Panobinostat plus bortezomib and dexamethasone versus placebo plus bortezomib and dexamethasone in patients with relapsed or relapsed and refractory multiple myeloma: a multicentre, randomised, double-blind phase 3 trial. Lancet Oncol 2014;15(11):1195-1206.59736 - Keeney GE, Gray MP, Morrison AK. Dexamethasone for acute asthma exacerbations in children: a meta-analysis. Pediatrics 2014;133:493-499.59737 - Altamimi S, Robertson G, Jastaniah W. Single-dose oral dexamethasone in the emergency management of children with exacerbations of mild to moderate asthma. Pediatr Emerg Care 2006;22:786-793.59738 - Gordon S, Tompkins T, Dayan PS. Randomized trial of single-dose intramuscular dexamethasone compared with prednisolone for children with acute asthma. Pediatr Emerg Care 2007;23:521-527.60044 - Stewart AK, Rajkumar SV, Dimopoulos MA, et al. Carfilzomib, lenalidomide, and dexamethasone for relapsed multiple myeloma. N Engl J Med 2015;372(2):142-152.60311 - Darzalex (daratumumab) injection package insert. Horsham, PA: Janssen Biotech, Inc.; 2020 Apr.60353 - Lonial S, Dimopoulos M, Palumbo A, et al. Elotuzumab therapy for relapsed or refractory multiple myeloma. N Engl J Med 2015;373(7):621-631.60354 - Empliciti (elotuzumab) injection package insert. Princeton, NJ: Bristol-Myers Squibb Company; 2019 Oct.60414 - Brownfoot FC, Gagliardi DI, Bain E, et al. Different corticosteroids and regimens for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2013;8:CD006764.60464 - Lieberman P, Nicklas RA, Randolf C, et al. Anaphylaxis - a practice parameter update 2015. Ann Allergy Asthma Immunol 2015;115(5):341-84.60756 - Crump M, Kuruvilla J, Couban S, et al. Randomized comparison of gemcitabine, dexamethasone, and cisplatin versus dexamethasone, cytarabine, and cisplatin chemotherapy before autologous stem-cell transplantation for relapsed and refractory aggressive lymphomas: NCIC-CTG LY.12. J Clin Oncol 2014;32(31):3490-3496.60760 - Dexamethasone sodium phosphate injection package insert. Eatontown, NJ:West-Ward Pharmaceuticals;2014 Sept.60761 - Dexamethasone tablets USP, Dexamethasone oral solution, and Dexamethasone Intensol (oral solution concentrate) package insert. Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.61073 - Dimopoulos MA, Anagnostopoulos A, Kyrtsonis MC, et al. Primary treatment of Waldenstrom macroglobulinemia with dexamethasone, rituximab, and cyclophosphamide. J Clin Oncol 2007;25(22):3344-3349.61131 - Dimopoulos MA, Garcia-Sanz R, Gavriatopoulou M, et al. Primary therapy of Waldenstrom macroglobulinemia (WM) with weekly bortezomib, low-dose dexamethasone, and rituximab (BDR): long-term results of a phase 2 study of the European Myeloma Network (EMN). Blood 2013;122(19):3276-3282.61207 - Palumbo A, Chanan-Khan A, Weisel K, et al. Daratumumab, Bortezomib, and Dexamethasone for Multiple Myeloma. N Engl J Med 2016;375(8):754-766.61321 - Cibeira MT, Oriol A, Lahuerta JJ, et al. A phase II trial of lenalidomide, dexamethasone and cyclophosphamide for newly diagnosed patients with systemic immunoglobulin light chain amyloidosis. Br J Haematol 2015;170(6):804-813.61322 - Palladini G, Russo P, Milani P, et al. A phase II trial of cyclophosphamide, lenalidomide and dexamethasone in previously treated patients with AL amyloidosis. Haematologica 2013;98(3):433-436.61323 - Kumar SK, Hayman SR, Buadi FK, et al. Lenalidomide, cyclophosphamide, and dexamethasone (CRd) for light-chain amyloidosis: long-term results from a phase 2 trial. Blood 2012;119(21):4860-4867.61331 - Dinner S, Witteles W, Afghahi A, et al. Lenalidomide, melphalan and dexamethasone in a population of patients with immunoglobulin light chain amyloidosis with high rates of advanced cardiac involvement. Haematologica 2013;98(10):1593-1599.61332 - Sanchorawala V, Patel JM, Sloan JM, et al. Melphalan, lenalidomide and dexamethasone for the treatment of immunoglobulin light chain amyloidosis: results of a phase II trial. Haematologica 2013;98(5):789-792.61407 - Dimopoulos MA, Oriol A, Nahi H, et al. Daratumumab, lenalidomide, and dexamethasone for multiple myeloma. N Engl J Med 2016;375(14):1319-1331.61633 - Maxidex (dexamethasone ophthalmic suspension 0.1%) package insert. Fort Worth, TX; Alcon Laboratories, Inc.; 2017 Nov.61715 - van Imhoff GW, McMillan A, Matasar MJ, et al. Ofatumumab versus rituximab salvage chemoimmunotherapy in relapsed or refractory diffuse large B-cell lymphoma: The ORCHARRD study. J Clin Oncol 2016. Epub ahead of print. doi: 10.1200/JCO.2016.69.0198.61788 - Durie BG, Hoering A, Abidi MH, et al. Bortezomib with lenalidomide and dexamethasone versus lenalidomide and dexamethasone alone in patients with newly diagnosed myeloma without intent for immediate autologous stem-cell transplant (SWOG S0777): a randomised, open-label, phase 3 trial. Lancet 2017;389(10068):519-527.61821 - Solomon SD, Chew E, Duh EJ, et al. Diabetic retinopathy: a position statement by the American Diabetes Association. Diabetic Care 2017;40:412-418.63796 - Dextenza (dexamethasone ophthalmic insert) package insert. Bedford, MA: Ocular Therapeutix, Inc.; 2019 Jun.64165 - Dexamethasone (Decadron) tablets package insert. Whitehouse Station, NJ: Merck & Co., Inc.; 2019 May.64365 - Facon T, Kumar S, Plesner T, et al. Daratumumab plus lenalidomide and dexamethasone for untreated myeloma. N Engl J Med 2019;380(22):2104-2115.64393 - Rubin DT, Ananthakrishnan AN, Siegel CA, et al.; American College of Gastroenterology Clinical Guideline: Ulcerative Colitis in Adults. Am J Gastroenterol. 2019;114:384–413.64397 - Lichtenstein GR, Loftus EV, Isaacs KL, et al. American College of Gastroenterology Clinical Guideline: Management of Crohn's Disease in Adults. Am J Gastroenterol. 2018;113:481–517.64412 - Richardson PG, Oriol A, Beksac M, et al. Pomalidomide, bortezomib, and dexamethasone for patients with relapsed or refractory multiple myeloma previously treated with lenalidomide (OPTIMISMM): a randomised, open-label, phase 3 trial. Lancet Oncol 2019;20(6):781-794.64435 - American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins-Obstetrics. Practice Bulletin No. 171: Management of Preterm Labor. Obstet Gynecol 2016;128:e155-e164.64528 - Moreau P, Attal M, Hulin C, et al. Bortezomib, thalidomide, and dexamethasone with or without daratumumab before and after autologous stem-cell transplantation for newly diagnosed multiple myeloma (CASSIOPEIA): a randomised, open-label, phase 3 study. Lancet 2019; 394(10192):29-38.64564 - Liyanage CK, Galappatthy P, Seneviratne SL. Corticosteroids in management of anaphylaxis; a systematic review of evidence. Eur Ann Allergy Clin Immunol 2017;49:196-207.64673 - Doyle LW, Cheong JL, Ehrenkranz RA, Halliday HL. Early (8 days) days systemic postnatal corticosteroids for prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Database of Systematic Reviews 2017, Issue 10. Art. No.: CD00114664674 - Doyle LW, Cheong JL, Ehrenkranz RA, Halliday HL. Late (greater than 8 days) systemic postnatal corticosteroids for prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Database of Systematic Reviews 2017, Issue 10. Art. No.: CD00114564807 - Global Strategy for Asthma Management and Prevention. Global Initiative for Asthma (GINA) 2020. Available from: http://www.ginasthma.org. Accessed May 20th, 2020.64934 - Shenoi RP, Timm N, AAP Committee on Drugs, AAP Committee on Emergency Medicine. Drugs used to treat pediatric emergencies. Pediatrics 2020;145:e20193450.65314 - COVID-19 Treatment Guidelines Panel. Coronavirus Diseases 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Accessed July 30, 2020. Available at on the World Wide Web at: https://covid19treatmentguidelines.nih.gov/.

    How Supplied

    Dexamethasone Acetate Solution for injection

    Decadron LA 8mg/ml Solution for Injection (00006-7644) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Acetate Suspension for injection

    Dalalone LA 8mg/ml Suspension for Injection (00456-1075) (Allergan USA, Inc.) (off market)

    Dexamethasone Acetate Suspension for injection

    Dalalone DP 16mg/ml Suspension for Injection (00456-1097) (Allergan USA, Inc.) (off market)

    Dexamethasone Acetate Suspension for injection

    Dalalone DP 16mg/ml Suspension for Injection (00785-9080) (UAD Laboratories Inc) (off market)

    Dexamethasone Elixir

    Baycadron 0.5mg/5ml Elixir (64679-0810) (Wockhardt USA, LLC) (off market)

    Dexamethasone Elixir

    Decadron 0.5mg/5ml Elixir (00006-7622) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Elixir

    Dexamethasone 0.5mg/5ml Elixir (00603-1147) (Par Pharmaceuticals, an Endo Company) (off market)

    Dexamethasone Elixir

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    Dexamethasone Elixir

    Dexamethasone 0.5mg/5ml Elixir (00677-0601) (Sun Pharmaceutical Industries, Inc.) (off market)

    Dexamethasone Elixir

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    Dexamethasone Implant

    Ozurdex 0.7mg Ophthalmic Implant (00023-3348) (Allergan USA, Inc.) null

    Dexamethasone Ophthalmic drops, suspension

    Maxidex 0.1% Ophthalmic Suspension (00998-0615) (Alcon Laboratories, Inc) nullMaxidex 0.1% Ophthalmic Suspension package photo

    Dexamethasone Ophthalmic drops, suspension

    Maxidex 0.1% Ophthalmic Suspension (00065-0615) (Alcon Laboratories, Inc) (off market)

    Dexamethasone Ophthalmic insert

    Dextenza 0.4mg Ophthalmic Insert (70382-0204) (Ocular Therapeutix, Inc.) null

    Dexamethasone Oral solution

    Decadron 0.5mg/5mL Elixir (58463-0010) (Pragma Pharmaceuticals, LLC) (off market)

    Dexamethasone Oral solution

    Dexamethasone 0.5mg/5ml Elixir (60432-0466) (Morton Grove Pharmaceuticals Inc, a subsidiary of Wockhardt, Ltd.) nullDexamethasone 0.5mg/5ml Elixir package photo

    Dexamethasone Oral solution

    Dexamethasone 0.5mg/5ml Elixir (64980-0509) (Rising Pharmaceuticals Inc) nullDexamethasone 0.5mg/5ml Elixir package photo

    Dexamethasone Oral solution

    Dexamethasone 0.5mg/5ml Elixir (00472-0972) (Teva/Actavis US) (off market)Dexamethasone 0.5mg/5ml Elixir package photo

    Dexamethasone Oral solution

    Dexamethasone 0.5mg/5mL Elixir (54879-0003) (STI Pharma LLC) null

    Dexamethasone Oral solution

    Dexamethasone 0.5mg/5ml Solution (00054-3177) (Hikma Pharmaceuticals USA Inc.) nullDexamethasone 0.5mg/5ml Solution package photo

    Dexamethasone Oral solution

    Dexamethasone Intensol 1mg/mL Solution (00054-3176) (Hikma Pharmaceuticals USA Inc.) nullDexamethasone Intensol 1mg/mL Solution package photo

    Dexamethasone Oral tablet

    Dexamethasone 0.25mg Tablet (49884-0083) (Par Pharmaceuticals, an Endo Company) (off market)

    Dexamethasone Oral tablet

    Decadron 0.5mg Tablet (00006-0041) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

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    Decadron 0.5mg Tablet (58463-0014) (Pragma Pharmaceuticals, LLC) null

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Decadron 0.75mg Tablet (00006-0063) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Oral tablet

    Decadron 0.75mg Tablet (58463-0015) (Pragma Pharmaceuticals, LLC) null

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    Dexamethasone Oral tablet

    Dexamethasone 1.5mg Tablet (00054-8181) (Hikma Pharmaceuticals USA Inc.) null

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    DexPak 13-day TaperPak 1.5mg Tablet (00095-0088) (Bausch Health US, LLC) (off market)

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    DexPak 6-day TaperPak 1.5mg Tablet (00095-0089) (ECR Pharmaceuticals) (off market)DexPak 6-day TaperPak 1.5mg Tablet package photo

    Dexamethasone Oral tablet

    DexPak Jr 10-day TaperPak 1.5mg Tablet (00095-0086) (ECR Pharmaceuticals) (off market)

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    HiDex 6-day Tablet (15014-0211) (Gentex Pharma LLC) null

    Dexamethasone Oral tablet

    LoCort 11-Day Tablet (71297-0211) (Allegis Holdings, LLC) (off market)

    Dexamethasone Oral tablet

    LoCort 7-Day Tablet (71297-0127) (Allegis Holdings, LLC) (off market)

    Dexamethasone Oral tablet

    TaperDex 12-Day Tablet (42195-0149) (Xspire Pharma Brand) null

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    TaperDex 7-Day Tablet (42195-0127) (Xspire Pharma Brand) null

    Dexamethasone Oral tablet

    ZCORT 7-Day Tapered 1.5mg Tablet (79043-0200) (Scite Pharma, LLC) null

    Dexamethasone Oral tablet

    Zema-Pak 10-day TaperPak 1.5mg Tablet (44183-0507) (Macoven Pharmaceuticals, LLC, a subsidiary of Currax Pharmaceuticals, LLC) (off market)

    Dexamethasone Oral tablet

    Zema-Pak 13-day TaperPak 1.5mg Tablet (44183-0508) (Macoven Pharmaceuticals, LLC, a subsidiary of Currax Pharmaceuticals, LLC) (off market)

    Dexamethasone Oral tablet

    Zema-Pak 6-day TaperPak 1.5mg Tablet (44183-0509) (Macoven Pharmaceuticals, LLC, a subsidiary of Currax Pharmaceuticals, LLC) (off market)

    Dexamethasone Oral tablet

    ZoDex 12-Day Tablet (42195-0150) (Xspire Pharma, LLC) (off market)

    Dexamethasone Oral tablet

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    ZonaCort 7 Day Tapered 1.5mg Tablet (70868-0107) (Key Therapeutics, LLC) (off market)

    Dexamethasone Oral tablet

    Dexamethasone 2mg Tablet (00054-4183) (Hikma Pharmaceuticals USA Inc.) null

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    Dexamethasone 2mg Tablet (43063-0266) (PD-Rx Pharmaceuticals, Inc.) null

    Dexamethasone Oral tablet

    Decadron 4mg Tablet (00006-0097) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Oral tablet

    Decadron 4mg Tablet (58463-0016) (Pragma Pharmaceuticals, LLC) null

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    Dexamethasone 4mg Tablet (00054-4184) (Hikma Pharmaceuticals USA Inc.) null

    Dexamethasone Oral tablet

    Dexamethasone 4mg Tablet (49884-0087) (Par Pharmaceuticals, an Endo Company) (off market)

    Dexamethasone Oral tablet

    Dexamethasone 4mg Tablet (49884-0087) (Par Pharmaceuticals, an Endo Company) (off market)

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    Dexamethasone 4mg Tablet (00182-1614) (Teva Pharmaceuticals USA) (off market)

    Dexamethasone Oral tablet

    Decadron 6mg Tablet (58463-0017) (Pragma Pharmaceuticals, LLC) null

    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

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    Dexamethasone Oral tablet

    Dexamethasone 6mg Tablet (49884-0129) (Par Pharmaceuticals, an Endo Company) (off market)

    Dexamethasone Oral tablet

    Dexamethasone 6mg Tablet (49884-0373) (Par Pharmaceuticals, an Endo Company) (off market)

    Dexamethasone Sodium Phosphate Inhalation vapour, solution

    Dexacort 84mcg Turbinaire Inhalant (53014-0203) (UCB Pharma Inc) (off market)

    Dexamethasone Sodium Phosphate Inhalation vapour, solution

    Dexacort PH 84mcg Turbinaire Inhalant (53014-0201) (UCB Pharma Inc) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    AK-Dex 0.1% Ophthalmic Solution (17478-0279) (Akorn Inc) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Decadron Phosphate 0.1% Ophthalmic Solution (00006-7643) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Dexamethasone Sodium Phosphate 0.1% Ophthalmic Solution (24208-0720) (Bausch Health US, LLC) nullDexamethasone Sodium Phosphate 0.1% Ophthalmic Solution package photo

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Dexamethasone Sodium Phosphate 0.1% Ophthalmic Solution (00904-3006) (Major Pharmaceuticals Inc, a Harvard Drug Group Company) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Dexamethasone Sodium Phosphate 0.1% Ophthalmic Solution (57319-0065) (Phoenix Pharmaceuticals Inc) null

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Dexamethasone Sodium Phosphate 0.1% Ophthalmic Solution (61314-0294) (Sandoz Inc. a Novartis Company) null

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Dexamethasone Sodium Phosphate 0.1% Ophthalmic Solution (60855-0720) (Sight Pharmaceuticals Inc) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic drops, solution

    Dexamethasone Sodium Phosphate 0.1% Ophthalmic Solution (11695-4188) (WA Butler Co) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic ointment

    Decadron Phosphate 0.05% Ophthalmic Ointment (00006-7615) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Sodium Phosphate Ophthalmic ointment

    Ocu-Dex 0.05% Ophthalmic Ointment (51944-3390) (Ocumed Inc) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Decadron 4mg/ml Solution for Injection (00006-7628) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 120mg/30mL Solution for Injection (55150-0239) (AuroMedics Pharma LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 120mg/30mL Solution for Injection (67457-0421) (Mylan Institutional LLC ) nullDexamethasone Sodium Phosphate 120mg/30mL Solution for Injection package photo

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 120mg/30ml Solution for Injection (NOVAPLUS) (00069-0192) (Mylan Institutional LLC ) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 120mg/30ml Solution for Injection (NOVAPLUS) (00069-0192) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 120mg/30mL Solution for Injection (NOVAPLUS) (67457-0484) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 20mg/5mL Solution for Injection (55150-0238) (AuroMedics Pharma LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 20mg/5mL Solution for Injection (00641-6146) (Hikma Pharmaceuticals USA Inc.) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 20mg/5ml Solution for Injection (NOVAPLUS) (00069-0178) (Mylan Institutional LLC ) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 20mg/5ml Solution for Injection (NOVAPLUS) (00069-0178) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 20mg/5mL Solution for Injection (NOVAPLUS) (67457-0418) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 20mg/5mL Solution for Injection (PREMIER ProRx) (63323-0165) (Fresenius Kabi USA, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00517-4901) (American Regent Inc, a division of Luitpold Pharmaceuticals) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00517-4930) (American Regent Inc, a division of Luitpold Pharmaceuticals) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00517-4905) (American Regent Inc, a division of Luitpold Pharmaceuticals) (off market)Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection package photo

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00641-2273) (Baxter Anesthesia/Critical Care) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (67457-0422) (Mylan Institutional LLC ) nullDexamethasone Sodium Phosphate 4mg/ml Solution for Injection package photo

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (67457-0423) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00069-4545) (Mylan Institutional LLC ) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00069-4547) (Mylan Institutional LLC ) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00069-4543) (Mylan Institutional LLC ) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00069-4547) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00069-4545) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (00069-4543) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (55150-0237) (AuroMedics Pharma LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (72572-0120) (Civica, Inc.) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (71266-1050) (Fagron Compounding Services dba Fagron Sterile Services LLC dba JCB Laboratories) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (63323-0165) (Fresenius Kabi USA, LLC) nullDexamethasone Sodium Phosphate 4mg/mL Solution for Injection package photo

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (00641-6145) (Hikma Pharmaceuticals USA Inc.) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/ml Solution for Injection (NOVAPLUS) (00069-0179) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (NOVAPLUS) (67457-0419) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 4mg/mL Solution for Injection (PREMIER ProRx) (63323-0165) (Fresenius Kabi USA, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Simplist Dexamethasone Sodium Phosphate 4mg/mL Prefilled Syringe Solution for Injection (76045-0106) (BD Rx Inc., a Fresenius Kabi USA Company) null

    Dexamethasone Sodium Phosphate Solution for injection

    Solurex 4mg/ml Solution for Injection (00314-0896) (Hyrex Pharmaceuticals) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 100mg/10ml Solution for Injection (67457-0420) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 100mg/10mL Solution for Injection (63323-0516) (Fresenius Kabi USA, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 100mg/10mL Solution for Injection (70069-0025) (Somerset Therapeutics, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 100mg/10mL Solution for Injection (NOVAPLUS) (67457-0483) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (00641-0367) (Baxter Anesthesia/Critical Care) (off market)Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection package photo

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (00641-0367) (Hikma Pharmaceuticals USA inc.) nullDexamethasone Sodium Phosphate 10mg/ml Solution for Injection package photo

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (00069-4541) (Mylan Institutional LLC ) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (00069-4541) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (00703-3524) (Teva Pharmaceuticals USA) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/mL Solution for Injection (72572-0122) (Civica, Inc.) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/mL Solution for Injection (71266-1040) (Fagron Compounding Services dba Fagron Sterile Services LLC dba JCB Laboratories) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/mL Solution for Injection (63323-0506) (Fresenius Kabi USA, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/mL Solution for Injection (70069-0021) (Somerset Therapeutics, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (NOVAPLUS) (00069-0177) (Mylan Institutional LLC ) null

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/ml Solution for Injection (NOVAPLUS) (00069-0177) (Pfizer Injectables) (off market)

    Dexamethasone Sodium Phosphate Solution for injection

    Dexamethasone Sodium Phosphate 10mg/mL Solution for Injection (PREMIER ProRx) (63323-0506) (Fresenius Kabi USA, LLC) null

    Dexamethasone Sodium Phosphate Solution for injection

    DoubleDex Kit (76420-0766) (Enovachem Manufacturing) null

    Dexamethasone Sodium Phosphate Solution for injection

    Simplist Dexamethasone Sodium Phosphate 10mg/mL Prefilled Syringe Solution for Injection (76045-0109) (BD Rx Inc., a Fresenius Kabi USA Company) null

    Dexamethasone Sodium Phosphate Solution for injection

    Decadron 24mg/ml Solution for Injection (00006-7646) (Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc.) (off market)

    Dexamethasone Sodium Phosphate Suspension for injection

    Dalalone 4mg/ml Suspension for Injection (00456-1074) (Allergan USA, Inc.) (off market)

    Dexamethasone Suspension for injection

    DEXYCU 9% Intraocular Suspension Kit (71879-0001) (EyePoint Pharmaceuticals) null

    Description/Classification

    Description

    Dexamethasone and its derivatives, dexamethasone sodium phosphate and dexamethasone acetate, are synthetic glucocorticoids used as anti-inflammatory or immunosuppressive agents. Dexamethasone is available as oral, parenteral, as well as topical ophthalmic and intraocular dosage forms. Dexamethasone is used for many conditions in adult and pediatric patients, including cerebral edema, prevention of transplant rejection, and many allergic, dermatologic, ophthalmic, and systemic inflammatory conditions. Systemic dexamethasone is usually selected for the management of cerebral edema because of its superior ability to penetrate the CNS. Dexamethasone is also commonly used in antiemetic regimens for chemotherapy patients. In general, prednisone is more commonly prescribed as a corticosteroid when systemic treatment is needed for most conditions. Dexamethasone has little to no mineralocorticoid activity and is therefore not used by itself in the management of adrenal insufficiency. Systemic corticosteroids may be added to other long-term maintenance medications in the management of uncontrolled severe persistent asthma. Once stabilization of asthma is achieved, regular attempts should be made to reduce or eliminate the use of systemic corticosteroids due to the side effects associated with chronic administration. Short courses of treatment may be used in the management of asthma exacerbations.[64807]

     

    Updates for coronavirus disease 2019 (COVID-19):

    The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend using dexamethasone in patients with COVID-19 who are mechanically ventilated and in patients with COVID-19 who require supplemental oxygen but are not on a mechanical ventilator. However, the NIH recommends against the use of dexamethasone in patients who do not require supplemental oxygen.[65314] These recommendations are based on preliminary results from the Randomized Evaluation of COVID-19 Therapy (RECOVERY) trial. The RECOVERY trial is a multicenter, open-label study that found dexamethasone reduced deaths in patients with severe respiratory complications to COVID-19. When compared to patients receiving usual care alone (n = 4,321), treatment with dexamethasone (n = 2,104) reduced deaths in ventilated patients (29.3% vs. 41.4%; RR 0.64; 95% CI, 0.51 to 0.81) and in other patients receiving oxygen only (23.3% vs. 26.2%; RR 0.82; 95% CI, 0.72 to 0.94). No benefit was observed in patients not requiring respiratory support (17.8% vs. 14%; RR 1.19; 95% CI, 0.91 to 1.55). Overall, significantly fewer dexamethasone patients than usual care patients died within 28 days (22.9% vs. 25.7%; RR 0.83; 95% CI, 0.75 to 0.93; p < 0.001).[65625]

    Classifications

    • Respiratory System
      • Agents for Reactive and Obstructive Airway Diseases
        • Corticosteroids
          • Respiratory Corticosteroids
    • Sensory Organs
      • Ophthalmologicals
        • Ophthalmological Corticosteroids
    • Systemic Hormonal Agents (excluding Sex Hormones)
      • Systemic Corticosteroids
        • Systemic Corticosteroid Combinations
        • Systemic Corticosteroids, Plain
    Revision Date: 07/20/2020, 03:06:51 PM

    References

    64807 - Global Strategy for Asthma Management and Prevention. Global Initiative for Asthma (GINA) 2020. Available from: http://www.ginasthma.org. Accessed May 20th, 2020.65314 - COVID-19 Treatment Guidelines Panel. Coronavirus Diseases 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Accessed July 30, 2020. Available at on the World Wide Web at: https://covid19treatmentguidelines.nih.gov/.65625 - Horby P, Lim WS, Eberson J, et al. Dexamethasone in hospitalized patients with COVID-19: Preliminary Report. NEJM 2020 July 17. Available on the World Wide Web at: DOI:10.1056/NEJMoa2021436. [Epub Ahead of Print]

    Administration Information

    General Administration Information

    For storage information, see the specific product information within the How Supplied section.

    Route-Specific Administration

    Oral Administration

    • Administer with food to minimize GI upset.
    • If given once daily, give in the morning to coincide with the body's normal cortisol secretion.

    Oral Liquid Formulations

    Dexamethasone Intensol (Oral Solution Concentrate)

    • 1 mg/mL concentrated solution; contains 30% alcohol.
    • Measure the appropriate dose, using only the calibrated dropper provided with product.
    • Mix the dose with liquid or semi-solid food such as water, juice, soda, applesauce, or pudding and stir the preparation for a few seconds.
    • Consume the entire mixture immediately; do not store for future use.[60761]

    Injectable Administration

    • Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
    • Some injectable formulations contain benzyl alcohol; avoid the use of these formulations in premature neonates, and use with caution in neonates.[60760]

    Intravenous Administration

    Direct IV injection:

    • Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be given directly from the vial.[60760]

     

    Intermittent or continuous IV infusion:

    • Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be added to 5% Dextrose injection or 0.9% Sodium Chloride injection, USP and given by IV infusion.
    • Use diluted solutions within 24 hours, as infusion solutions generally do not contain preservatives.[60760]

    Intramuscular Administration

    • Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be administered intramuscularly.[60760]

    Other Injectable Administration

    Intra-articular, Soft tissue, or Intralesional injection

    • Dexamethasone sodium phosphate solution for injection 4 mg/mL may be administered into joints, soft tissues, or lesions, but administration of dexamethasone via these routes requires specialized techniques.
    • Only clinicians familiar with these methods of administration and with management of potential complications should administer dexamethasone by these routes.
    • Frequent intra-articular injections may result in damage to joint tissues.
    • Dexamethasone sodium phosphate injection is particularly recommended for use in conjunction with one of the less soluble, longer-acting steroids for intra-articular and soft tissue injection.[60760]

    Ophthalmic Administration

    Ophthalmic solution or suspension:

    • Apply ophthalmic solution or suspension topically to the eye.
    • For ophthalmic suspensions, shake well prior to each administration.
    • Instruct patient on appropriate instillation technique.
    • Do not to touch the tip of the dropper or tube to the eye, fingertips, or other surfaces.
    • To prevent contamination, each dropper is for one individual, do not share among patients.[54348] [61633]

     

    Intraocular Administration

    • For administration by the physician at the end of the ophthalmic surgical procedure.

    Dexycu Intraocular Suspension

    Preparation of intraocular suspension:

    • Prepare a sterile field. Remove the components of the administration kit from their respective pouches and place onto the sterile field.
    • Withdraw the syringe plunger approximately 1 inch. Place the syringe ring on the plunger (slit facing the plunger). Apply slight downward pressure until the syringe ring "snaps" into place.
    • Place the 18-gauge needle firmly on the syringe. Remove the cap from the needle. Depress the plunger completely and then withdraw the plunger to fill the syringe with air.
    • Mix using a vortex mixer or vigorously shake the vial sideways for a minimum of 30 seconds; the suspended drug material must be used immediately after shaking.
    • Remove the blue plastic flip-cap from the vial and wipe the top of the rubber stopper with an alcohol pad. Invert the vial.
    • Insert the needle into the vial and inject the air into the vial. Making sure the needle tip is immersed in the drug material pooled in the neck of the inverted vial, fill the syringe by slowly withdrawing the plunger approximately 0.2 mL. Remove the needle from the vial and discard the unused portion in the vial.
    • Remove the needle from the syringe. Firmly place the cannula on the syringe and remove the plastic cap. Hold the syringe vertically with the cannula pointing up. Depress the plunger to expel air bubbles from the syringe.
    • Affix the syringe guide over the syringe ring on the plunger.
    • Depress the plunger until the syringe guide/ring mechanism comes gently into contact with the flange of the syringe. Lightly tap/flick the barrel of the syringe to remove any excess drug from the tip of the cannula. Do not wipe or touch the tip of the cannula to remove excess drug.
    • Remove the syringe guide, leaving the syringe ring in place. CAUTION: DO NOT MOVE THE PLUNGER. The space between the syringe ring and the top of the plunger is the medication injection volume that will be applied to the patient's eye; the syringe is now ready for injection.[48640]

     

    Intraocular Administration:

    • In a single slow-motion, inject 0.005 mL of the drug material behind the iris in the inferior portion of the posterior chamber. If the sphere of the administered drug after intraocular injection appears to be larger than 2 mm in diameter, excess drug material may be removed by irrigation and aspiration in the sterile surgical setting.
    • Some drug material will remain in the syringe after the injection; this is necessary for accurate dosing. Discard the unused portion remaining in the syringe after administration.[48640]

    Dextenza Ophthalmic Insert

    Intracanalicular Administration:

    • Do not use if pouch has been damaged or opened. Do not re-sterilize.
    • Carefully remove foam carrier and transfer to a clean and dry area. If necessary, dilate the punctum with an ophthalmic dilator. Care should be taken not to perforate the canaliculus during dilation or placement of the insert. If perforation occurs, do not place the insert in the eye.
    • After drying the punctal area, using blunt (non-toothed) forceps, grasp the insert and place into the lower lacrimal canaliculus. The insert should be placed just below the punctal opening. Excessive squeezing of the insert may cause deformation.
    • To aid in the hydration of the insert, 1 to 2 drops of balanced salt solution can be instilled into the punctum. The insert hydrates quickly upon contact with moisture. If the insert begins to hydrate before fully inserted, discard the product and use a new insert.
    • The insert can be visualized when illuminated by a blue light source (e.g., slit lamp or hand held blue light) with yellow filter.[63796]
    • The insert is for single-use only.
    • Insert is resorbable; removal not required.

    Otic Administration

    Otic Administration of Ophthalmic Solution:

    • Clean the ear canal thoroughly and sponge dry prior to administration.
    • Instill the solution directly into the ear canal.
    • Alternatively, a gauze wick may be saturated with solution and packed into the ear canal. Keep the gauze wick moist with solution and remove from ear after 12 to 24 hours.[54348]

    Other Administration Route(s)

    Intravitreal Implant Administration

    • Intravitreal implantation should be performed only by surgeons who have observed or assisted in surgical implantation of the implant. Consult specialized instructions regarding insertion of the implant.
    • Administer via intravitreal injection with the provided single-use plastic applicator.
    • Use controlled aseptic conditions, which include the use of sterile gloves, a sterile drape, and a sterile eyelid speculum (or equivalent).
    • Use each applicator for a single treatment only. If the contralateral eye requires treatment, a new applicator must be used and the sterile field should be changed.
    • After the intravitreal injection, monitor patients for elevation in intraocular pressure and for endophthalmitis. Monitoring may consist of a check for reperfusion of the optic nerve head immediately after the injection, tonometry within 30 minutes after the injection, and biomicroscopy 2 to 7 days after the injection.
    • Instruct patients to promptly report any symptoms suggestive of endophthalmitis.[41921]

    Clinical Pharmaceutics Information

    From Trissel's 2‚Ñ¢ Clinical Pharmaceutics Database

    Dexamethasone sodium phosphate

    pH Range
    10 mg/mL- pH range of 7 to 8.5 4 mg/mL- pH range of 7.5 to 10.5 In NS 0.5 to 2 mg/mL- pH 7.3 to 7.5
    ReferencesAnon. Manufacturer's information and labeling. (Package insert).
    ReferencesSchneider JJ, Wilson KM, Ravenscroft PJ. A study of the osmolality and pH of subcutaneous drug infusion solutions. Austral J Hosp Pharm. 1997; 27
    Osmolality/Osmolarity
    Dexamethasone sodium phosphate injections are near isotonicity. The 4-mg/mL concentration of dexamethasone sodium phosphate had a measured osmolality of 356 mOsm/kg. Dexamethasone sodium phosphate diluted to concentrations of 0.5, 1, and 2 mg/mL in sodium chloride 0.9% had measured osmolalities of 269, 260, and 238 mOsm/kg, respectively.
    ReferencesAnon. Manufacturer's information and labeling. (Package insert).
    ReferencesBretschneider H. Osmolalities of commercially supplied drugs often used in anesthesia. Anesth Analg. 1987; 66
    ReferencesSchneider JJ, Wilson KM, Ravenscroft PJ. A study of the osmolality and pH of subcutaneous drug infusion solutions. Austral J Hosp Pharm. 1997; 27
    Stability
    Dexamethasone sodium phosphate injection in intact containers stored as directed by the manufacturer is stable until the labeled expiration date. Dexamethasone sodium phosphate is sensitive to heat; the vials should not be autoclaved. Lugo and Nahata reported that dexamethasone sodium phosphate1 mg/mL in bacteriostatic sodium chloride 0.9% packaged in glass vials remained clear and was stable exhibiting little or no loss by HPLC analysis in 28 days stored at room temperature or refrigerated. Infusion Solutions: Dexamethasone sodium phosphate diluted for infusion has been found to be stable for extended periods up to 14 days at room temperature in dextrose 5% and up to 22 days in sodium chloride 0.9%. Packaged in Syringes: Dexamethasone sodium phosphate injection packaged in glass syringes or syringe cartridges has been reported to be stable for periods ranging from 91 days to 196 days. In plastic syringes, conflicting information exists, but stability-indicating HPLC analysis indicates the drug is stable at room temperature for periods up to 55 days. Lau et al. evaluated dexamethasone sodium phosphate 10 mg/mL packaged in Glaspak disposable glass syringes and polypropylene plastic syringes. No loss of drug was found by stability-indicating HPLC analysis in 90 days at 4 and 23 degree C. This is consistent with Levin et al. and Kirschenbaum et al. who reported room temperature drug stability for 3 months in Tubex cartridges and for 196 days in disposable glass syringes, respectively. Lau et al also reported that the 10-mg/mL concentration packaged in 1- and 3-mL Monoject polypropylene plastic syringes exhibited 3% loss in 35 days and 7% loss in 55 days at room temperature using a stability-indicating HPLC analysis specific for dexamethasone. However Speaker et al. reported substantial changes in ultraviolet light absorbance for dexamethasone 4 mg/mL packaged in 3-mL Becton Dickinson, Monoject, and Terumo plastic syringes. The changes were attributed to loss of dexamethasone; losses ranged from 5 to 20% in one day. The UV analysis is non-specific, and the changes could be from other components. Gupta reported that dexamethasone sodium phosphate 1 and 0.1 mg/ml in sodium chloride 0.9% packaged in 3- and 5-ml Becton Dickinson polypropylene syringes was stable when stored at 25 ?C. The solutions remained clear throughout the study, and less than 3% loss occurred by HPLC analysis in 22 days. Dobrinas et al. evaluated the stability of dexamethasone sodium phosphate 4 mg/mL in aqueous solution for use as intraocular injections during ophthalmic surgery. The solution was packaged in 1-mL syringes with tip seals, placed in light protective plastic bags, and stored frozen at -18 degree C for 6 months. Samples were thawed at room temperature for evaluation. The syringes remained sterile, endotoxin-free, and tightly sealed when challenged with a methylene blue 1% solution. Stability-indicating HPLC analysis found little or no drug loss over 6 months of frozen storage. Paramedic Vehicles: Valenzuela et al. reported the stability of dexamethasone exposed to temperatures ranging from 26 to 38 degree C under simulated summer conditions in paramedic vehicles over 4 weeks. Gas chromatography coupled with mass spectrometry found no change in the drug over 4 weeks under these simulated use conditions.
    ReferencesAnon. Manufacturer's information and labeling. (Package insert).
    ReferencesChin A, Suk Y, Moon K, et al. Stability of granisetron hydrochloride with dexamethasone sodium phosphate for 14 days. Am J Health-Syst Pharm. 1996; 53
    ReferencesDobrinas M, Fleury-Souverain S, Sadeghipour F, et al. Stability of ophthalmic injections of ceftazidime, vancomycin and dexamethasone in aqueous humor after freezing, storage and thawing (accessed at http://pharmacie.hug-ge/rd/posters). Pharm Hopitaux Univ Geneve. 2007;
    ReferencesGupta VD. Chemical stability of dexamethasone sodium phosphate after reconstitution in 0.9% sodium chloride injection and storage in polypropylene syringes. Int J Pharmaceut Compound. 2002; 6
    ReferencesKirschenbaum BE, Latiolais CJ. Injectable medications - a guide to stability and reconstitution. New York, NY: McMahon Group. Data on file. 1993;
    ReferencesLau DWC, Law S, Walker SE, et al. Dexamethasone phosphate stability and contamination of solutions stored in syringes. PDA J Pharm Sci Tech. 1996; 50
    ReferencesLevin HJ, Fieber RA, Levi RS. Stability data for Tubex filled by hospital pharmacists. Hosp Pharm. 1973; 8
    ReferencesLugo RA, Nahata MC. Stability of diluted dexamethasone sodium phosphate injection at two temperatures. Ann Pharmacother. 1994; 28
    ReferencesValenzuela TD, Criss EA, Hammargen WM, et al. Thermal stability of prehospital medications. Ann Emerg Med. 1989; 18
    Light Exposure
    No unacceptable adverse effect on drug concentration due to normal fluorescent light exposure was observed in a stability study of dexamethasone sodium phosphate in infusion solutions and in syringes.
    ReferencesHagan RL, Mallett MS, Fox JL. Stability of ondansetron hydrochloride and dexamethasone sodium phosphate in infusion bags and syringes for 32 days. Am J Health-Syst Pharm. 1996; 53
    ReferencesLau DWC, Law S, Walker SE, et al. Dexamethasone phosphate stability and contamination of solutions stored in syringes. PDA J Pharm Sci Tech. 1996; 50
    Freezing
    The manufacturer states that dexamethasone sodium phosphate injection should be protected from freezing during storage. Rolin et al. found little or no loss of dexamethasone sodium phosphate in an admixture with ondansetron hydrochloride mixed in dextrose 5% when stored for 3 months frozen at -20 degree C. Dobrinas et al. evaluated the stability of dexamethasone sodium phosphate 4 mg/mL in aqueous solution for use as intraocular injections during ophthalmic surgery. The solution was packaged in 1-mL syringes with tip seals, placed in light protective plastic bags, and stored frozen at -18 degree C for 6 months. Samples were thawed at room temperature for evaluation. The syringes remained sterile, endotoxin-free, and tightly sealed when challenged with a methylene blue 1% solution. Stability-indicating HPLC analysis found little or no drug loss over 6 months of frozen storage.
    ReferencesAnon. Manufacturer's information and labeling. (Package insert).
    ReferencesDobrinas M, Fleury-Souverain S, Sadeghipour F, et al. Stability of ophthalmic injections of ceftazidime, vancomycin and dexamethasone in aqueous humor after freezing, storage and thawing (accessed at http://pharmacie.hug-ge/rd/posters). Pharm Hopitaux Univ Geneve. 2007;
    ReferencesRolin C, Hecq JD, Vanbeckbergen DF, et al. Stability of ondansetron and dexamethasone infusion upon refrigeration. Ann Pharmacother. 2011; 45
    Filtration
    Dexamethasone sodium phosphate has not shown loss due to binding to cellulose ester membranes filters (Ivex-2 and S-A-I-F), polycarbonate membrane filters (In-Sure Filter set), and stainless steel depth filters (Argyle Filter Connector). Mueller et al. reported no loss of dexamethasone sodium phosphate from ViaSpan organ cold storage solution filtered through Pall SQ40S 40-micron blood transfusion filters. Dexamethasone sodium phosphate 80 mcg/mL underwent no loss due to filtration through a Pall Supor membrane filter.
    ReferencesAnon. Pall Medical Supor-membrane IV filter device drug-adsorption data. Data on file. 2004; 8
    ReferencesMueller BJ, Guessford SA, Chen TT, et al. Effect of inline filtration on ViaSpan cold-storage solution. Am J Health-Syst Pharm. 1998; 55
    ReferencesRusmin S, Welton S, DeLuca P, et al. Effect of inline filtration on the potency of drugs administered intravenously. Am J Hosp Pharm. 1977; 34
    ReferencesStiles ML, Allen LV Jr. Retention of drugs during inline filtration of parenteral solutions. Infusion. 1979; 3
    Sorption Leaching
    Dexamethasone sodium phosphate has been shown not to undergo sorption to polyvinyl chloride (PVC) plastic bags and PVC administration tubing, polyethylene tubing, Silastic tubing, cellulose propionate burettes, and polypropylene or polypropylene/polyethylene plastic syringes. In addition, Xu et al. reported no sorption occurred to a polyurethane central catheter from Arrow International as well as no leaching of the chlorhexidine antimicrobial in it.
    ReferencesChin A, Suk Y, Moon K, et al. Stability of granisetron hydrochloride with dexamethasone sodium phosphate for 14 days. Am J Health-Syst Pharm. 1996; 53
    ReferencesGupta VD. Chemical stability of dexamethasone sodium phosphate after reconstitution in 0.9% sodium chloride injection and storage in polypropylene syringes. Int J Pharmaceut Compound. 2002; 6
    ReferencesHagan RL, Mallett MS, Fox JL. Stability of ondansetron hydrochloride and dexamethasone sodium phosphate in infusion bags and syringes for 32 days. Am J Health-Syst Pharm. 1996; 53
    ReferencesKowaluk EA, Roberts MA, Blackburn HD, et al. Interactions between drugs and polyvinyl chloride infusion bags. Am J Hosp Pharm. 1981; 38
    ReferencesKowaluk EA, Roberts MS, Polack AE. Interactions between drugs and intravenous delivery systems. Am J Hosp Pharm. 1982; 39
    ReferencesLau DWC, Law S, Walker SE, et al. Dexamethasone phosphate stability and contamination of solutions stored in syringes. PDA J Pharm Sci Tech. 1996; 50
    ReferencesXu QA, Zhang Y, Trissel LA, et al. Adequacy of a new chlorhexidine-bearing polyurethane central catheter for administration of 82 selected parenteral drugs. Ann Pharmacother. 2000; 34
    Other Information
    Dolasetron: Walker et al. reported that the pH-dependency of dolasetron solubility (See pH Effects) is most likely responsible for the variable amounts and time frames of precipitate formation that may occur when dolasetron mesylate and dexamethasone sodium phosphate are admixed or given by simultaneous Y-site administration. Multiple Drugs: Study 1: Targett et al. reported the physical and chemical stability of 5-drug combinations at 2 concentrations that included the drugs noted below. The mixture was packaged in Terumo polypropylene syringes with tip caps and stored at room temperature and under refrigeration. The mixtures were physically stable over 2 weeks. HPLC analysis found midazolam was stable for 14 days under refrigeration but was stable at room temperature for only 12 days at the higher concentration and 5 days at the lower concentration exhibiting more than 10% loss after those times. The other drugs were all stable throughout the 14-day study period at both storage temperatures. Concentration 1- Morphine tartrate 400 mg Dexamethasone sodium phosphate 8 mg Droperidol 2 mg Scopolamine hydrobromide 20 mg Midazolam HCl 5 mg Concentration 2- Morphine tartrate 40 mg Dexamethasone sodium phosphate 8 mg Droperidol 2 mg Scopolamine hydrobromide 20 mg Midazolam HCl 5 mg Sodium chloride 0.9% qs 10 mL Study 2: Negro et al. evaluated the compatibility of morphine hydrochloride (Grunenthal) and also tramadol hydrochloride (Andromaco) in 3-, 4-, and 5-drug combinations with five other drugs, including dexamethasone sodium phosphate, diluted in sodium chloride 0.9% in elastomeric pump reservoirs for subcutaneous infusion for palliative care in cancer patients when stored at room temperature of 25 degree C and protected from exposure to light. Morphine hydrochloride 1.68 mg/mL or Tramadol hydrochloride 11.18 mg/mL was tested with dexamethasone sodium phosphate (Merck) 0.44 mg/mL, haloperidol lactate (Esteve) 0.21 mg/mL, hyoscine butylbromide (Boehringer-Ingelheim) 1.68 mg/mL, metoclopramide hydrochloride 1.11 mg/mL, and midazolam hydrochloride (Roche) 0.5 mg/mL. Morphine hydrochloride 5 mg/mL or Tramadol hydrochloride 33.3 mg/mL was tested with dexamethasone sodium phosphate (Merck) 1.33 mg/mL, haloperidol lactate (Esteve) 0.62 mg/mL, hyoscine butylbromide (Boehringer-Ingelheim) 5 mg/mL, metoclopramide hydrochloride 3.33 mg/mL, midazolam hydrochloride (Roche) 1.5 mg/mL. All 3-, 4-, and 5-drug combinations that contained dexamethasone sodium phosphate with midazolam hydrochloride and/or haloperidol lactate resulted in precipitation immediately upon preparation. The precipitation was most likely free dexamethasone that formed due to the lower pH of the admixtures containing haloperidol lactate and/or midazolam hydrochloride. All 3-, 4-, and 5-drug combinations without dexamethasone sodium phosphate and midazolam hydrochloride and/or haloperidol lactate remained compatible for 7 days.
    ReferencesTargett PL, Keefe PA, Merridew CG. Compatibility and stability of drug adjuvants and morphine tartrate in 10 mL polypropylene syringes. Austral J Hosp Pharm. 1997; 27
    ReferencesWalker SE, Dip SL. Stability and compatibility of combinations of dolasetron and dexamethasone. Can J Hosp Pharm. 1998; 51
    Stability Max
    Maximum reported stability periods: In D5W- 14 days at room temperature. In NS- 22 days at room temperature.
    ReferencesChin A, Suk Y, Moon K, et al. Stability of granisetron hydrochloride with dexamethasone sodium phosphate for 14 days. Am J Health-Syst Pharm. 1996; 53
    ReferencesGupta VD. Chemical stability of dexamethasone sodium phosphate after reconstitution in 0.9% sodium chloride injection and storage in polypropylene syringes. Int J Pharmaceut Compound. 2002; 6
    • [object Object]
    Revision Date: 06/25/2020, 11:13:59 AMCopyright 2004-2020 by Lawrence A. Trissel. All Rights Reserved.

    References

    41921 - Ozurdex (dexamethasone intravitreal implant) package insert. Irvine, CA: Allergan, Inc.; 2018 May.48640 - Dexycu (dexamethasone intraocular suspension) package insert. Watertown, MA: EyePoint Pharmaceuticals US, Inc.; 2020 Jun.54348 - Dexamethasone sodium phosphate ophthalmic solution package insert. Bridgewater, NJ: Bausch and Lomb Inc.; 2016 June.60760 - Dexamethasone sodium phosphate injection package insert. Eatontown, NJ:West-Ward Pharmaceuticals;2014 Sept.60761 - Dexamethasone tablets USP, Dexamethasone oral solution, and Dexamethasone Intensol (oral solution concentrate) package insert. Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.61633 - Maxidex (dexamethasone ophthalmic suspension 0.1%) package insert. Fort Worth, TX; Alcon Laboratories, Inc.; 2017 Nov.63796 - Dextenza (dexamethasone ophthalmic insert) package insert. Bedford, MA: Ocular Therapeutix, Inc.; 2019 Jun.

    Adverse Reactions

    Moderate

    • adrenocortical insufficiency
    • amnesia
    • angina
    • blurred vision
    • candidiasis
    • cataracts
    • conjunctival hyperemia
    • conjunctivitis
    • corneal edema
    • Cushing's syndrome
    • delirium
    • depression
    • diabetes mellitus
    • edema
    • EEG changes
    • elevated hepatic enzymes
    • erythema
    • esophagitis
    • euphoria
    • exophthalmos
    • fluid retention
    • gastritis
    • glycosuria
    • growth inhibition
    • hallucinations
    • hepatomegaly
    • hypercholesterolemia
    • hyperemia
    • hyperglycemia
    • hypernatremia
    • hypertension
    • hyperthyroidism
    • hypocalcemia
    • hypokalemia
    • hypotension
    • hypothalamic-pituitary-adrenal (HPA) suppression
    • hypothyroidism
    • immunosuppression
    • impaired cognition
    • impaired wound healing
    • iritis
    • mania
    • memory impairment
    • meningitis
    • metabolic alkalosis
    • myasthenia
    • myopathy
    • neuritis
    • ocular infection
    • ocular inflammation
    • osteopenia
    • osteoporosis
    • palpitations
    • paresis
    • peripheral neuropathy
    • phlebitis
    • photophobia
    • physiological dependence
    • postmenopausal bleeding
    • pseudotumor cerebri
    • psychosis
    • sinus tachycardia
    • skin ulcer
    • sodium retention
    • withdrawal

    Severe

    • anaphylactoid reactions
    • angioedema
    • arachnoiditis
    • arrhythmia exacerbation
    • avascular necrosis
    • bone fractures
    • bradycardia
    • cardiac arrest
    • cardiomyopathy
    • corneal erosion
    • endophthalmitis
    • esophageal ulceration
    • exfoliative dermatitis
    • GI bleeding
    • GI perforation
    • heart failure
    • increased intracranial pressure
    • keratitis
    • keratoconjunctivitis
    • macular edema
    • myocardial infarction
    • ocular hemorrhage
    • ocular hypertension
    • optic neuritis
    • pancreatitis
    • papilledema
    • peptic ulcer
    • pulmonary edema
    • retinal detachment
    • retinopathy
    • seizures
    • skin atrophy
    • stroke
    • tendon rupture
    • thromboembolism
    • thrombosis
    • vasculitis
    • visual impairment

    Mild

    • abdominal pain
    • acne vulgaris
    • acneiform rash
    • alopecia
    • amenorrhea
    • anxiety
    • appetite stimulation
    • arthralgia
    • arthropathy
    • dizziness
    • dysmenorrhea
    • ecchymosis
    • emotional lability
    • fever
    • foreign body sensation
    • headache
    • hiccups
    • hirsutism
    • hyperhidrosis
    • infection
    • injection site reaction
    • insomnia
    • irritability
    • lacrimation
    • lethargy
    • leukocytosis
    • malaise
    • menstrual irregularity
    • myalgia
    • mydriasis
    • nausea
    • ocular hypotonia
    • ocular irritation
    • ocular pain
    • ocular pruritus
    • paresthesias
    • perineal pain
    • petechiae
    • pruritus
    • ptosis
    • purpura
    • rash
    • restlessness
    • skin hyperpigmentation
    • skin hypopigmentation
    • striae
    • syncope
    • telangiectasia
    • urticaria
    • vertigo
    • vomiting
    • weakness
    • weight gain
    • xerophthalmia
    • xerosis

    Pharmacologic doses of systemic corticosteroids (e.g. dexamethasone) administered for prolonged periods can result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. Exogenously administered corticosteroids exert a negative feedback effect on the pituitary, inhibiting the secretion of adrenocorticotropin (ACTH). This results in a decrease in ACTH-mediated synthesis of endogenous corticosteroids and androgens by the adrenal cortex. The severity of secondary adrenocortical insufficiency varies among individuals and is dependent on the dose, frequency, time of administration, and duration of therapy. Systemic administration of the drug on alternate days may help to alleviate this adverse effect. Patients with HPA suppression will require increased doses of corticosteroid therapy during periods of physiologic stress. Acute adrenal insufficiency and even death can occur with abrupt discontinuation of therapy. Discontinuation of prolonged oral corticosteroid therapy should be gradual since HPA suppression can last for up to 12 months following cessation of therapy. Patients may continue to need supplemental corticosteroid treatment during periods of physiologic stress or infectious conditions, even after the drug has been discontinued. A withdrawal syndrome unrelated to adrenocortical insufficiency can occur following sudden discontinuance of corticosteroid therapy. This syndrome includes symptoms such as appetite loss, malaise, lethargy, nauseousness, head pain/ache, joint pain, muscle pain, fever, exfoliative dermatitis, loss of weight, and hypotension. These effects are believed to be due to the sudden change in corticosteroid concentration rather than to low corticosteroid levels. Increased intracranial pressure with papilledema (i.e., pseudotumor cerebri) has also been reported with glucocorticoids usually after treatment withdrawal.[60760] [60761] [64165]

    Prolonged dexamethasone therapy can adversely affect the endocrine system, resulting in hypercorticism (Cushing's syndrome including fat abnormalities such as buffalo hump and moon face), hypertrichosis or hirsutism, menstrual irregularity including amenorrhea, postmenopausal bleeding, or dysmenorrhea, a decrease or increase in motility and number of spermatozoa, hyperthyroidism, hypothyroidism, glycosuria, hyperglycemia, and aggravation of diabetes mellitus in susceptible patients. In a review of 93 studies of corticosteroid use, the development of diabetes mellitus was determined to occur 4 times more frequently in steroid recipients compared to control groups.[24362] [60760] [60761] [64165]

    Because of retardation of bone growth, children receiving prolonged systemic corticosteroid therapy, like dexamethasone, may have growth inhibition. Growth inhibition has been observed in the absence of laboratory evidence of hypothalamic-pituitary-adrenal (HPA) suppression, suggesting that growth velocity is a more sensitive indicator of systemic corticosteroid exposure in pediatric patients.[60760] [60761] [64165]

    Endogenous glucocorticoids are responsible for protein metabolism; prolonged therapy with pharmaceutical glucocorticoids like dexamethasone can result in various musculoskeletal and joint manifestations, including myopathy (myalgia, muscle wasting, muscle weakness or myasthenia, and quadriplegia), arthralgia, tendon rupture, bone matrix atrophy (osteoporosis and osteopenia), bone fractures such as vertebral compression fractures or fractures of long bones, and avascular necrosis of femoral or humeral heads. These effects are more likely to occur in older or debilitated patients. Of note, abrupt cessation of corticosteroids can cause arthralgia and myalgia. Glucocorticoids interact with calcium metabolism at many sites, including: decreasing the synthesis by osteoblasts of the principal proteins of bone matrix, malabsorption of calcium in both the nephron and the gut, and reduction of sex hormone concentrations. Although all of these actions probably contribute to glucocorticoid-induced osteoporosis, the actions on osteoblasts are most important. Glucocorticoids do not modify vitamin D metabolism. Intra-articular injections of corticosteroids can cause Charcot-like arthropathy and post-injection flare. Atrophy at the site of injection has been reported following administration of soluble glucocorticoids.[24837] [60760] [60761] [64165]

    Adverse gastrointestinal (GI) effects associated with systemic corticosteroid (e.g., dexamethasone) administration include nausea and vomiting. Abdominal pain or distention, appetite stimulation, weight gain, pancreatitis, gastritis, hiccups, peptic ulcer with possible GI perforation and GI bleeding, perforation of the small and large bowel (particularly in patients with inflammatory bowel disease), and esophageal ulceration (ulcerative esophagitis) have also been reported.[60760] [60761] [64165] Although it was once believed that corticosteroids contributed to the development of peptic ulcer disease, in a review of 93 studies of corticosteroid use, the incidence of peptic ulcer disease was not found to be higher in steroid recipients compared to control groups. While most of these studies did not utilize endoscopy, it is unlikely that corticosteroids contribute to the development of peptic ulcer disease.[24362]

    Corticosteroid therapy including dexamethasone can mask the symptoms of infection and should generally be avoided during an acute viral, fungal, or bacterial infection. Leukocytosis is a common physiologic effect of systemic corticosteroid therapy and may need to be differentiated from the leukocytosis that occurs with inflammatory or infectious processes.[30943] [65096] [65097] Immunosuppression from corticosteroids is most likely to occur in patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily), systemic corticosteroid therapy for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) and/or concomitant immunosuppressant agents; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods may also be at risk. Corticosteroid-induced immunosuppression may result in the activation of latent viral (e.g., herpes) or bacterial (e.g., tuberculosis) infections and should not be used in patients with an active infection except when appropriate anti-infective therapy is instituted concomitantly. Patients receiving immunosuppressive doses of corticosteroids should be advised to avoid exposure to measles or varicella (chickenpox) and, if exposed to these diseases, to seek medical advice immediately. Monitoring systemic corticosteroid recipients for signs of opportunistic fungal infection is recommended, as cases of oropharyngeal candidiasis have been reported. Development of Kaposi's sarcoma has also been associated with prolonged administration of corticosteroids; discontinuation of the corticosteroid may result in clinical improvement.[60760] [60761] [64165] Bronchitis was noted in 5% of dexamethasone ophthalmic implant recipients during clinical trials and at an incidence higher than with placebo; secondary ophthalmic infection or exacerbation of infection has also been reported with other ophthalmic and intraocular dosage forms.[41921] [48640] [54348]

    Various adverse dermatologic effects reported during systemic corticosteroid therapy include skin atrophy (thin fragile skin), increased sweating (hyperhidrosis), acne vulgaris, striae, acneiform rash, alopecia, xerosis, perineal pain and irritation, purpura, rash (unspecified), telangiectasia, facial erythema, petechiae, ecchymosis or easy bruising, and suppression of reactions to skin tests. An increased susceptibility to skin ulcer may occur in patients with impaired circulation. Hypersensitivity reactions may manifest as allergic dermatitis, urticaria, anaphylactoid reactions, and/or angioedema. Burning or tingling in the perineal area may occur following IV injection of corticosteroids. Parenteral corticosteroid therapy has also produced skin hypopigmentation, skin hyperpigmentation, scarring, and other types of injection site reaction (e.g., induration, delayed pain or soreness, subcutaneous and cutaneous atrophy, and sterile abscesses).[60760] [60761] [64165]

    In general, systemic corticosteroids like dexamethasone can lead to impaired wound healing.[60760] [60761] [64165]

    Prolonged administration of systemic dexamethasone can result in edema and fluid retention due to sodium retention; electrolyte disturbances (hypokalemia, hypokalemic metabolic alkalosis, hypernatremia, hypocalcemia); and hypertension.[60760] [60761] [64165] In a review of 93 studies of corticosteroid use, hypertension was found to develop 4 times as often in steroid recipients compared to control groups.[24362] In another study, an increased risk of heart failure was observed for medium-dose glucocorticoid use as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. Medium exposure was defined as less than 7.5 mg daily of prednisolone or the equivalent given orally, rectally, or parenterally.[30697] Increased blood pressure was noted in 13% of dexamethasone ophthalmic insert recipients for one of the products during clinical trials.[41921]

    Adverse neurologic effects have been reported during prolonged systemic dexamethasone administration and include insomnia, vertigo or dizziness, restlessness, amnesia and memory impairment, increased motor activity, impaired cognition, paresthesias, ischemic peripheral neuropathy, seizures, neuritis, and EEG changes. Mental disturbances, including depression, anxiety, euphoria, personality changes, emotional lability, delirium, dementia, hallucinations, irritability, mania, mood swings, schizophrenic reactions, withdrawn behavior, and psychosis have also been reported; emotional lability and psychotic problems can be exacerbated by corticosteroid therapy. Headache may be a sign of elevated intracranial pressure.[60760] [60761] [64165] Arachnoiditis, meningitis, paresis, paraplegia, and sensory disturbances have occurred after intrathecal administration. Serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids. Specific events reported include, but are not limited to, spinal cord infarction, paraplegia, quadriplegia, cortical blindness, and stroke.[60760] Headache was noted in 1% to 4% of dexamethasone ophthalmic insert/implant recipients during clinical trials, at incidences higher than with placebo.[41921] [63796]

    Dexamethasone can cause increased intraocular pressure or ocular hypertension, the magnitude of which depends on the formulation used, indication for use, and the frequency and duration of dosing. Ocular hypertension can occur after 1 to 6 weeks of topical ophthalmic therapy, and it usually is reversible upon discontinuance of the drug. Use of the intravitreal implant has resulted in ocular hypertension (glaucoma) in 5% of patients in clinical trials, and increased ocular pressure (IOP) occurred in 25% to 35% of patients receiving the intravitreal implant. In retinal vein occlusion (RVO) and uveitis trials, IOP peaked at 60 days, returning to baseline by day 180. During the initial treatment period with the intravitreal implant for RVO and uveitis, 1% of patients required laser or surgical procedures to manage elevated IOP. In a 2 year observational study with the intravitreal implant, among patients who received more than 2 injections, increased IOP was reported in 24% (n = 68) patients. Frequently check IOP during receipt of ophthalmic preparations of dexamethasone. In diseases that cause thinning of the cornea or sclera, topical ocular steroids have been known to cause perforation. Intravitreal injections have also been associated with endophthalmitis, ocular inflammation, and retinal detachment. In clinical trials, the use of the intravitreal implant has resulted in ocular hemorrhage (conjunctival hemorrhage) (22% to 23%), ocular pain (8%), conjunctival hyperemia (7%), conjunctivitis (6%), vitreous floaters (5%), conjunctival edema (5%), xerophthalmia (5%), vitreous opacities (3%), retinal aneurysm (3%), foreign body sensation (2%), corneal erosion (2%), keratitis (2%), anterior chamber inflammation (2%), retinal tear (2%), eyelid ptosis (2%), vitreous hemorrhage (ocular hemorrhage, 6%), and vitreous detachment (2% to 4%). Postmarketing, implant misplacement, device dislocation with or without corneal edema, and ocular hypotonia (associated with vitreous leakage due to injection) were noted. Patients with an absent or torn posterior capsule of the lens are at increased risk of migration of the intravitreal implant into the anterior chamber.[41921] The most common ocular adverse reactions that occurred in patients treated with dexamethasone ophthalmic insert were: anterior chamber inflammation including iritis and iridocyclitis (10%), increased intraocular pressure (6%), reduced visual acuity (2%), ocular pain (1%), cystoid macular edema (1%), corneal edema (1%), and conjunctival hyperemia (1%).[63796] Ocular irritation including transient stinging, burning, or tearing and keratoconjunctivitis may occur during use of ophthalmic dexamethasone. Allergic reactions have also been reported; ocular pruritus can occur. Ocular discomfort (10%) and eye irritation (1%) were the most frequently reported adverse reactions in clinical studies with dexamethasone ophthalmic suspension. All other adverse reactions from these studies occurred with a frequency less than 1% including keratitis, conjunctivitis, dry eye (xerophthalmia), photophobia, blurred vision, ocular pruritus, foreign body sensation, increased lacrimation, abnormal ocular sensation, eyelid margin crusting, and ocular hyperemia. Postmarketing adverse reactions with dexamethasone topical ophthalmic suspension use include corneal erosion, dizziness, ocular pain, eyelid ptosis, headache, hypersensitivity reactions, and mydriasis.[61633] In patients receiving dexamethasone intraocular suspension for injection, the most common adverse reactions occurring in 5% to 15% of patients included intraocular pressure or ocular hypertension, corneal edema and iritis. Other ocular adverse reactions occurring in 1% to 5% of patients included corneal endothelial cell loss, blepharitis, ocular pain, cystoid macular edema, xerophthalmia, ocular inflammation, posterior capsule opacification, blurred vision, reduced visual acuity, vitreous floaters, foreign body sensation, photophobia, and vitreous detachment.[48640] Prolonged use of dexamethasone therapy by any route can result in ocular nerve damage including optic neuritis and visual defects. Temporary or permanent visual impairment, including blurred vision and blindness, has been reported with glucocorticoid administration by several routes of administration including intranasal and ophthalmic administration. Other ocular adverse reactions resulting from systemic corticosteroid therapy can include corneal perforation, exophthalmos, slowing of corneal wound healing, increased intraocular pressure, glaucoma with possible damage to the optic nerves, blurred vision, or retinopathy.[60760] [60761] [64165] Consider referring patients who develop ocular symptoms or use systemic corticosteroid-containing products for more than 6 weeks to an ophthalmologist for evaluation.[41921] [48640] [60760] [60761] [61633] [64165] Dexamethasone (by any route) can reduce host resistance to infection. Secondary fungal and viral infections of the eye (ocular infection) can be masked or exacerbated by corticosteroid therapy. Investigate the possibility of fungal infection if patients have persistent corneal ulceration. Prolonged use of dexamethasone therapy by any route has resulted in posterior subcapsular cataracts.[48640] [60760] [60761] [64165] The mechanism of corticosteroid-induced cataract formation is uncertain but may involve disruption of sodium-potassium pumps in the lens epithelium leading to accumulation of water in lens fibers and agglutination of lens proteins.[24813] The incidence of cataracts with initial use of the intravitreal implant in clinical trials of patients with RVO or uveitis was 5% within the first 6 months; however, the overall incidence after a second intravitreal implant injection was higher after 1 year. In diabetic macular edema (DME) trials, the incidence of cataract development in patients who had a phakic study eye was higher in the dexamethasone group (68%) compared with sham (21%). Among these patients, 61% of dexamethasone subjects vs. 8% of sham-controlled subjects underwent cataract surgery. In a 2 year observational study, among patients who received more than 2 injections, the most frequent adverse reaction was cataract 54% (n = 96 out of 178 phakic eyes at baseline).[41921]

    Hypercholesterolemia, atherosclerosis, fat embolism, palpitations, sinus tachycardia, bradycardia, syncope, vasculitis, necrotizing angiitis, thrombosis, thromboembolism, and phlebitis, specifically, thrombophlebitis, have been associated with systemic corticosteroid therapy such as dexamethasone. Systemic glucocorticoid use appears to increase the risk of cardiovascular events such as myocardial infarction, left ventricular rupture (in persons who recently experienced a myocardial infarction), angina, angioplasty, coronary revascularization, stroke, transient ischemic attack, cardiomegaly, arrhythmia exacerbation and ECG changes, hypertrophic cardiomyopathy (in premature infants), congestive heart failure and pulmonary edema, cardiac arrest or cardiovascular death.[60760] [60761] [64165] As determined from observational data, the rate of cardiovascular events was 17 per 1,000 person-years among 82,202 non-users of glucocorticoids. In contrast, the rate was 23.9 per 1,000 person-years among 68,781 glucocorticoid users. Furthermore, the rate of cardiovascular events was 76.5 per 1,000 person-years for high exposure patients. After adjustment for known covariates by multivariate analysis, high-dose glucocorticoid use was associated with a 2.56-fold increased risk of cardiovascular events as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. High glucocorticoid exposure was defined as at least 7.5 mg daily of prednisolone (or equivalent) given orally, rectally, or parenterally whereas medium exposure was defined as less than the above dosage by any of the 3 routes. Low-dose exposure was defined as inhaled, topical, or nasal usage only.[30697]

    Cases of elevated hepatic enzymes (usually reversible upon discontinuation) and hepatomegaly have been associated with corticosteroid receipt such as dexamethasone.[60760] [60761] [64165]

    Revision Date: 07/09/2020, 05:30:27 PM

    References

    24362 - Conn HO, Poynard T. Corticosteroids and peptic ulcer: meta-analysis of adverse events during steroid therapy. J Intern Med 1994;236:619-32.24813 - Cumming RG, Mitchell P, Leeder SR, et al. Use of inhaled corticosteroids and the risk of cataracts. N Engl J Med 1997;337:8-14.24837 - Reid IR. Preventing glucocorticoid-induced osteoporosis. N Engl J Med 1997;337:420-1.30697 - Wei L, MacDonald TM, Walker BR. Taking glucocorticoids by prescription is associated with subsequent cardiovascular disease. Ann Intern Med 2004;141:764-70.30943 - Schimmer B, Parker K. Adrenocorticotropic hormone; adrenocortical steroids and their synthetic analogs; inhibitors of the synthesis and actions of adrenocortical hormones. In: Hardman JG, Limbird LE, Molinoff PB, et al., eds. Goodman and Gilman's the Pharmacological Basis of Therapeutics, 10th edition. New York: McGraw Hill, 2001;1649-1674.41921 - Ozurdex (dexamethasone intravitreal implant) package insert. Irvine, CA: Allergan, Inc.; 2018 May.48640 - Dexycu (dexamethasone intraocular suspension) package insert. Watertown, MA: EyePoint Pharmaceuticals US, Inc.; 2020 Jun.54348 - Dexamethasone sodium phosphate ophthalmic solution package insert. Bridgewater, NJ: Bausch and Lomb Inc.; 2016 June.60760 - Dexamethasone sodium phosphate injection package insert. Eatontown, NJ:West-Ward Pharmaceuticals;2014 Sept.60761 - Dexamethasone tablets USP, Dexamethasone oral solution, and Dexamethasone Intensol (oral solution concentrate) package insert. Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.61633 - Maxidex (dexamethasone ophthalmic suspension 0.1%) package insert. Fort Worth, TX; Alcon Laboratories, Inc.; 2017 Nov.63796 - Dextenza (dexamethasone ophthalmic insert) package insert. Bedford, MA: Ocular Therapeutix, Inc.; 2019 Jun.64165 - Dexamethasone (Decadron) tablets package insert. Whitehouse Station, NJ: Merck & Co., Inc.; 2019 May.65096 - Abramson N, Melton B. Leukocytosis: basic of clinical assessment. Am Fam Physician 2000;62:2053-60.65097 - Shoenfeld Y, Gurewich Y, Gallant LA, et al. Prednisone-induced leukocytosis. Influenced of dosage, method and duration of administration on the degree of leukocytosis. Am J Med 1981;71:773-8.

    Contraindications/Precautions

    Absolute contraindications are italicized.

    • corticosteroid hypersensitivity
    • fungal infection
    • glaucoma
    • herpes simplex keratitis (dendritic keratitis)
    • ocular infection
    • rupture of posterior ocular lens capsule
    • abrupt discontinuation
    • adrenal insufficiency
    • benzyl alcohol hypersensitivity
    • breast-feeding
    • cataracts
    • corneal abrasion
    • Cushing's syndrome
    • diabetes mellitus
    • diverticulitis
    • epidural administration
    • geriatric
    • GI perforation
    • growth inhibition
    • head trauma
    • heart failure
    • helminth infection
    • hepatic disease
    • herpes infection
    • hypertension
    • hyperthyroidism
    • hypothalamic-pituitary-adrenal (HPA) suppression
    • hypothyroidism
    • immunosuppression
    • impaired wound healing
    • increased intracranial pressure
    • increased intraocular pressure
    • infection
    • measles
    • myasthenia gravis
    • myocardial infarction
    • myopia
    • neonates
    • neuromuscular disease
    • osteopenia
    • osteoporosis
    • peptic ulcer disease
    • pregnancy
    • premature neonates
    • psychosis
    • renal disease
    • seizure disorder
    • sulfite hypersensitivity
    • surgery
    • thyroid disease
    • tuberculosis
    • ulcerative colitis
    • vaccination
    • varicella
    • viral infection
    • visual disturbance

    Epidural administration of corticosteroids should be used with great caution. Rare, but serious adverse reactions, including cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been associated with epidural administration of injectable corticosteroids. These events have been reported with and without the use of fluoroscopy. Many cases were temporally associated with the corticosteroid injection; reactions occurred within minutes to 48 hours after injection. Some cases of neurologic events were confirmed through magnetic resonance imaging (MRI) or computed tomography (CT) scan. Many patients did not recover from the reported adverse effects. Discuss the benefits and risks of epidural corticosteroid injections with the patient before treatment. If a decision is made to proceed with corticosteroid epidural administration, counsel patients to seek emergency medical attention if they experience symptoms after injection such as vision changes, tingling in the arms or legs, dizziness, severe headache, seizures, or sudden weakness or numbness of face, arm, or leg.[57053]

    Although true corticosteroid hypersensitivity is rare, patients who have demonstrated a prior hypersensitivity reaction to dexamethasone should not receive any form of dexamethasone. It is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids. It is advisable that patients who have a hypersensitivity reaction to any corticosteroid undergo skin testing, which, although not a conclusive predictor, may help to determine if hypersensitivity to another corticosteroid exists. Such patients should be carefully monitored during and following the administration of any corticosteroid.[27616] [54285] [54286] [64165] [48640] [41921] [63796] [49533] [54348]

    Prolonged administration of pharmacological doses of systemic, nasal, inhaled or topical corticosteroids (resulting in systemic absorption) may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients. Adrenal suppression and increased intracranial pressure have been reported with the use and/or withdrawal of various corticosteroid formulations in pediatric patients.[60760] [51792] Acute adrenal insufficiency and even death may occur following abrupt discontinuation of systemic therapy. In addition, a withdrawal syndrome unrelated to adrenocortical insufficiency may occur following sudden discontinuation of corticosteroid therapy.[60760] [60761] [64165] These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid concentrations. Withdraw prolonged systemic corticosteroid therapy (duration of treatment of more than 2 weeks) gradually. HPA suppression can last for up to 12 months following cessation of systemic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid. HPA-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as post-surgical stress, acute blood loss, or infectious conditions, even after the corticosteroid has been discontinued. Encourage patients currently receiving chronic corticosteroid therapy or who have had corticosteroids discontinued within the last 12 months to carry identification advising the need for administration of corticosteroids in situations of increased stress.[54138] [54286] [64165] [60760] [60761]

    Potential adverse effects of chronic corticosteroid therapy should be weighed against the clinical benefits obtained and the availability of other treatment alternatives. Prolonged systemic corticosteroid therapy can lead to osteopenia, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fractures of long bones secondary to decreased bone formation, increased bone resorption, and protein catabolism in any patient.[60760] [60761] [64165] A high-protein diet may alleviate or prevent the adverse effects associated with protein catabolism. The elderly, post-menopausal, and pediatric patients may be more susceptible to the effects on bone. Chronic systemic dexamethasone therapy may cause growth inhibition in pediatric patients due to hypothalamic-pituitary-adrenal axis suppression and inhibition of bone growth. Corticosteroids should be titrated to the lowest effective dose. Because bone development is critical in pediatric patients, monitoring is warranted in patients receiving high-dose or chronic corticosteroid treatment. Use of the lowest effective dose is recommended to minimize the occurrence of systemic adverse effects. Monitor growth routinely.[51792] [60760] [60761] [64165]

    Patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily) or systemic corticosteroid therapy, such as dexamethasone, for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) are at risk to develop immunosuppression; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Treatment with topical or inhaled corticosteroids lessens the risk of immunosuppression; although localized effects may be seen in some patients. When given in combination with other immunosuppressive agents, there is a risk of over-immunosuppression.[60760] [60761] [64165] Intra-articularly injected corticosteroids are systemically absorbed and may cause immunosuppression. Advise patients to contact their health care provider if they develop fever or other signs or symptoms of infection. Local injection of a corticosteroid into a previously infected joint is not usually recommended. Examine any joint fluid to exclude a septic process. Injection into unstable joints is generally not recommended.[60760]

    If surgery is required, patients should advise their physician that they received prolonged systemic corticosteroid therapy, such as dexamethasone, within the last 12 months and state the disease for which they were being treated. For systemic therapy, identification cards that include disease state, type and dose of corticosteroid, and physician should always be carried with the patient. Long-acting dexamethasone injection preparations, which are no longer marketed in the U.S., are not suitable for use in acute stress situations. To avoid drug-induced adrenal insufficiency, a supportive corticosteroid dosage may be required in times of stress (such as trauma, surgery, or severe illness) both during treatment with these injections and for a year afterward.[60760] [60761] [64165]

    Corticosteroids may increase the risks related to infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminth infection. The degree to which the dose, route, and duration of corticosteroid administration correlate with the specific risks of infection is not well characterized, however, with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. Corticosteroids may also mask some signs of current infection. Although the FDA-approved product labeling states that corticosteroids are contraindicated in patients with systemic fungal infections, most clinicians believe that systemic corticosteroids can be administered to these patients as long as appropriate therapy is administered simultaneously. Avoid the use of dexamethasone in patients with a fungal infection or bacterial infection that is not adequately controlled with anti-infective agents. Activation of latent disease or exacerbation of intercurrent infection due to pathogens such as Amoeba, Candida, Cryptococcus, Mycobacterium, Nocardia, Pneumocystis, or Toxoplasma can occur in patients receiving systemic corticosteroids. Rule out infection with latent or active amebiasis before initiating corticosteroid therapy in patients who have spent time in the tropics or who have unexplained diarrhea. Use corticosteroids with caution in patients with known or suspected Strongyloides (threadworm) infestation as the immunosuppressive effects may lead to disseminated infection, severe enterocolitis, and sepsis. Reserve systemic corticosteroid therapy in active tuberculosis for patients with fulminating or disseminated disease and only in conjunction with appropriate antituberculosis therapy. Reactivation of tuberculosis may occur in patients with latent tuberculosis or tuberculin reactivity; close observation for disease reactivation is needed if corticosteroids are indicated in such patients. Furthermore, chemoprophylaxis is advised if prolonged corticosteroid therapy is needed. Advise patients receiving immunosuppressive doses of systemic corticosteroids to avoid exposure to persons with a viral infection (i.e., measles or varicella) because these diseases may be more serious or even fatal in immunosuppressed patients. Instruct patients to get immediate medical advice if exposure occurs. If exposed to chickenpox, prophylaxis with varicella-zoster immune globulin may be indicated. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin may be indicated. Avoid the use of corticosteroids in active ocular herpes infection due to the risk of corneal perforation. Corticosteroids should not be used in cerebral malaria.[60760] [60761] [64165] The use of ophthalmic dexamethasone formulations is contraindicated in most forms of cornea and conjunctiva viral infection including epithelial herpes simplex keratitis (dendritic keratitis), vaccinia, and varicella, and also in mycobacterial infection of the eye and fungal diseases of ocular structures.[48640] [41921] [63796] [49533] [54348]

    Do not use high doses of systemic corticosteroids such as dexamethasone for the treatment of traumatic brain injury. An increase in early mortality (at 2 weeks) and late mortality (at 6 months) was noted in patients with head trauma who were determined not to have other clear indications for corticosteroid treatment; in the trial, patients received methylprednisolone hemisuccinate.[60760]

    Corticosteroid therapy, including systemic dexamethasone therapy, has been associated with left ventricular free-wall rupture in patients with recent myocardial infarction, and should therefore be used cautiously in these patients. As sodium retention with resultant edema and potassium loss may occur in patients receiving systemic corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal disease or insufficiency.[60760] [60761] [64165]

    Systemic corticosteroids, such as dexamethasone, may decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus. This may especially occur in patients predisposed to diabetes mellitus. When corticosteroid therapy is necessary in patients with diabetes mellitus, changes in insulin, oral antidiabetic agent dosage, and/or diet may be required.[60760] [60761] [64165]

    An acute myopathy has been observed with the use of high doses of systemic corticosteroids, most often occurring in patients with neuromuscular disease disorders (e.g., myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular blocking drugs. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.[60760] [60761] [64165]

    Existing emotional instability or psychosis may be aggravated by corticosteroids. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychosis. Use dexamethasone with caution in patients with a seizure disorder; systemic steroids can lower the seizure threshold.[60760] [60761] [64165]

    Metabolic clearance of corticosteroids is decreased in hypothyroidism and increased in hyperthyroidism. Changes in thyroid disease status of a patient may necessitate an adjustment in systemic dexamethasone dosage.[60760] [60761] [64165]

    Systemic corticosteroids should be used with caution in patients with active or latent peptic ulcer disease, diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative colitis, since steroids may increase the risk of a gastrointestinal (GI) perforation. Signs of peritoneal irritation following GI perforation in patients receiving corticosteroids may be minimal or absent. Corticosteroids should not be used in patients where there is a possibility of impending GI perforation, abscess, or pyogenic infection. There is an enhanced effect due to decreased metabolism of systemic corticosteroids in patients with severe hepatic disease with cirrhosis.[60760] [60761] [64165]

    Systemic corticosteroids, like dexamethasone, may cause impaired wound healing. Ophthalmic and ocular dosage forms may cause impairment of wound healing within or near the site of application.[60760] [60761] [64165] [48640] [41921] [63796] [49533] [54348]

    Prolonged use of corticosteroids including dexamethasone may result in glaucoma with damage to the optic nerve, defects in visual acuity and fields of vision. Corticosteroids can cause cataracts and exacerbate pre-existing glaucoma. Periodically assess patients receiving corticosteroids chronically for cataract formation, visual disturbance, or increased intraocular pressure. Consider referring patients who develop ocular symptoms or use systemic corticosteroid-containing products for more than 6 weeks to an ophthalmologist for evaluation.[60760] [60761] [64165] Ophthalmic dexamethasone is more likely than other ophthalmic agents to increase intraocular pressure, so intraocular pressure should be measured every 2 to 4 weeks for the first 2 months of therapy, and every 1 to 2 months thereafter. Ophthalmic dexamethasone therapy should be undertaken with caution in patients with a history of open-angle glaucoma, myopia, Krukenberg's spindle, or diabetes because these patients have an increased risk of developing ocular hypertension during therapy. There is also an increase in the propensity for secondary ocular infection caused by fungal or viral infections. Ophthalmic dexamethasone should be used with caution in patients with corneal abrasion.[54348] [61633] [41921] [48640] [63796] The dexamethasone intravitreal implant is contraindicated in patients with glaucoma who have cup to disc ratio more than 0.8. Dexamethasone intravitreal implant is also contraindicated in patients who have a tear or a rupture of posterior ocular lens capsule; these patients with an absent or torn posterior capsule of the lens are at increased risk of migration of the intravitreal implant into the anterior chamber. Laser posterior capsulotomy in pseudophakic patients is not a contraindication for the dexamethasone intravitreal implant.[41921] The safety and efficacy of dexamethasone intravitreal implant. ophthalmic injection suspension, and ophthalmic insert have not been established in pediatric patients.[41921] [48640] [63796]

    Corticosteroid therapy usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (less than 2 weeks); low to moderate dose; long-term alternate-day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); ophthalmic administration, or by intra-articular, bursal or tendon injection. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise a concern about the safety of immunization with live-virus vaccines. In general, patients with severe immunosuppression due to large doses of corticosteroids should not receive vaccination with live-virus vaccines. When cancer chemotherapy or immunosuppressive therapy is being considered (e.g., for patients with Hodgkin's disease or organ transplantation), vaccination should precede the initiation of chemotherapy or immunotherapy by 2 or more weeks. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy. In patients who have received high-dose, systemic corticosteroids for 2 or more weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.[60760] [60761]

    There are no adequate, well-controlled studies for the use of dexamethasone in pregnant women; therefore, the manufacturers recommend that the drug be used during pregnancy only if the potential benefit to the mother outweighs the potential risk to the fetus. Corticosteroids have been shown to be teratogenic in many species when given in systemic doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring.[60760] [60761] [64165] In addition, dexamethasone has been shown to be teratogenic in mice and rabbits following topical ophthalmic application in multiples of the therapeutic dose.[61633] Topical ocular administration of dexamethasone to pregnant mice and rabbits during organogenesis produced embryofetal lethality, cleft palate and multiple visceral malformations.[41921] [63796] Topical and otic corticosteroids should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Dexamethasone injections have been used medically later in pregnancy to induce fetal lung maturation in patients at risk for pre-term delivery; use is for select circumstances and for a limited duration of time.[33038] [33039] [33040] An infant who is born to a woman receiving large doses of systemic corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary.

    Systemic use of dexamethasone has not been studied during breast-feeding; corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Caution is warranted, and some manufacturers recommend to discontinue breast-feeding if systemic dexamethasone treatment is needed.[60760] [60761] [64165] However, experts generally consider inhaled corticosteroids and oral corticosteroids (e.g., prednisone and prednisolone), acceptable to use during breast-feeding.[33723] [33724] [31822] There is no information regarding dexamethasone effects on breastfed infants or milk production or its presence in human milk following placement of the intravitreal implant or intracanalicular insert to inform risk to an infant during lactation.[41921] [63796] However, the systemic concentration of dexamethasone following administration of the intracanalicular insert is low.[63796] It is not known whether topical ophthalmic administration of dexamethasone could result in sufficient systemic absorption to produce detectable quantities in breast milk.[61633] [49533] Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition.

    The routine use of high-dose (greater than 0.5 mg/kg/day) dexamethasone for either the prevention or treatment of chronic lung disease in premature neonates is not recommended by the American Academy of Pediatrics (AAP) due to a lack of survival benefit and concern about long-term adverse outcomes, particularly increased rates of cerebral palsy. Studies utilizing lower doses of dexamethasone (less than 0.2 mg/kg/day) have not reported increased rates of adverse neurodevelopmental effects; however, due to the small number of patients included in these studies, the AAP states that there is insufficient evidence to recommend the use of low-dose dexamethasone and further study is warranted.[54338] In a geographical cohort study of 148 extremely premature pediatric patients (born less than 28 weeks gestation), 55 (27%) received postnatal dexamethasone (mean cumulative dose 7.7 mg/kg) during the neonatal period. Patients receiving dexamethasone had smaller total brain tissue volume (mean difference -3.6%, p value = 0.04) and smaller white matter, thalami, and basal ganglia volumes (p is less than 0.05 for all) when compared with participants who did not receive postnatal dexamethasone. There was also a trend of smaller total brain and white matter volumes with an increased dose of postnatal dexamethasone.[56910] Avoid the use of dexamethasone injectable formulations containing benzyl alcohol in premature neonates and neonates. Administration of benzyl alcohol to neonates can result in 'gasping syndrome,' which is a potentially fatal condition characterized by metabolic acidosis and CNS, respiratory, circulatory, and renal dysfunction; it is also characterized by high concentrations of benzyl alcohol and its metabolites in the blood and urine. While the minimum amount of benzyl alcohol at which toxicity may occur is not known, 'gasping syndrome' has been associated with daily benzyl alcohol exposure above 99 mg/kg/day in neonates and low-birth-weight neonates. Additional symptoms may include gradual neurological deterioration, seizures, intracranial hemorrhage, hematologic abnormalities, skin breakdown, hepatic failure, renal failure, hypotension, bradycardia, and cardiovascular collapse. Rare cases of death, primarily in premature neonates, have been reported. Further, an increased incidence of kernicterus, especially in small, premature neonates has been reported. Practitioners administering this and other medications containing benzyl alcohol should consider the combined daily metabolic load of benzyl alcohol from all sources. Premature neonates, neonates with low birth weight, and patients who receive a high dose may be more likely to develop toxicity.[60760]

    Use systemic corticosteroids with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient. Geriatric and debilitated patients are especially susceptible to corticosteroid-induced decreases in bone mineral density and resultant fractures. Detrimental effects on bone metabolism, such as osteoporosis, are a risk with chronic, systemically-administered corticosteroids.[60760] [60761] [64165] According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration.[63923] The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities (LTCFs); the need for continued use of a systemic glucocorticoid should be documented, along with monitoring for adverse consequences with intermediate or longer-term use.[60742]

    Some commercially available formulations of dexamethasone injection or ophthalmic solutionmay contain sulfites; some parenteral products also contain benzyl alcohol. Sulfites and benzyl alcohol may cause allergic reactions in some people. They should be used with caution in patients with known sulfite hypersensitivity or benzyl alcohol hypersensitivity. Patients who have asthma are more likely to experience a sulfite sensitivity reaction than non-asthmatic patients.[54285] [54348]

    Revision Date: 07/22/2020, 03:18:19 PM

    References

    27616 - Butani L. Corticosteroid-induced hypersensitivity reactions. Ann Allergy Asthma Immunol 2002;89(5):439-445.31822 - NAEPP Working Group Report on Managing Asthma During Pregnancy. Recommendations for Pharmacologic Treatment-Update 2004. NIH Publication No. 05-3279. Bethesda, MD: U.S. Department of Health and Human Services; National Institutes of Health; National Heart, Lung, and Blood Institute, 200433038 - Di Renzo GC, Roura LC, European Association of Perinatal Medicine-Study Group on Preterm Birth. International guidelines: Guidelines for the management of spontaneous preterm labor. J Perinat Med 2006;34:359-66.33039 - ACOG Committee on Practice Bulletins. ACOG Practice Bulletin: Management of preterm labor. Int J Gynecol Obstet 2003;82:127-35.33040 - Ballard PL, Ballard RA. Scientific basis and therapeutic regimens for use of antenatal glucocorticoids. Am J Obstet Gynecol 1995;173:254-62.33723 - Greenberger PA, Patterson R. The management of asthma during pregnancy and lactation. Clin Rev Allergy 1987;5:317-24.33724 - Ellsworth A. Pharmacotherapy of asthma while breastfeeding. J Hum Lact 1994;10:39-41.41921 - Ozurdex (dexamethasone intravitreal implant) package insert. Irvine, CA: Allergan, Inc.; 2018 May.48640 - Dexycu (dexamethasone intraocular suspension) package insert. Watertown, MA: EyePoint Pharmaceuticals US, Inc.; 2020 Jun.49533 - Maxidex (dexamethasone) ophthalmic ointment package insert. Ft. Worth, TX: Alcon Laboratories, Inc.; 2006 Dec.51792 - Patradoon-Ho P, Gunasekera H, Ryan MM. Inhaled corticosteroids, adrenal suppression and benign intracranial hypertension. Med J Aust 2006;185:279-28054138 - Shulman DI, Palmert MR, Kemp SF. Adrenal insufficiency: still a cause of morbidity and death in childhood. Pediatrics 2007;119(2):e484-494.54285 - Dexamethasone sodium phosphate injection solution. Schaumburg, IL: APP Pharmaceuticals, LLC; 2008 Apr.54286 - Dexamethasone tablets USP, Dexamethasone oral solution, and Dexamethasone Intensol (oral solution concentrate) package insert. Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.54338 - American Academy of Pediatrics Committee on Fetus and Newborn. Postnatal corticosteroids to prevent or treat bronchopulmonary dysplasia. Pediatrics 2010;126:800-8.54348 - Dexamethasone sodium phosphate ophthalmic solution package insert. Bridgewater, NJ: Bausch and Lomb Inc.; 2016 June.56910 - Cheong JL, Burnett AC, Lee KJ. Association between postnatal dexamethasone for treatment of bronchopulmonary dysplasia and brain volumes at adolescence in infants born very preterm. J Pediatr. 2014; 164(4): 737-743.57053 - Food and Drug Administration (US FDA) Drug Medwatch-FDA requires label changes to warn of rare but serious neurologic problems after epidural corticosteroid injections for pain. Retrieved April 23, 2014. Available on the World Wide Web at http://www.fda.gov/downloads/Drugs/DrugSafety/UCM394286.pdf.60742 - Health Care Financing Administration. Interpretive Guidelines for Long-term Care Facilities. Title 42 CFR 483.25(l) F329: Unnecessary Drugs. Revised 2015.60760 - Dexamethasone sodium phosphate injection package insert. Eatontown, NJ:West-Ward Pharmaceuticals;2014 Sept.60761 - Dexamethasone tablets USP, Dexamethasone oral solution, and Dexamethasone Intensol (oral solution concentrate) package insert. Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.61633 - Maxidex (dexamethasone ophthalmic suspension 0.1%) package insert. Fort Worth, TX; Alcon Laboratories, Inc.; 2017 Nov.63796 - Dextenza (dexamethasone ophthalmic insert) package insert. Bedford, MA: Ocular Therapeutix, Inc.; 2019 Jun.63923 - The American Geriatrics Society 2019 Beers Criteria Update Expert Panel. American Geriatrics Society 2019 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2019;00:1-21.64165 - Dexamethasone (Decadron) tablets package insert. Whitehouse Station, NJ: Merck & Co., Inc.; 2019 May.

    Mechanism of Action

    Glucocorticoids are naturally occurring hormones that prevent or suppress inflammation and immune responses when administered at pharmacological doses. At the molecular level, unbound glucocorticoids readily cross cell membranes and bind with high affinity to specific cytoplasmic receptors. This binding induces a response by modifying transcription and, ultimately, protein synthesis to achieve the steroid's intended action. Such actions can include: inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of the inflammatory response, and suppression of humoral immune responses. Some of the net effects include reduction in edema or scar tissue and a general suppression in an immune response. The degree of clinical effect is normally related to the dose administered. The anti-inflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, collectively called lipocortins. Lipocortins, in turn, control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor molecule arachidonic acid. Likewise, the numerous adverse effects related to corticosteroid use usually depend on the dose administered and the duration of therapy.[30943][50600]

    Revision Date: 06/25/2020, 06:57:57 PM

    References

    30943 - Schimmer B, Parker K. Adrenocorticotropic hormone; adrenocortical steroids and their synthetic analogs; inhibitors of the synthesis and actions of adrenocortical hormones. In: Hardman JG, Limbird LE, Molinoff PB, et al., eds. Goodman and Gilman's the Pharmacological Basis of Therapeutics, 10th edition. New York: McGraw Hill, 2001;1649-1674.50600 - Barnes PJ. Anti-inflammatory actions of glucocorticoids: molecular mechanisms. Clin Sci (Lond). 1998;94(6):557-572.

    Pharmacokinetics

    Dexamethasone is administered via oral, intravenous, intramuscular, intraarticular, intravitreal, ophthalmic, and otic routes. Certain dosage forms, like inhalational products, have been removed from marketing. Circulating drug binds weakly to plasma proteins, with only the unbound portion of a dose being active. Systemic dexamethasone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Corticosteroids distribute into breast milk and cross the placenta. Systemic dexamethasone is metabolized by the liver to inactive metabolites. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine. The plasma elimination half-life of dexamethasone is approximately 1.8 to 3.5 hours whereas the biological half-life is 36 to 54 hours.[34477]

     

    Affected cytochrome P450 (CYP450) isoenzymes and drug transporters: CYP3A4, P-glycoprotein (P-gp)

    Dexamethasone is an inducer of CYP3A4 and is a substrate for both P-glycoprotein (P-gp) and CYP3A4.[34477]

    Route-Specific Pharmacokinetics

    Oral Route

    Dexamethasone is rapidly and well absorbed after oral administration.[38183] In adults, bioavailability has been reported to be in the range of approximately 60% to 100%, with no significant differences between the elixir and tablet formulations.[54046][54366] Peak concentrations occur 1 to 2 hours after oral administration.[54046] However, 1 study of 13 patients (aged 14 to 28 years) with congenital adrenal hyperplasia reported a mean time to peak concentrations for oral dexamethasone of 45 minutes (range 30 to 120 minutes).[54352]

    Intravenous Route

    Peak concentrations were reached approximately 60 minutes after single-dose administration of IV dexamethasone in neonates.[54368]

    Intramuscular Route

    The onset and duration of action of dexamethasone injection ranges from 2 days to 3 weeks and is dependent on whether the drug is administered by intra-articular or IM injection and by the extent of the local blood supply.

    Other Route(s)

    Intra-articular Route

    The onset and duration of action of dexamethasone injection ranges from 2 days to 3 weeks and is dependent on whether the drug is administered by intra-articular or IM injection and by the extent of the local blood supply.

     

    Ophthalmic Route

    Following ophthalmic administration, dexamethasone is absorbed through the aqueous humor and distribute into the local tissues, with only minimal systemic absorption occurring. Ophthalmic doses are metabolized locally.

     

    Intravitreal Implant Route

    After the insertion of the dexamethasone intravitreal implant (0.35 mg or 0.7 mg) in 21 patients, plasma concentrations were obtained on days 1, 7, 30, 60, and 90. Overall, the majority of dexamethasone plasma concentration measurements were below the lower limit of quantitation (LLOQ = 50 pg/mL). Ten of the 73 samples in the patients receiving the 0.7 mg dose and 2 of the 42 samples in the patients receiving the 0.35 mg dose were above the LLOQ (range, 52 to 94 pg/mL). The highest plasma concentration (94 pg/mL) was observed in one patient who had received the 0.7 mg dose. Age, body weight, and gender did not affect the plasma dexamethasone concentrations. In vitro metabolism studies of the intravitreal implant showed no metabolites.[41921]

     

    Intraocular Route

    Systemic exposure to dexamethasone was evaluated in a subgroup of patients enrolled in 2 studies (n = 25 for the first study and n = 13 for the second study). The patients received a single intraocular injection of dexamethasone containing 342 mcg or 517 mcg of dexamethasone at the end of cataract surgery and blood samples were collected prior to surgery and at the several time points post-surgery between Day 1 and up to Day 30. In the first study, the dexamethasone plasma concentrations on post-surgery Day 1 ranged from 0.09 to 0.86 ng/mL and from 0.07 to 1.16 ng/mL following administration of dexamethasone 342 mcg and 517 mcg, respectively. In the second study, dexamethasone plasma concentrations on post-surgery Day 1 ranged from 0.349 to 2.79 ng/mL following administration of dexamethasone 517 mcg. In both the studies, dexamethasone plasma concentrations declined over time and very few patients had quantifiable dexamethasone plasma concentrations at the final time point of sampling (Day 15 or Day 30).[48640]

     

    Intracanalicular Route

    Systemic exposure to dexamthasone was evaluated in 16 healthy volunteers. Plasma samples were obtained prior to and at several time points on Days 1 to 29. Dexamethasone plasma concentrations were detectable (above 50 pg/mL, the lower limit of quantification of the assay) in 11% of samples (21 of 189), and ranged from 0.05 ng/mL to 0.81 ng/mL.[63796]

    Special Populations

    Hepatic Impairment

    In adult patients with chronic liver disease, dexamethasone clearance is reduced and the elimination half-life is prolonged. Pharmacokinetic data are unavailable in pediatric patients with hepatic impairment.[54046]

    Renal Impairment

    In adult patients with renal impairment, dexamethasone clearance is increased and the elimination half-life is shorter. This is due to decreased protein binding of dexamethasone to albumin in uremic patients. Pharmacokinetic data are unavailable in pediatric patients with renal impairment.[54046]

    Pediatrics

    Infants, Children, and Adolescents

    Pharmacokinetics of dexamethasone in pediatric patients are similar to adults. In a pharmacokinetic study in 12 pediatric patients (4 months to 16 years) who received IV dexamethasone (0.1 to 0.3 mg/kg/dose), the mean elimination half-life of dexamethasone was 4.34 hours (range 2.33 to 9.54 hours), which is similar to that reported in adults. The mean volume of distribution (Vd) was 2.07 L/kg (range 0.48 to 8.99 L/kg).[54361] Another study that included adolescents and adults (14 to 28 years) reported a mean elimination half-life of 3.53 hours (range 2.18 to 4.5 hours) after dexamethasone administration.[54352]

     

    Neonates

    Clearance of dexamethasone in neonates is a function of gestational age (GA) with premature neonates having a slower clearance. In a pharmacokinetic study in 9 neonates (mean GA 27.3 weeks [range 25 to 30 weeks]; mean postnatal age 21.8 days), mean clearance was 1.69 mL/kg/minute in neonates with a GA less than 27 weeks compared with 7.57 mL/kg/minute in neonates with a GA more than 27 weeks. Corresponding elimination half-life values were 10.2 and 4.9 hours, respectively. The mean Vd was 1.78 L/kg, which was also correlated with GA (1.26 vs 2.19 L/kg for neonates with GA less than 27 weeks and more than 27 weeks, respectively). The mean Vd was higher than what has been reported in adults (0.77 L/kg).[54358] Another study in 7 extremely low birth weight neonates (mean GA 25.6 weeks; mean birthweight 735 g) found similar results after administration of single-dose IV dexamethasone. In this study, mean values for clearance, Vd, and elimination half-life were 2.4 mL/kg/minute, 1.9 L/kg, and 9.26 hours, respectively.[54368]

    Revision Date: 06/25/2020, 07:02:51 PM

    References

    34477 - Kovarik JM, Purba HS, Pongowski M, et al. Pharmacokinetics of dexamethasone and valspodar, a P-glycoprotein (mdr1) modulator: implications for coadministration. Pharmacother 1998;18:1230-6.38183 - Sparrow A, Geelhoed G. Prednisolone versus dexamethasone in croup: a randomised equivalence trial. Arch Dis Child. 2006;91:580-583.41921 - Ozurdex (dexamethasone intravitreal implant) package insert. Irvine, CA: Allergan, Inc.; 2018 May.48640 - Dexycu (dexamethasone intraocular suspension) package insert. Watertown, MA: EyePoint Pharmaceuticals US, Inc.; 2020 Jun.54046 - Czock D, Keller F, Rasche FM, et al. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clin Pharmacokinet 2005;44:61-98.54352 - Young MC, Cook N, Read GF, et al. The pharmacokinetics of low-dose dexamethasone in congenital adrenal hyperplasia. Eur J Clin Pharmacol 1989;37:75-77.54358 - Lugo RA, Nahata MC, Menke JA, et al. Pharmacokinetics of dexamethasone in premature neonates. Eur J Clin Pharmacol 1996;49:477-483.54361 - Richter O, Ern B, Reinhardt D, et al. Pharmacokinetics of dexamethasone in children. Pediatr Pharmacol 1983;3:329-337.54366 - Duggan DE, Yeh KC, Matalia N, et al. Bioavailability of oral dexamethasone. Clin Pharmacol Ther 1975;18:205-209.54368 - Charles B, Schild P, Steer P, et al. Pharmacokinetics of dexamethasone following single-dose intravenous administration to extremely low birth weight infants. Dev Pharmacol Ther 1993;20:205-210.63796 - Dextenza (dexamethasone ophthalmic insert) package insert. Bedford, MA: Ocular Therapeutix, Inc.; 2019 Jun.

    Pregnancy/Breast-feeding

    pregnancy

    There are no adequate, well-controlled studies for the use of dexamethasone in pregnant women; therefore, the manufacturers recommend that the drug be used during pregnancy only if the potential benefit to the mother outweighs the potential risk to the fetus. Corticosteroids have been shown to be teratogenic in many species when given in systemic doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring.[60760] [60761] [64165] In addition, dexamethasone has been shown to be teratogenic in mice and rabbits following topical ophthalmic application in multiples of the therapeutic dose.[61633] Topical ocular administration of dexamethasone to pregnant mice and rabbits during organogenesis produced embryofetal lethality, cleft palate and multiple visceral malformations.[41921] [63796] Topical and otic corticosteroids should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Dexamethasone injections have been used medically later in pregnancy to induce fetal lung maturation in patients at risk for pre-term delivery; use is for select circumstances and for a limited duration of time.[33038] [33039] [33040] An infant who is born to a woman receiving large doses of systemic corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary.

    breast-feeding

    Systemic use of dexamethasone has not been studied during breast-feeding; corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Caution is warranted, and some manufacturers recommend to discontinue breast-feeding if systemic dexamethasone treatment is needed.[60760] [60761] [64165] However, experts generally consider inhaled corticosteroids and oral corticosteroids (e.g., prednisone and prednisolone), acceptable to use during breast-feeding.[33723] [33724] [31822] There is no information regarding dexamethasone effects on breastfed infants or milk production or its presence in human milk following placement of the intravitreal implant or intracanalicular insert to inform risk to an infant during lactation.[41921] [63796] However, the systemic concentration of dexamethasone following administration of the intracanalicular insert is low.[63796] It is not known whether topical ophthalmic administration of dexamethasone could result in sufficient systemic absorption to produce detectable quantities in breast milk.[61633] [49533] Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition.

    Revision Date: 06/25/2020, 01:54:36 PM

    References

    31822 - NAEPP Working Group Report on Managing Asthma During Pregnancy. Recommendations for Pharmacologic Treatment-Update 2004. NIH Publication No. 05-3279. Bethesda, MD: U.S. Department of Health and Human Services; National Institutes of Health; National Heart, Lung, and Blood Institute, 200433038 - Di Renzo GC, Roura LC, European Association of Perinatal Medicine-Study Group on Preterm Birth. International guidelines: Guidelines for the management of spontaneous preterm labor. J Perinat Med 2006;34:359-66.33039 - ACOG Committee on Practice Bulletins. ACOG Practice Bulletin: Management of preterm labor. Int J Gynecol Obstet 2003;82:127-35.33040 - Ballard PL, Ballard RA. Scientific basis and therapeutic regimens for use of antenatal glucocorticoids. Am J Obstet Gynecol 1995;173:254-62.33723 - Greenberger PA, Patterson R. The management of asthma during pregnancy and lactation. Clin Rev Allergy 1987;5:317-24.33724 - Ellsworth A. Pharmacotherapy of asthma while breastfeeding. J Hum Lact 1994;10:39-41.41921 - Ozurdex (dexamethasone intravitreal implant) package insert. Irvine, CA: Allergan, Inc.; 2018 May.49533 - Maxidex (dexamethasone) ophthalmic ointment package insert. Ft. Worth, TX: Alcon Laboratories, Inc.; 2006 Dec.60760 - Dexamethasone sodium phosphate injection package insert. Eatontown, NJ:West-Ward Pharmaceuticals;2014 Sept.60761 - Dexamethasone tablets USP, Dexamethasone oral solution, and Dexamethasone Intensol (oral solution concentrate) package insert. Eatontown, NJ: West-Ward Pharmaceuticals Corp; 2016 March.61633 - Maxidex (dexamethasone ophthalmic suspension 0.1%) package insert. Fort Worth, TX; Alcon Laboratories, Inc.; 2017 Nov.63796 - Dextenza (dexamethasone ophthalmic insert) package insert. Bedford, MA: Ocular Therapeutix, Inc.; 2019 Jun.64165 - Dexamethasone (Decadron) tablets package insert. Whitehouse Station, NJ: Merck & Co., Inc.; 2019 May.

    Interactions

    Level 1 (Severe)

    • Alefacept
    • Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir
    • Dolutegravir; Rilpivirine
    • Emtricitabine; Rilpivirine; Tenofovir alafenamide
    • Emtricitabine; Rilpivirine; Tenofovir disoproxil fumarate
    • Iopamidol
    • Live Vaccines
    • Metyrapone
    • Ombitasvir; Paritaprevir; Ritonavir
    • Rilpivirine

    Level 2 (Major)

    • Abemaciclib
    • Amiodarone
    • Amoxicillin; Clarithromycin; Lansoprazole
    • Amoxicillin; Clarithromycin; Omeprazole
    • Artemether; Lumefantrine
    • Atazanavir
    • Atazanavir; Cobicistat
    • Avapritinib
    • Axitinib
    • Bedaquiline
    • Bicalutamide
    • Capmatinib
    • Cariprazine
    • Caspofungin
    • Clarithromycin
    • Cobicistat
    • Cobimetinib
    • Conivaptan
    • Corticorelin, Ovine
    • Dabrafenib
    • Daclatasvir
    • Darunavir
    • Darunavir; Cobicistat
    • Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide
    • Deflazacort
    • Desmopressin
    • Dofetilide
    • Dronedarone
    • Efalizumab
    • Elbasvir; Grazoprevir
    • Elvitegravir
    • Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide
    • Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate
    • Encorafenib
    • Entrectinib
    • Erdafitinib
    • Erlotinib
    • Etravirine
    • Fedratinib
    • Flibanserin
    • Glasdegib
    • Guanfacine
    • Halofantrine
    • Hylan G-F 20
    • Idelalisib
    • Iohexol
    • Isavuconazonium
    • Ivabradine
    • Ixabepilone
    • Lapatinib
    • Lefamulin
    • Lemborexant
    • Levomethadyl
    • Lorlatinib
    • Lumateperone
    • Macimorelin
    • Mifepristone
    • Mitotane
    • Muromonab-CD3
    • Natalizumab
    • Neratinib
    • Nisoldipine
    • Olaparib
    • Pazopanib
    • Pemigatinib
    • Penicillamine
    • Perampanel
    • Pimavanserin
    • Rimegepant
    • Ritodrine
    • Roflumilast
    • Romidepsin
    • Saquinavir
    • Sargramostim, GM-CSF
    • Selpercatinib
    • Selumetinib
    • Simeprevir
    • Sipuleucel-T
    • Sirolimus
    • Sofosbuvir; Velpatasvir
    • Sofosbuvir; Velpatasvir; Voxilaprevir
    • Sonidegib
    • Sorafenib
    • Sunitinib
    • Tazemetostat
    • Telithromycin
    • Temsirolimus
    • Tolvaptan
    • Toremifene
    • Ubrogepant
    • Ulipristal
    • Vemurafenib
    • Venetoclax
    • Vigabatrin
    • Voxelotor
    • Zanubrutinib

    Level 3 (Moderate)

    • Abatacept
    • Acetaminophen; Aspirin, ASA; Caffeine
    • Acetaminophen; Butalbital
    • Acetaminophen; Butalbital; Caffeine
    • Acetaminophen; Butalbital; Caffeine; Codeine
    • Acetaminophen; Caffeine; Dihydrocodeine
    • Acetaminophen; Caffeine; Magnesium Salicylate; Phenyltoloxamine
    • Acetaminophen; Caffeine; Phenyltoloxamine; Salicylamide
    • Acetaminophen; Chlorpheniramine; Dextromethorphan; Phenylephrine
    • Acetaminophen; Chlorpheniramine; Phenylephrine; Phenyltoloxamine
    • Acetaminophen; Codeine
    • Acetaminophen; Dextromethorphan; Guaifenesin; Phenylephrine
    • Acetaminophen; Dextromethorphan; Phenylephrine
    • Acetaminophen; Guaifenesin; Phenylephrine
    • Acetaminophen; Hydrocodone
    • Acetaminophen; Oxycodone
    • Acetazolamide
    • Acetohexamide
    • Adalimumab
    • Albiglutide
    • Aliskiren; Amlodipine; Hydrochlorothiazide, HCTZ
    • Aliskiren; Hydrochlorothiazide, HCTZ
    • Alogliptin; Metformin
    • Alpha-glucosidase Inhibitors
    • Ambenonium Chloride
    • Amifampridine
    • Amiloride; Hydrochlorothiazide, HCTZ
    • Aminosalicylate sodium, Aminosalicylic acid
    • Amlodipine; Hydrochlorothiazide, HCTZ; Olmesartan
    • Amlodipine; Hydrochlorothiazide, HCTZ; Valsartan
    • Amphotericin B
    • Amphotericin B cholesteryl sulfate complex (ABCD)
    • Amphotericin B lipid complex (ABLC)
    • Amphotericin B liposomal (LAmB)
    • Amprenavir
    • Antithymocyte Globulin
    • Apalutamide
    • Argatroban
    • Aripiprazole
    • Arsenic Trioxide
    • Asparaginase Erwinia chrysanthemi
    • Aspirin, ASA
    • Aspirin, ASA; Butalbital; Caffeine
    • Aspirin, ASA; Butalbital; Caffeine; Codeine
    • Aspirin, ASA; Caffeine; Dihydrocodeine
    • Aspirin, ASA; Caffeine; Orphenadrine
    • Aspirin, ASA; Carisoprodol
    • Aspirin, ASA; Carisoprodol; Codeine
    • Aspirin, ASA; Citric Acid; Sodium Bicarbonate
    • Aspirin, ASA; Dipyridamole
    • Aspirin, ASA; Omeprazole
    • Aspirin, ASA; Oxycodone
    • Aspirin, ASA; Pravastatin
    • Atenolol; Chlorthalidone
    • Atracurium
    • Atropine; Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate
    • Atropine; Hyoscyamine; Phenobarbital; Scopolamine
    • Azilsartan; Chlorthalidone
    • Belladonna Alkaloids; Ergotamine; Phenobarbital
    • Benazepril; Hydrochlorothiazide, HCTZ
    • Bendroflumethiazide; Nadolol
    • Benzhydrocodone; Acetaminophen
    • Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate
    • Bepridil
    • Bismuth Subsalicylate
    • Bismuth Subsalicylate; Metronidazole; Tetracycline
    • Bisoprolol; Hydrochlorothiazide, HCTZ
    • Bivalirudin
    • Boceprevir
    • Brentuximab vedotin
    • Brexpiprazole
    • Brigatinib
    • Bromocriptine
    • Brompheniramine; Carbetapentane; Phenylephrine
    • Brompheniramine; Dextromethorphan; Phenylephrine
    • Brompheniramine; Guaifenesin; Hydrocodone
    • Brompheniramine; Hydrocodone; Pseudoephedrine
    • Budesonide
    • Budesonide; Formoterol
    • Budesonide; Glycopyrrolate; Formoterol
    • Bupivacaine; Lidocaine
    • Bupropion
    • Bupropion; Naltrexone
    • Buspirone
    • Butabarbital
    • Calcium Carbonate
    • Calcium Carbonate; Magnesium Hydroxide
    • Calcium Carbonate; Risedronate
    • Calcium Carbonate; Simethicone
    • Canagliflozin
    • Canagliflozin; Metformin
    • Candesartan; Hydrochlorothiazide, HCTZ
    • Captopril; Hydrochlorothiazide, HCTZ
    • Carbamazepine
    • Carbetapentane; Chlorpheniramine; Phenylephrine
    • Carbetapentane; Diphenhydramine; Phenylephrine
    • Carbetapentane; Guaifenesin; Phenylephrine
    • Carbetapentane; Phenylephrine
    • Carbetapentane; Phenylephrine; Pyrilamine
    • Carbinoxamine; Hydrocodone; Phenylephrine
    • Carbinoxamine; Hydrocodone; Pseudoephedrine
    • Carbinoxamine; Phenylephrine
    • Ceritinib
    • Certolizumab pegol
    • Chlophedianol; Guaifenesin; Phenylephrine
    • Chlorothiazide
    • Chlorpheniramine; Codeine
    • Chlorpheniramine; Dextromethorphan; Phenylephrine
    • Chlorpheniramine; Dihydrocodeine; Phenylephrine
    • Chlorpheniramine; Dihydrocodeine; Pseudoephedrine
    • Chlorpheniramine; Guaifenesin; Hydrocodone; Pseudoephedrine
    • Chlorpheniramine; Hydrocodone
    • Chlorpheniramine; Hydrocodone; Phenylephrine
    • Chlorpheniramine; Hydrocodone; Pseudoephedrine
    • Chlorpheniramine; Phenylephrine
    • Chlorpropamide
    • Chlorthalidone
    • Chlorthalidone; Clonidine
    • Cholestyramine
    • Choline Salicylate; Magnesium Salicylate
    • Cimetidine
    • Cisapride
    • Cisatracurium
    • Citalopram
    • Clindamycin
    • Clozapine
    • Codeine
    • Codeine; Guaifenesin
    • Codeine; Phenylephrine; Promethazine
    • Codeine; Promethazine
    • Crizotinib
    • Cyclosporine
    • Dapagliflozin
    • Dapagliflozin; Metformin
    • Dapagliflozin; Saxagliptin
    • Dapsone
    • Deferasirox
    • Denosumab
    • Dextran
    • Dextromethorphan; Diphenhydramine; Phenylephrine
    • Dextromethorphan; Guaifenesin; Phenylephrine
    • Dextromethorphan; Quinidine
    • Digoxin
    • Dihydrocodeine; Guaifenesin; Pseudoephedrine
    • Dipeptidyl Peptidase-4 Inhibitors
    • Diphenhydramine; Hydrocodone; Phenylephrine
    • Diphenhydramine; Phenylephrine
    • Doravirine
    • Doravirine; Lamivudine; Tenofovir disoproxil fumarate
    • Doxacurium
    • Dronabinol
    • Droperidol
    • Dulaglutide
    • Echinacea
    • Elagolix
    • Elagolix; Estradiol; Norethindrone acetate
    • Eliglustat
    • Empagliflozin
    • Empagliflozin; Linagliptin
    • Empagliflozin; Linagliptin; Metformin
    • Empagliflozin; Metformin
    • Enalapril; Hydrochlorothiazide, HCTZ
    • Enzalutamide
    • Ephedrine
    • Eprosartan; Hydrochlorothiazide, HCTZ
    • Ertugliflozin
    • Ertugliflozin; Metformin
    • Ertugliflozin; Sitagliptin
    • Erythromycin
    • Erythromycin; Sulfisoxazole
    • Esomeprazole
    • Esomeprazole; Naproxen
    • Estrogens
    • Eszopiclone
    • Exenatide
    • Fentanyl
    • Fluconazole
    • Fluoxymesterone
    • food
    • Fosamprenavir
    • Fosinopril; Hydrochlorothiazide, HCTZ
    • Gallium Ga 68 Dotatate
    • Gefitinib
    • Gemcitabine
    • Gentamicin
    • Glecaprevir; Pibrentasvir
    • Glimepiride
    • Glimepiride; Pioglitazone
    • Glimepiride; Rosiglitazone
    • Glipizide
    • Glipizide; Metformin
    • Glyburide
    • Glyburide; Metformin
    • Glycerol Phenylbutyrate
    • Golimumab
    • Guaifenesin; Hydrocodone
    • Guaifenesin; Hydrocodone; Pseudoephedrine
    • Guaifenesin; Phenylephrine
    • Haloperidol
    • Hemin
    • Heparin
    • Hetastarch
    • Homatropine; Hydrocodone
    • Hydantoins
    • Hydralazine; Hydrochlorothiazide, HCTZ
    • Hydrochlorothiazide, HCTZ
    • Hydrochlorothiazide, HCTZ; Irbesartan
    • Hydrochlorothiazide, HCTZ; Lisinopril
    • Hydrochlorothiazide, HCTZ; Losartan
    • Hydrochlorothiazide, HCTZ; Methyldopa
    • Hydrochlorothiazide, HCTZ; Metoprolol
    • Hydrochlorothiazide, HCTZ; Moexipril
    • Hydrochlorothiazide, HCTZ; Olmesartan
    • Hydrochlorothiazide, HCTZ; Propranolol
    • Hydrochlorothiazide, HCTZ; Quinapril
    • Hydrochlorothiazide, HCTZ; Spironolactone
    • Hydrochlorothiazide, HCTZ; Telmisartan
    • Hydrochlorothiazide, HCTZ; Triamterene
    • Hydrochlorothiazide, HCTZ; Valsartan
    • Hydrocodone
    • Hydrocodone; Ibuprofen
    • Hydrocodone; Phenylephrine
    • Hydrocodone; Potassium Guaiacolsulfonate
    • Hydrocodone; Potassium Guaiacolsulfonate; Pseudoephedrine
    • Hydrocodone; Pseudoephedrine
    • Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate
    • Ibritumomab Tiuxetan
    • Ibrutinib
    • Ibuprofen; Oxycodone
    • Ifosfamide
    • Incretin Mimetics
    • Indapamide
    • Indinavir
    • Inebilizumab
    • Infliximab
    • Insulin Degludec; Liraglutide
    • Insulin Glargine; Lixisenatide
    • Insulins
    • Isoniazid, INH; Pyrazinamide, PZA; Rifampin
    • Isoniazid, INH; Rifampin
    • Isoproterenol
    • Itraconazole
    • Ketoconazole
    • L-Asparaginase Escherichia coli
    • Ledipasvir; Sofosbuvir
    • Letermovir
    • Levetiracetam
    • Lidocaine
    • Lidocaine; Prilocaine
    • Linagliptin; Metformin
    • Liraglutide
    • Lixisenatide
    • Loop diuretics
    • Loperamide
    • Loperamide; Simethicone
    • Lopinavir; Ritonavir
    • Lumacaftor; Ivacaftor
    • Lurasidone
    • Magnesium Salicylate
    • Mannitol
    • Maraviroc
    • Mecasermin rinfabate
    • Mecasermin, Recombinant, rh-IGF-1
    • Mefloquine
    • Meglitinides
    • Mephobarbital
    • Metformin
    • Metformin; Pioglitazone
    • Metformin; Repaglinide
    • Metformin; Rosiglitazone
    • Metformin; Saxagliptin
    • Metformin; Sitagliptin
    • Methazolamide
    • Methenamine; Sodium Acid Phosphate
    • Methenamine; Sodium Acid Phosphate; Methylene Blue; Hyoscyamine
    • Methyclothiazide
    • Metolazone
    • Micafungin
    • Mivacurium
    • Moxifloxacin
    • Nanoparticle Albumin-Bound Paclitaxel
    • Nateglinide
    • Neostigmine
    • Netupitant, Fosnetupitant; Palonosetron
    • Neuromuscular blockers
    • Nicardipine
    • Nilotinib
    • Nonsteroidal antiinflammatory drugs
    • Ocrelizumab
    • Omeprazole
    • Omeprazole; Amoxicillin; Rifabutin
    • Omeprazole; Sodium Bicarbonate
    • Ondansetron
    • Oxycodone
    • Oxymetholone
    • Ozanimod
    • Pancuronium
    • Pegaspargase
    • Peginterferon Alfa-2a
    • Phenobarbital
    • Phenylephrine
    • Phenylephrine; Promethazine
    • Physostigmine
    • Pimozide
    • Posaconazole
    • Potassium
    • Potassium Chloride
    • Potassium Phosphate; Sodium Phosphate
    • Pramlintide
    • Prasterone, Dehydroepiandrosterone, DHEA (Dietary Supplements)
    • Prasterone, Dehydroepiandrosterone, DHEA (FDA-approved)
    • Praziquantel
    • Primidone
    • Propranolol
    • Pyridostigmine
    • Quetiapine
    • Quinidine
    • Quinolones
    • Rapacuronium
    • Regular Insulin
    • Remdesivir
    • Repaglinide
    • Ribociclib
    • Ribociclib; Letrozole
    • Rifabutin
    • Rifampin
    • Rifamycins
    • Rifapentine
    • Rilonacept
    • Ritonavir
    • Rituximab
    • Rituximab; Hyaluronidase
    • Rocuronium
    • Ruxolitinib
    • Salicylates
    • Salsalate
    • Sapropterin
    • Semaglutide
    • SGLT2 Inhibitors
    • Siponimod
    • Sodium Benzoate; Sodium Phenylacetate
    • Sodium Chloride
    • Sodium Phenylbutyrate
    • Sodium Phosphate Monobasic Monohydrate; Sodium Phosphate Dibasic Anhydrous
    • Somatropin, rh-GH
    • Succinylcholine
    • Sufentanil
    • Sulfonylureas
    • Tasimelteon
    • Telaprevir
    • Telbivudine
    • Telotristat Ethyl
    • Terbinafine
    • Testosterone
    • Thalidomide
    • Thiazide diuretics
    • Thiazolidinediones
    • Thyroid hormones
    • Ticagrelor
    • Tobramycin
    • Tolazamide
    • Tolbutamide
    • Tranexamic Acid
    • Tuberculin Purified Protein Derivative, PPD
    • Tubocurarine
    • Tucatinib
    • Vancomycin
    • Vecuronium
    • Vincristine
    • Vincristine Liposomal
    • Vorapaxar
    • Voriconazole
    • Vorinostat
    • Warfarin
    • Zolpidem

    Level 4 (Minor)

    • Albendazole
    • Aldesleukin, IL-2
    • Alemtuzumab
    • Aliskiren; Amlodipine
    • Alosetron
    • Altretamine
    • Aminolevulinic Acid
    • Amlodipine
    • Amlodipine; Atorvastatin
    • Amlodipine; Benazepril
    • Amlodipine; Celecoxib
    • Amlodipine; Olmesartan
    • Amlodipine; Telmisartan
    • Amlodipine; Valsartan
    • Antitumor antibiotics
    • Aprepitant, Fosaprepitant
    • Armodafinil
    • Avanafil
    • Azathioprine
    • Basiliximab
    • Bexarotene
    • Bortezomib
    • Bosentan
    • Cabozantinib
    • Carmustine, BCNU
    • Carvedilol
    • Cenobamate
    • Chlorambucil
    • Clofarabine
    • Delavirdine
    • Denileukin Diftitox
    • Econazole
    • Escitalopram
    • Estramustine
    • Hydroxyurea
    • Imatinib
    • Interferon Alfa-2a
    • Interferon Alfa-2b
    • Interferon Alfa-2b; Ribavirin
    • Isotretinoin
    • Lansoprazole
    • Lansoprazole; Naproxen
    • Lomustine, CCNU
    • Lurbinectedin
    • Melphalan
    • Mepenzolate
    • Methoxsalen
    • Mitoxantrone
    • Modafinil
    • Nelarabine
    • Oritavancin
    • Perindopril; Amlodipine
    • Photosensitizing agents (topical)
    • Potassium-sparing diuretics
    • Purine analogs
    • Rivaroxaban
    • Sildenafil
    • Tadalafil
    • Tositumomab
    • Tretinoin, ATRA
    • Zafirlukast
    • Zonisamide
    Abatacept: (Moderate) Concomitant use of immunosuppressives, as well as long-term corticosteroids, may potentially increase the risk of serious infection in abatacept treated patients. Advise patients taking abatacept to seek immediate medical advice if they develop signs and symptoms suggestive of infection. [8565] Abemaciclib: (Major) Avoid coadministration of dexamethasone with abemaciclib due to decreased exposure to abemaciclib and its active metabolites, which may lead to reduced efficacy. Consider alternative treatments. Abemaciclib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with moderate CYP3A4 inducers is predicted to decrease the relative potency adjusted unbound AUC of abemaciclib plus its active metabolites (M2, M18, and M20) by 53%, 41%, and 29% respectively. [54286] [62393] Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Acetaminophen; Butalbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Acetaminophen; Butalbital; Caffeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Acetaminophen; Butalbital; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] Acetaminophen; Caffeine; Dihydrocodeine: (Moderate) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine. [30282] [54286] Acetaminophen; Caffeine; Magnesium Salicylate; Phenyltoloxamine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Acetaminophen; Caffeine; Phenyltoloxamine; Salicylamide: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Acetaminophen; Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Acetaminophen; Chlorpheniramine; Phenylephrine; Phenyltoloxamine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Acetaminophen; Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] Acetaminophen; Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Acetaminophen; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Acetaminophen; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Acetaminophen; Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Acetaminophen; Oxycodone: (Moderate) Monitor for reduced efficacy of oxycodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of oxycodone as needed. If dexamethasone is discontinued, consider a dose reduction of oxycodone and frequently monitor for signs of respiratory depression and sedation. Oxycodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease oxycodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. [39926] [54286] Acetazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with acetazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy. [26417] [28267] Acetohexamide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Adalimumab: (Moderate) Closely monitor for the development of signs and symptoms of infection if coadministration of a corticosteroid with adalimumab is necessary. Adalimumab treatment increases the risk for serious infections that may lead to hospitalization or death. Patients taking concomitant immunosuppressants including corticosteroids may be at greater risk of infection. [27939] Albendazole: (Minor) Concomitant administration of albendazole with dexamethasone increases the plasma concentration of albendazole sulfoxide, presumably via reduction in albendazole sulfoxide clearance. [4768] Albiglutide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Aldesleukin, IL-2: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [41853] [7592] [7714] Alefacept: (Severe) Patients receiving other immunosuppressives should not receive concurrent therapy with alefacept; there is the possibility of excessive immunosuppression and subsequent risks of infection and other serious side effects. [4657] Alemtuzumab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Aliskiren; Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Aliskiren; Amlodipine; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Aliskiren; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Alogliptin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Alosetron: (Minor) Dexamethasone can induce the activity of CYP3A4 and increase the metabolism of alosetron by increasing the metabolism of the drug, thus potentially reducing the effect of alosetron. [5112] Alpha-glucosidase Inhibitors: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Altretamine: (Minor) Concurrent use of altretamine with other agents which cause bone marrow or immune suppression such as corticosteroids may result in additive effects. [4661] [7714] Ambenonium Chloride: (Moderate) Concomitant use of anticholinesterase agents, such as ambenonium chloride, and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents used to treat myasthenia should be withdrawn at least 24 hours before initiating corticosteroid therapy. [29779] [30015] [30028] [42863] [56146] [64165] Amifampridine: (Moderate) Carefully consider the need for concomitant treatment with systemic corticosteroids and amifampridine, as coadministration may increase the risk of seizures. If coadministration occurs, closely monitor patients for seizure activity. Seizures have been observed in patients without a history of seizures taking amifampridine at recommended doses. Systemic corticosteroids may increase the risk of seizures in some patients. [45339] [63790] Amiloride; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Aminolevulinic Acid: (Minor) Corticosteroids administered prior to or concomitantly with photosensitizing agents used in photodynamic therapy may decrease the efficacy of the treatment. [6625] Aminosalicylate sodium, Aminosalicylic acid: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Amiodarone: (Major) Use caution when coadministering amiodarone with drugs which may induce hypokalemia and, or hypomagnesemia, including corticosteroids. Since antiarrhythmic drugs may be ineffective or may be arrhythmogenic in patients with hypokalemia, any potassium or magnesium deficiency should be corrected before instituting and during amiodarone therapy. [26417] [28224] [29377] Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Atorvastatin: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Benazepril: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Celecoxib: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Hydrochlorothiazide, HCTZ; Olmesartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Hydrochlorothiazide, HCTZ; Valsartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Olmesartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Telmisartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amlodipine; Valsartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Amoxicillin; Clarithromycin; Lansoprazole: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage. [28238] [34477] (Minor) Monitor for decreased efficacy of lansoprazole if coadministration with dexamethasone is necessary. Lansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased lansoprazole plasma concentrations. [40596] [54286] Amoxicillin; Clarithromycin; Omeprazole: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage. [28238] [34477] (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29564] [54286] Amphotericin B cholesteryl sulfate complex (ABCD): (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly. [30011] [40134] Amphotericin B lipid complex (ABLC): (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly. [30011] [40134] Amphotericin B liposomal (LAmB): (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly. [30011] [40134] Amphotericin B: (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly. [30011] [40134] Amprenavir: (Moderate) Exercise caution when administering dexamethasone and amprenavir concurrently. Dexamethasone decreases amprenavir serum concentrations. Amprenavir may be less effective in patients taking these agents together. [5074] Antithymocyte Globulin: (Moderate) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [6303] [7714] Antitumor antibiotics: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Apalutamide: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with apalutamide is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and apalutamide is a strong CYP3A4 inducer. [54286] [62874] Aprepitant, Fosaprepitant: (Minor) Aprepitant, fosaprepitant is indicated for the treatment of chemotherapy-induced nausea/vomiting (CINV) in combination with dexamethasone and a 5HT3 antagonist; the pharmacokinetic interactions discussed here are accounted for in the recommended dosing for this indication. No dosage adjustment is needed when dexamethasone is used in combination with a single 40-mg dose of oral aprepitant. Dexamethasone is a CYP3A4 substrate. Aprepitant, when administered as a 3-day oral regimen (125 mg/80 mg/80 mg), is a moderate CYP3A4 inhibitor and inducer. The AUC of dexamethasone (8 mg PO on days 1, 2, and 3) was increased by approximately 2-fold on days 1 and 2 when given with a single 150-mg dose of IV fosaprepitant. After a 5-day regimen of oral aprepitant (125 mg/80 mg/80 mg/80 mg/80 mg), the AUC of dexamethasone increased 2.2-fold on days 1 and 5. A single dose of aprepitant 40 mg increased the AUC of dexamethasone by 1.45-fold, which was not considered clinically significant. [30676] [40027] Argatroban: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Aripiprazole: (Moderate) Because aripiprazole is metabolized by CYP3A4, concurrent use of CYP3A4 inducers such as dexamethasone may result in decreased plasma concentrations of aripiprazole. If these agents are used in combination, the patient should be carefully monitored for a decrease in aripiprazole efficacy. An increase in aripiprazole dosage may be clinically warranted in some patients. Avoid concurrent use of Abilify Maintena with a CYP3A4 inducer when the combined treatment period exceeds 14 days because aripiprazole blood concentrations decline and may become suboptimal. There are no dosing recommendations for Aristada or Aristada Initio during concurrent use of a mild or moderate CYP3A4 inducer. [30011] [31327] [53394] [63328] Armodafinil: (Minor) Armodafinil is partially metabolized via CYP3A4/5 isoenzymes. CYP3A4 inducers, such as dexamethasone, may potentially increase the metabolism of armodafinil. Decreased serum levels of armodafinil could potentially result in decreased efficacy of the drug. [10318] Arsenic Trioxide: (Moderate) Caution is advisable during concurrent use of arsenic trioxide and corticosteroids as electrolyte imbalance caused by corticosteroids may increase the risk of QT prolongation with arsenic trioxide. [26417] [59438] Artemether; Lumefantrine: (Major) Dexamethasone is a substrate/inducer and both components of artemether; lumefantrine are substrates of the CYP3A4 isoenzyme; therefore, coadministration may lead to decreased artemether; lumefantrine concentrations. Concomitant use warrants caution due to a possible reduction in antimalarial activity. [11334] [35401] [6759] Asparaginase Erwinia chrysanthemi: (Moderate) Concomitant use of L-asparaginase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions. [55362] Aspirin, ASA: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Butalbital; Caffeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Butalbital; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Caffeine; Dihydrocodeine: (Moderate) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine. [30282] [54286] (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Caffeine; Orphenadrine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Carisoprodol: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Citric Acid; Sodium Bicarbonate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Dipyridamole: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Omeprazole: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29564] [54286] (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Oxycodone: (Moderate) Monitor for reduced efficacy of oxycodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of oxycodone as needed. If dexamethasone is discontinued, consider a dose reduction of oxycodone and frequently monitor for signs of respiratory depression and sedation. Oxycodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease oxycodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. [39926] [54286] (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Aspirin, ASA; Pravastatin: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Atazanavir: (Major) Avoid concurrent use of dexamethasone with atazanavir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to atazanavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; atazanavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone) whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [28142] [58000] Atazanavir; Cobicistat: (Major) Avoid concurrent use of dexamethasone with atazanavir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to atazanavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; atazanavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone) whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [28142] [58000] (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [51664] [58000] Atenolol; Chlorthalidone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Atracurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Atropine; Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Atropine; Hyoscyamine; Phenobarbital; Scopolamine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Phenobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Avanafil: (Minor) Avanafil is primarily metabolized by CYP3A4, and although no studies have been performed, concomitant administration of CYP3A4 inducers, such as dexamethasone, may decrease avanafil plasma levels. Concomitant use is not recommended. [4718] [49866] Avapritinib: (Major) Avoid coadministration of avapritinib with dexamethasone due to the risk of decreased avapritinib efficacy. Avapritinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer is predicted to decrease the AUC and Cmax of avapritinib by 62% and 55%, respectively. [54286] [64922] Axitinib: (Major) Avoid coadministration of axitinib with dexamethasone due to the risk of decreased efficacy of axitinib. Selection of a concomitant medication with no or minimal CYP3A4 induction potential is recommended. Axitinib is a CYP3A4/5 substrate and dexamethasone is a CYP3A4 inducer. Coadministration with a strong CYP3A4/5 inducer significantly decreased the plasma exposure of axitinib in healthy volunteers. [34477] [48494] [54286] Azathioprine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [4710] [7714] Azilsartan; Chlorthalidone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Basiliximab: (Minor) Because systemically administered corticosteroids have immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives. [4746] Bedaquiline: (Major) Avoid concurrent use of dexamethasone with bedaquiline. Dexamethasone is a CYP3A4 inducer, which may result in decreased bedaquiline systemic exposure (AUC) and possibly reduced therapeutic effect. [34477] [52746] Belladonna Alkaloids; Ergotamine; Phenobarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Phenobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Benazepril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Bendroflumethiazide; Nadolol: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Benzhydrocodone; Acetaminophen: (Moderate) Concurrent use of benzhydrocodone with dexamethasone may decrease hydrocodone plasma concentrations, decrease opioid efficacy, and potentially lead to a withdrawal syndrome in those with physical dependence to opioid agonists. If concomitant use is necessary, consider increasing the benzhydrocodone dosage until stable drug effects are achieved. Monitor for signs of opioid withdrawal. Discontinuation of dexamethasone may increase the risk of increased opioid-related adverse reactions, such as fatal respiratory depression. If dexamethasone is discontinued, consider a benzhydrocodone dosage reduction and monitor patients for respiratory depression and sedation at frequent intervals. Benzhydrocodone is a prodrug of hydrocodone. Dexamethasone is an inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of hydrocodone. [48640] [62889] Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Bepridil: (Moderate) Hypokalemia-producing agents, including corticosteroids, may increase the risk of bepridil-induced arrhythmias and should therefore be administered cautiously in patients receiving bepridil therapy. [3085] [4953] Bexarotene: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents, such as bexarotene. [30943] Bicalutamide: (Major) Bicalutamide is metabolized by cytochrome P450 3A4. Drugs that are potent inducers of CYP3A4 activity, such as dexamethasone, will decrease the plasma concentrations of bicalutamide.It is not known if bicalutamide dosing adjustments are necessary. [7874] Bismuth Subsalicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Bisoprolol; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Bivalirudin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Boceprevir: (Moderate) Coadministration of dexamethasone and boceprevir is not recommended. If coadministered, close clinical monitoring for increased dexamethasone-related adverse events and for decreased boceprevir efficacy is advised. If dexamethasone dose adjustments are made, re-adjust the dose upon completion of boceprevir treatment. Predictions about the interaction can be made based on the metabolic pathways of dexamethasone and boceprevir. Dexamethasone is an inducer and substrate of the hepatic isoenzyme CYP3A4; boceprevir is an inhibitor and substrate of this isoenzyme. Additionally, both dexamethasone and boceprevir are substrates for the drug efflux transporter P-glycoprotein (PGP). When used in combination, the plasma concentrations of dexamethasone may be elevated and the plasma concentration of boceprevir may be deceased, resulting in an increased potential for dexamethasone-related adverse events and boceprevir treatment failure. [44314] [6759] Bortezomib: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Bosentan: (Minor) A dose adjustment of systemic dexamethasone may be necessary if bosentan is initiated or withdrawn during therapy. Bosentan may increase the metabolism of dexamethasone resulting in decreased exposure. Bosentan is an inducer of CYP3A4; dexamethasone is a CYP3A4 substrate. [28496] Brentuximab vedotin: (Moderate) Concomitant administration of brentuximab vedotin and dexamethasone may decrease the exposure of monomethyl auristatin E (MMAE), one of the 3 components released from brentuximab vedotin. MMAE is a CYP3A4 substrate and dexamethasone is a potent CYP3A4 inducer; therefore, the efficacy of brentuximab may be reduced. [45378] [48640] Brexpiprazole: (Moderate) Because brexpiprazole is partially metabolized by CYP3A4, concurrent use of CYP3A4 inducers such as dexamethasone may result in decreased plasma concentrations of brexpiprazole. If these agents are used in combination, the patient should be carefully monitored for a decrease in brexpiprazole efficacy. An increase in brexpiprazole dosage may be clinically warranted in some patients. [59949] [6759] Brigatinib: (Moderate) Avoid coadministration of brigatinib with dexamethasone due to decreased plasma exposure to brigatinib which may result in decreased efficacy. If concomitant use is unavoidable, after 7 days of concomitant treatment with dexamethasone, increase the dose of brigatinib as tolerated in 30 mg increments to a maximum of twice the original brigatinib dose. After discontinuation of dexamethasone, resume the brigatinib dose that was tolerated prior to initiation of dexamethasone. Brigatinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a moderate CYP3A inducer is predicted to decrease the AUC of brigatinib by approximately 50%. [54286] [61909] Bromocriptine: (Moderate) Caution and close monitoring are advised if bromocriptine and dexamethasone are used together. Concurrent use may decrease the plasma concentrations of bromocriptine resulting in loss of efficacy. Bromocriptine is extensively metabolized by the liver via CYP3A4; dexamethasone is a moderate inducer of CYP3A4. [35591] [54285] Brompheniramine; Carbetapentane; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Brompheniramine; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Brompheniramine; Guaifenesin; Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Brompheniramine; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Budesonide: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone. [28001] Budesonide; Formoterol: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone. [28001] Budesonide; Glycopyrrolate; Formoterol: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone. [28001] Bupivacaine; Lidocaine: (Moderate) Concomitant use of systemic lidocaine and dexamethasone may decrease lidocaine plasma concentrations. Higher lidocaine doses may be required; titrate to effect. Lidocaine is a CYP3A4 and CYP1A2 substrate; dexamethasone induces CYP3A4. [32857] [54286] Bupropion: (Moderate) Because bupropion is associated with a dose-related risk of seizures, extreme caution is recommended during concurrent use of other drugs that may lower the seizure threshold such as systemic corticosteroids. Low initial dosing and slow dosage titration of bupropion is recommended if these combinations must be used; the patient should be closely monitored. [41057] [41086] Bupropion; Naltrexone: (Moderate) Because bupropion is associated with a dose-related risk of seizures, extreme caution is recommended during concurrent use of other drugs that may lower the seizure threshold such as systemic corticosteroids. Low initial dosing and slow dosage titration of bupropion is recommended if these combinations must be used; the patient should be closely monitored. [41057] [41086] Buspirone: (Moderate) Potent inducers of hepatic cytochrome P450 3A4, such as dexamethasone, may increase the rate of buspirone metabolism. [28001] Butabarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butabarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Cabozantinib: (Minor) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with cabozantinib is necessary. Dexamethasone is a P-glycoprotein (P-gp) substrate. Cabozantinib is a P-gp inhibitor and has the potential to increase plasma concentrations of P-gp substrates; however, the clinical relevance of this finding is unknown. [34477] [52506] [54286] [60738] Calcium Carbonate: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. [8255] [8256] Calcium Carbonate; Magnesium Hydroxide: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. [8255] [8256] Calcium Carbonate; Risedronate: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. [8255] [8256] Calcium Carbonate; Simethicone: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function. [8255] [8256] Canagliflozin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Canagliflozin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Candesartan; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Capmatinib: (Major) Avoid coadministration of capmatinib and dexamethasone due to the risk of decreased capmatinib exposure, which may reduce its efficacy. Capmatinib is a CYP3A substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer decreased capmatinib exposure by 44%. [34477] [54286] [65377] Captopril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Carbamazepine: (Moderate) Hepatic microsomal enzyme inducers, including carbamazepine, can increase the metabolism of dexamethasone. Dosage adjustments may be necessary, and closer monitoring of clinical and/or adverse effects is warranted when carbamazepine is used with dexamethasone. [41237] Carbetapentane; Chlorpheniramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Carbetapentane; Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Carbetapentane; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Carbetapentane; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Carbetapentane; Phenylephrine; Pyrilamine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Carbinoxamine; Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Carbinoxamine; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Carbinoxamine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Cariprazine: (Major) Cariprazine and its active metabolites are extensively metabolized by CYP3A4. Concurrent use of cariprazine with CYP3A4 inducers, such as dexamethasone, has not been evaluated and is not recommended because the net effect on active drug and metabolites is unclear. [30011] [60164] Carmustine, BCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [5946] [7714] [7944] Carvedilol: (Minor) Increased concentrations of dexamethasone may occur if it is coadministered with carvedilol; exercise caution. Carvedilol is a P-glycoprotein (P-gp) inhibitor and dexamethasone is a P-gp substrate. [34477] [51834] [58220] Caspofungin: (Major) Data suggest that coadministration of inducers or mixed inducers/inhibitors of hepatic drug clearance along with caspofungin may result in reduced caspofungin blood concentrations. The reductions may be clinically significant. It is not known how caspofungin drug clearance is induced. Drugs that may lead to reductions in caspofungin concentrations include dexamethasone. For adult patients receiving dexamethasone, an increase in the caspofungin dose to 70 mg/day should be considered. For pediatric patients receiving dexamethasone, a daily dosage of 70 mg/m2, not to exceed 70 mg, should be considered. [28782] Cenobamate: (Minor) A dose adjustment of systemic dexamethasone may be necessary if cenobamate is initiated or withdrawn during therapy. Cenobamate may increase the metabolism of dexamethasone resulting in decreased exposure. Cenobamate is a moderate inducer of CYP3A4; dexamethasone is a CYP3A4 substrate. [54286] [64768] Ceritinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ceritinib with dexamethasone is necessary, due to increased dexamethasone exposure; Cushings syndrome and adrenal suppression could potentially occur with long-term use. Consider the use of corticosteroids such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, especially for long-term use. Ceritinib is a strong CYP3A4 inhibitor and dexamethasone is primarily metabolized by CYP3A4. Another strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. [54286] [57094] Certolizumab pegol: (Moderate) The safety and efficacy of certolizumab in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with certolizumab may be at a greater risk of developing an infection. Many of the serious infections occurred in patients on immunosuppressive therapy who received certolizumab. [10783] Chlophedianol; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Chlorambucil: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [4757] [7714] Chlorothiazide: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Chlorpheniramine; Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Chlorpheniramine; Dihydrocodeine; Phenylephrine: (Moderate) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine. [30282] [54286] (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Chlorpheniramine; Dihydrocodeine; Pseudoephedrine: (Moderate) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine. [30282] [54286] Chlorpheniramine; Guaifenesin; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Chlorpheniramine; Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Chlorpheniramine; Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Chlorpheniramine; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Chlorpheniramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Chlorpropamide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Chlorthalidone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Chlorthalidone; Clonidine: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Cholestyramine: (Moderate) Cholestyramine may increase the clearance of corticosteroids. [8844] Choline Salicylate; Magnesium Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Cimetidine: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Cisapride: (Moderate) Cisapride is metabolized by the hepatic cytochrome P450 enzyme system, specifically the CYP3A4 isoenzyme. Inducers of CYP3A4, such as dexamethasone, may increase the clearance of cisapride. [4718] [5137] Cisatracurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Citalopram: (Moderate) Caution is advisable during concurrent use of citalopram and corticosteroids as electrolyte imbalance caused by corticosteroids may increase the risk of QT prolongation with citalopram. [26417] [28269] Clarithromycin: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage. [28238] [34477] Clindamycin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Clofarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7557] [7714] Clozapine: (Moderate) Caution is advisable during concurrent use of dexamethasone and clozapine. Dexamethasone is an inducer of CYP3A4, one of the isoenzymes responsible for the metabolism of clozapine. According to the manufacturer, patients receiving clozapine in combination with a weak to moderate CYP3A4 inducer should be monitored for loss of effectiveness. Consideration should be given to increasing the clozapine dose if necessary. Concurrent use with strong CYP3A4 inducers is not recommended. Topical corticosteroids are not likely to interact. [28262] [6759] Cobicistat: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [51664] [58000] Cobimetinib: (Major) Avoid the concurrent use of cobimetinib with dexamethasone due to decreased cobimetinib efficacy. Cobimetinib is a CYP3A substrate in vitro, and dexamethasone is a moderate inducer of CYP3A. Based on simulations, cobimetinib exposure would decrease by 73% when coadministered with a moderate CYP3A inducer. [34477] [54286] [60281] Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] Codeine; Guaifenesin: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] Codeine; Phenylephrine; Promethazine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Codeine; Promethazine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. [33654] [34883] [54286] Conivaptan: (Major) Coadministration of conivaptan, a CYP3A4/P-glycoprotein (P-gp) inhibitor and CYP3A4 substrate, and dexamethasone, a CYP3A4/P-gp substrate and CYP3A4 inducer, may result in elevated dexamethasone concentrations and decreased conivaptan concentrations. According to the manufacturer of conivaptan, concomitant use of conivaptan and CYP3A substrates should be avoided. Treatment with dexamethasone may be initiated no sooner than 1 week after completion of conivaptan therapy. In addition, conivaptan has been associated with hypokalemia (9.8%). Although not studied, consider the potential for additive hypokalemic effects if conivaptan is coadministered with drugs known to induce hypokalemia, such as corticosteroids. [26417] [31764] [34477] [54286] Corticorelin, Ovine: (Major) Patients pretreated with dexamethasone have demonstrated an inhibited or blunted response to corticotropin, ovine. Patients receiving corticotropin, ovine should not be pretreated with dexamethasone; no specific guidelines are available. [6759] Crizotinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of crizotinib with dexamethasone is necessary due to increased dexamethasone exposure. Dexamethasone is a CYP3A4 substrate and crizotinib is a moderate CYP3A inhibitor. A strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, increasing the risk of corticosteroid-related side effects. [45458] [54286] Cyclosporine: (Moderate) Convulsions have been reported during concurrent use of cyclosporine and other corticosteroids. In addition, mutual inhibition of metabolism occurs with concurrent use of cyclosporine and dexamethasone; therefore, the potential for adverse events associated with either drug may be increased. Coadministration should be approached with caution. [29779] [30015] [30028] [36319] [41361] Dabrafenib: (Major) Use dabrafenib and dexamethasone together with caution; concentrations of either agent may be decreased. Use an alternate agent in place of dexamethasone if possible. If concomitant use cannot be avoided, monitor patients for loss of dexamethasone efficacy. Dexamethasone and dabrafenib are both CYP3A4 substrates and moderate CYP3A4 inducers. [54286] [54802] Daclatasvir: (Major) The dose of daclatasvir, a CYP3A4 substrate, must be increased to 90 mg PO once daily when administered in combination with moderate CYP3A4 inducers, such as dexamethasone. Taking these drugs together may decrease daclatasvir serum concentrations, potentially resulting in reduced antiviral efficacy and antimicrobial resistance. Conversely, the therapeutic effects of dexamethasone, a P-glycoprotein (P-gp) substrate, may be increased by daclatasvir, a P-gp inhibitor. [34477] [54286] [60001] Dapagliflozin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Dapagliflozin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Dapagliflozin; Saxagliptin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Dapsone: (Moderate) Closely monitor for a reduction in dapsone efficacy and signs of hemolytic anemia if coadministration with dexamethasone is necessary. Dapsone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration may decrease plasma concentrations of dapsone and increase the formation of dapsone hydroxylamine (a metabolite associated with hemolysis). [34335] [34470] [60612] Darunavir: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [32432] [58000] Darunavir; Cobicistat: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [32432] [58000] (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [51664] [58000] Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [32432] [58000] (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [51664] [58000] Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir: (Severe) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. [34477] [54286] [58664] (Severe) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir or ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. [34477] [54286] [58664] (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate. [4718] [5070] [5206] Deferasirox: (Moderate) Because gastric ulceration and GI bleeding have been reported in patients taking deferasirox, use caution when coadministering with other drugs known to increase the risk of peptic ulcers or gastric hemorrhage including corticosteroids. [31807] Deflazacort: (Major) Avoid concomitant use of deflazacort and dexamethasone. Concurrent use may significantly decrease concentrations of 21-desDFZ, the active metabolite of deflazacort, resulting in loss of efficacy. Deflazacort is a CYP3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Administration of deflazacort with multiple doses of rifampin (a strong CYP3A4 inducer) resulted in geometric mean exposures that were approximately 95% lower compared to administration alone. [54286] [61750] Delavirdine: (Minor) Since dexamethasone may induce metabolism of delavirdine, concomitant use of these agents should be done with caution. Delavirdine therapy may be less effective due to decreased plasma levels in patients taking these drugs concomitantly. [5206] Denileukin Diftitox: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Denosumab: (Moderate) The safety and efficacy of denosumab use in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with denosumab may be at a greater risk of developing an infection. [40862] Desmopressin: (Major) Desmopressin, when used in the treatment of nocturia is contraindicated with corticosteroids because of the risk of severe hyponatremia. Desmopressin can be started or resumed 3 days or 5 half-lives after the corticosteroid is discontinued, whichever is longer. [61806] Dextran: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Dextromethorphan; Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Dextromethorphan; Quinidine: (Moderate) Quinidine is a substrate of the CYP3A4 isoenzyme. Inducers of CYP3A4 such as dexamethasone may increase hepatic elimination of quinidine with the potential for reduced efficacy of quinidine. [10571] [6759] Digoxin: (Moderate) Hypokalemia, hypomagnesemia, or hypercalcemia increase digoxin's effect. Corticosteroids can precipitate digoxin toxicity via their effect on electrolyte balance. It is recommended that serum potassium, magnesium, and calcium be monitored regularly in patients receiving digoxin. [28272] [29377] Dihydrocodeine; Guaifenesin; Pseudoephedrine: (Moderate) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine. [30282] [54286] Dipeptidyl Peptidase-4 Inhibitors: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Diphenhydramine; Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Dofetilide: (Major) Corticosteroids can cause increases in blood pressure, sodium and water retention, and hypokalemia, predisposing patients to interactions with certain other medications. Corticosteroid-induced hypokalemia could also enhance the proarrhythmic effects of dofetilide. [49489] Dolutegravir; Rilpivirine: (Severe) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine. [44376] [54286] Doravirine: (Moderate) Concurrent administration of doravirine and dexamethasone may result in decreased doravirine exposure, resulting in potential loss of virologic control. Doravirine is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. [54286] [63484] Doravirine; Lamivudine; Tenofovir disoproxil fumarate: (Moderate) Concurrent administration of doravirine and dexamethasone may result in decreased doravirine exposure, resulting in potential loss of virologic control. Doravirine is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. [54286] [63484] Doxacurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Dronabinol: (Moderate) Use caution if coadministration of dronabinol with dexamethasone is necessary, and monitor for a decrease in the efficacy of dronabinol. Dronabinol is a CYP2C9 and 3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Concomitant use may result in decreased plasma concentrations of dronabinol. [30431] [34477] [54286] [60951] Dronedarone: (Major) The concomitant use of dronedarone and CYP3A4 inducers should be avoided. Dronedarone is metabolized by CYP3A and is an inhibitor of CYP3A and P-gp. Dexamethasone induces CYP3A4 and is a substrate for CYP3A4 and P-gp. Coadministration of CYP3A4 inducers, such as dexamethasone, with dronedarone may result in reduced plasma concentration and subsequent reduced effectiveness of dronedarone therapy; the plasma concentrations of dexamethasone may also be increased. [36101] Droperidol: (Moderate) Caution is advised when using droperidol in combination with corticosteroids which may lead to electrolyte abnormalities, especially hypokalemia or hypomagnesemia, as such abnormalities may increase the risk for QT prolongation or cardiac arrhythmias. [5468] Dulaglutide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Echinacea: (Moderate) Echinacea possesses immunostimulatory activity and may theoretically reduce the response to immunosuppressant drugs like corticosteroids. For some patients who are using corticosteroids for serious illness, such as cancer or organ transplant, this potential interaction may result in the preferable avoidance of Echinacea. Although documentation is lacking, coadministration of echinacea with immunosuppressants is not recommended by some resources. [25398] [32073] [61902] [61905] Econazole: (Minor) In vitro studies indicate that corticosteroids inhibit the antifungal activity of econazole against C. albicans in a concentration-dependent manner. When the concentration of the corticosteroid was equal to or greater than that of econazole on a weight basis, the antifungal activity of econazole was substantially inhibited. When the corticosteroid concentration was one-tenth that of econazole, no inhibition of antifungal activity was observed. [6968] Efalizumab: (Major) Patients receiving immunosuppressives should not receive concurrent therapy with efalizumab because of the possibility of increased infections and malignancies. [7127] [7714] Elagolix: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with elagolix is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and elagolix is a weak to moderate CYP3A4 inducer. [54286] [63387] Elagolix; Estradiol; Norethindrone acetate: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with elagolix is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and elagolix is a weak to moderate CYP3A4 inducer. [54286] [63387] Elbasvir; Grazoprevir: (Major) If possible, avoid concurrent administration of elbasvir with dexamethasone. Dexamethasone is a moderate CYP3A inducer, while elbasvir is a substrate of CYP3A. Use of these drugs together is expected to decrease the plasma concentrations of elbasvir, and may result in decreased virologic response. [54286] [60523] (Major) If possible, avoid concurrent administration of grazoprevir with dexamethasone. Dexamethasone is a moderate CYP3A inducer, while grazoprevir is a substrate of CYP3A. Use of these drugs together is expected to decrease the plasma concentrations of grazoprevir, and may result in decreased virologic response. Conversely, concentrations of dexamethasone (also a CYP3A substrate) may be increased when given with grazoprevir (a weak CYP3A inhibitor). [54286] [60523] Eliglustat: (Moderate) Coadministration of dexamethasone and eliglustat may result in increased plasma concentrations of dexamethasone. Monitor patients closely for corticosteroid-related adverse effects; if appropriate, consider reducing the dexamethasone dosage and titrating to clinical effect. Dexamethasone is a P-glycoprotein (P-gp) substrate; eliglustat is a P-gp inhibitor. [34477] [57803] Elvitegravir: (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme. [51664] [58001] [60269] Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [51664] [58000] (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme. [51664] [58001] [60269] Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. [51664] [58000] (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme. [51664] [58001] [60269] Empagliflozin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Empagliflozin; Linagliptin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Empagliflozin; Linagliptin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Empagliflozin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Severe) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine. [44376] [54286] Emtricitabine; Rilpivirine; Tenofovir disoproxil fumarate: (Severe) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine. [44376] [54286] Enalapril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Encorafenib: (Major) Avoid coadministration of encorafenib and dexamethasone due to decreased encorafenib exposure and potential loss of efficacy. Encorafenib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Coadministration with CYP3A4 inducers has not been studied with encorafenib; however, in clinical trials, steady-state encorafenib exposures were lower than encorafenib exposures after the first dose, suggesting CYP3A4 auto-induction. [54286] [63317] Entrectinib: (Major) Avoid coadministration of entrectinib with dexamethasone due to decreased entrectinib exposure and risk of decreased efficacy. Entrectinib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Coadministration of a moderate CYP3A4 inducer is predicted to reduce the entrectinib AUC by 56%. [54286] [64567] Enzalutamide: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with enzalutamide is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and enzalutamide is a strong CYP3A4 inducer. [51727] [54286] Ephedrine: (Moderate) Ephedrine may enhance the metabolic clearance of corticosteroids. Decreased blood concentrations and lessened physiologic activity may necessitate an increase in corticosteroid dosage. [8844] Eprosartan; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Erdafitinib: (Major) If coadministration of erdafitinib and dexamethasone is necessary at the initiation of erdafitinib therapy, administer the dose of erdafitinib as recommended (8 mg once daily with potential to increase the dose to 9 mg on days 14 to 21 based on phosphate levels and tolerability). If dexamethasone must be added to erdafitinib therapy after the initial dose increase period (days 14 to 21), increase the dose of erdafitinib up to 9 mg. If dexamethasone is discontinued, continue erdafitinib at the same dose in the absence of drug-related toxicity. Erdafitinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [54286] [64064] Erlotinib: (Major) Avoid the coadministration of erlotinib with dexamethasone if possible due to the risk of decreased erlotinib efficacy. If concomitant use is unavoidable, increase the dose of erlotinib by 50 mg increments at 2-week intervals as tolerated, to a maximum of 450 mg. Also, monitor for symptoms of gastrointestinal (GI) perforation (e.g., severe abdominal pain, fever, nausea, and vomiting); permanently discontinue erlotinib in patients who develop GI perforation. Erlotinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration may decrease plasma concentrations of erlotinib. The pooled incidence of GI perforation clinical trials of erlotinib ranged from 0.1% to 0.4%, including fatal cases; patients receiving concomitant dexamethasone may be at increased risk. [30555] [54286] Ertugliflozin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Ertugliflozin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Ertugliflozin; Sitagliptin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Erythromycin: (Moderate) Caution is warranted with the use of dexamethasone and erythromycin. Erythromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of corticosteroids such as dexamethasone. [28251] Erythromycin; Sulfisoxazole: (Moderate) Caution is warranted with the use of dexamethasone and erythromycin. Erythromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of corticosteroids such as dexamethasone. [28251] Escitalopram: (Minor) Escitalopram is metabolized by CYP2C19 and CYP3A4. Dexamethasone can induce the metabolism of various CYP 450 isoenzymes, including those involved in escitalopram metabolism. Although no clinical data are available to support a clinically significant interaction, escitalopram may need to be administered in higher doses in patients chronically taking dexamethasone. [4718] [4997] Esomeprazole: (Moderate) Monitor for decreased efficacy of esomeprazole if coadministration with dexamethasone is necessary. Esomeprazole is extensively metabolized in the liver by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased esomeprazole plasma concentrations. The manufacturer of esomeprazole recommends avoidance with strong inducers because decreased exposure of esomeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29524] [54286] Esomeprazole; Naproxen: (Moderate) Monitor for decreased efficacy of esomeprazole if coadministration with dexamethasone is necessary. Esomeprazole is extensively metabolized in the liver by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased esomeprazole plasma concentrations. The manufacturer of esomeprazole recommends avoidance with strong inducers because decreased exposure of esomeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29524] [54286] Estramustine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [4744] [7714] Estrogens: (Moderate) Estrogens have been associated with elevated serum concentrations of corticosteroid binding globulin (CBG), leading to increased total circulating corticosteroids, although the free concentrations of these hormones may be lower; the clinical significance is not known. Estrogens are CYP3A4 substrates and dexamethasone is a CYP3A4 inducer; concomitant use may decrease the clinical efficacy of estrogens. Patients should be monitored for signs of decreased clinical effects of estrogens (e.g., breakthrough bleeding), oral contraceptives, or non-oral combination contraceptives if these drugs are used together. [4718] [4744] [6395] Eszopiclone: (Moderate) Potent inducers of CYP3A4, such as dexmethasone, may cause a reduction in the plasma concentration of eszopiclone. [28001] [30571] Etravirine: (Major) Dexamethasone can induce the activity of CYP3A4 and increase the metabolism of etravirine; decreased antiviral efficacy may be seen. While concomitant administration has not been evaluated, a potentially significant interaction may occur. Use these drugs concomitantly with caution, or consider alternative corticosteroids, particularly for long-term use. [33718] Exenatide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Fedratinib: (Major) Avoid coadministration of fedratinib with dexamethasone as concurrent use may decrease fedratinib exposure which may result in decreased therapeutic response. Fedratinib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. The coadministration of fedratinib with a moderate CYP3A4 inducer has not been evaluated. [54286] [64568] Fentanyl: (Moderate) Consider an increased dose of fentanyl and monitor for evidence of opioid withdrawal if concurrent use of dexamethasone is necessary. If dexamethasone is discontinued, consider reducing the fentanyl dosage and monitor for evidence of respiratory depression. Coadministration of a CYP3A4 inducer like dexamethasone with fentanyl, a CYP3A4 substrate, may decrease exposure to fentanyl resulting in decreased efficacy or onset of withdrawal symptoms in a patient who has developed physical dependence to fentanyl. Fentanyl plasma concentrations will increase once the inducer is stopped, which may increase or prolong the therapeutic and adverse effects, including serious respiratory depression. [29623] [29763] [32731] [40943] [54286] Flibanserin: (Major) The concomitant use of flibanserin with CYP3A4 inducers significantly decreases flibanserin exposure compared to the use of flibanserin alone. Therefore, concurrent use of flibanserin and CYP3A4 inducers, such as dexamethasone, is not recommended. [60099] [6759] Fluconazole: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Fluoxymesterone: (Moderate) Coadministration of corticosteroids and fluoxymesterone may increase the risk of edema, especially in patients with underlying cardiac or hepatic disease. Corticosteroids with greater mineralocorticoid activity, such as fludrocortisone, may be more likely to cause edema. Administer these drugs in combination with caution. [11342] Food: (Moderate) The incidence of marijuana associated adverse effects may change following coadministration with dexamethasone. Dexamethasone is an inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of marijuana's most psychoactive compound, delta-9-tetrahydrocannabinol (Delta-9-THC). When given concurrently with dexamethasone, the amount of Delta-9-THC converted to the active metabolite 11-hydroxy-delta-9-tetrahydrocannabinol (11-OH-THC) may be increased. These changes in Delta-9-THC and 11-OH-THC plasma concentrations may result in an altered marijuana adverse event profile. [42135] [42448] [6759] Fosamprenavir: (Moderate) Dexamethasone decreases amprenavir serum concentrations. Therefore, use caution when administering dexamethasone and fosamprenavir concurrently. Fosamprenavir may be less effective in patients taking these agents together. [5747] Fosinopril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Gallium Ga 68 Dotatate: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia. Also, corticotropin may cause calcium loss and sodium and fluid retention. Mannitol itself can cause hypernatremia. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly. [6524] Gefitinib: (Moderate) Monitor for clinical response of gefitinib if used concomitantly with dexamethasone. Gefitinib is metabolized significantly by CYP3A4 and dexamethasone is a CYP3A4 inducer; coadministration may increase gefitinib metabolism and decrease gefitinib concentrations. While the manufacturer has provided no guidance regarding the use of gefitinib with mild or moderate CYP3A4 inducers, administration of a single 500 mg gefitinib dose with a concurrent strong CYP3A4 inducer (rifampin) resulted in reduced mean AUC of gefitinib by 83%. [34477] [45935] [54286] Gemcitabine: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Gentamicin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Glasdegib: (Major) Avoid coadministration of glasdegib and dexamethasone due to the potential for decreased glasdegib exposure and risk of decreased efficacy. If concurrent use cannot be avoided, increase the glasdegib dosage (i.e., from 100 mg PO daily to 200 mg PO daily; or from 50 mg PO daily to 100 mg PO daily). Resume the previous dose of glasdegib after dexamethasone has been discontinued for 7 days. Glasdegib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer was predicted to decrease the glasdegib AUC value by 55% [54286] [63777] Glecaprevir; Pibrentasvir: (Moderate) Caution is advised with the coadministration of glecaprevir and dexamethasone as coadministration may increase serum concentrations of dexamethasone and increase the risk of adverse effects. Dexamethasone is a substrate of P-glycoprotein (P-gp); glecaprevir is a P-gp inhibitor. [34477] [62201] (Moderate) Caution is advised with the coadministration of pibrentasvir and dexamethasone as coadministration may increase serum concentrations of dexamethasone and increase the risk of adverse effects. Dexamethasone is a substrate of P-glycoprotein (P-gp); pibrentasvir is a P-gp inhibitor. [34477] [62201] Glimepiride: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glimepiride; Pioglitazone: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glimepiride; Rosiglitazone: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glipizide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glipizide; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glyburide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glyburide; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Glycerol Phenylbutyrate: (Moderate) Corticosteroids may induce elevated blood ammonia concentrations. Corticosteroids should be used with caution in patients receiving glycerol phenylbutyrate. Monitor ammonia concentrations closely. [53022] Golimumab: (Moderate) The safety and efficacy of golimumab in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with golimumab may be at a greater risk of developing an infection. [35501] Guaifenesin; Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Guaifenesin; Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Guanfacine: (Major) Dexamethasone may significantly decrease guanfacine plasma concentrations. FDA-approved labeling for extended-release (ER) guanfacine recommends that, if these agents are taken together, doubling the recommended dose of guanfacine should be considered; if dexamethasone is added in a patient already receiving guanfacine, this escalation should occur over 1 to 2 weeks. If dexamethasone is discontinued, decrease the guanfacine ER dosage back to the recommended dose over 1 to 2 weeks. Specific recommendations for immediate-release (IR) guanfacine are not available. Guanfacine is primarily metabolized by CYP3A4, and dexamethasone is a moderate CYP3A4 inducer. [43566] [54286] Halofantrine: (Major) Due to the risks of cardiac toxicity of halofantrine in patients with hypokalemia and/or hypomagnesemia, the use of halofantrine should be avoided in combination with agents that may lead to electrolyte losses, such as corticosteroids. [4968] Haloperidol: (Moderate) Caution is advisable during concurrent use of haloperidol and corticosteroids as electrolyte imbalance caused by corticosteroids may increase the risk of QT prolongation with haloperidol. [28307] Hemin: (Moderate) Hemin works by inhibiting aminolevulinic acid synthetase. Corticosteroids increase the activity of this enzyme should not be used with hemin. [6702] Heparin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Hetastarch: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Homatropine; Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Hydantoins: (Moderate) Hydantoin anticonvulsants induce hepatic microsomal enzymes and may increase the metabolism of dexamethasone, leading to reduced efficacy. Depending on the individual clinical situation and the indication for the interacting medication, enzyme-induction interactions may not always produce reductions in treatment efficacy. [28001] [28771] Hydralazine; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Irbesartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Lisinopril: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Losartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Methyldopa: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Metoprolol: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Moexipril: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Olmesartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Propranolol: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] (Moderate) Patients receiving corticosteroids during propranolol therapy may be at increased risk of hypoglycemia due to the loss of counter-regulatory cortisol response. This effect may be more pronounced in infants and young children. If concurrent use is necessary, carefully monitor vital signs and blood glucose concentrations as clinically indicated. [56853] Hydrochlorothiazide, HCTZ; Quinapril: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Spironolactone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Telmisartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Triamterene: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrochlorothiazide, HCTZ; Valsartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Hydrocodone; Ibuprofen: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Hydrocodone; Phenylephrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Hydrocodone; Potassium Guaiacolsulfonate: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Hydrocodone; Potassium Guaiacolsulfonate; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Hydrocodone; Pseudoephedrine: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [30011] [30379] [56303] Hydroxyurea: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Hylan G-F 20: (Major) The safety and efficacy of hylan G-F 20 given concomitantly with other intra-articular injectables have not been established. Other intra-articular injections may include intra-articular steroids (betamethasone, dexamethasone, hydrocortisone, prednisolone, methylprednisolone, and triamcinolone). [45238] [45239] Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] Ibritumomab Tiuxetan: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Ibrutinib: (Moderate) Use ibrutinib and dexamethasone together with caution; decreased ibrutinib levels may occur resulting in reduced ibrutinib efficacy. Monitor patients for signs of decreased ibrutinib efficacy if these agents are used together. Ibrutinib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A inducer. Simulations suggest that coadministration with a moderate CYP3A4 inducer may decrease ibrutinib exposure by 3-fold. [54286] [56410] Ibuprofen; Oxycodone: (Moderate) Monitor for reduced efficacy of oxycodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of oxycodone as needed. If dexamethasone is discontinued, consider a dose reduction of oxycodone and frequently monitor for signs of respiratory depression and sedation. Oxycodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease oxycodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. [39926] [54286] Idelalisib: (Major) Avoid concomitant use of idelalisib, a strong CYP3A inhibitor, with dexamethasone, a CYP3A substrate, as dexamethasone toxicities may be significantly increased. The AUC of a sensitive CYP3A substrate was increased 5.4-fold when coadministered with idelalisib. [57675] [6759] Ifosfamide: (Moderate) Closely monitor for increased ifosfamide-related toxicities (e.g., neurotoxicity, nephrotoxicity) if coadministration with dexamethasone is necessary. The significance of this interaction is unknwon, however, as dexamethasone is widely used as an antiemetic with chemotherapy such as ifosfamide. Ifosfamide is metabolized to its active alkylating metabolites by CYP3A4; dexamethasone is a moderate CYP3A4 inducer. Concomitant use may increase the formation of the neurotoxic/nephrotoxic ifosfamide metabolite, chloroacetaldehyde. [51027] [54286] Imatinib: (Minor) Any drug that induces cytochrome P450 3A4, such as dexamethasone, may increase the metabolism of imatinib and decrease imatinib concentrations and clinical effects. [4966] Incretin Mimetics: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Indapamide: (Moderate) Additive hypokalemia may occur when indapamide is coadministered with other drugs with a significant risk of hypokalemia such as systemic corticosteroids. Coadminister with caution and careful monitoring. [26417] Indinavir: (Moderate) Dexamethasone is a moderate inducer of CYP3A4. Coadministration with other drugs that are metabolized by CYP3A4 (e.g., indinavir) may increase their clearance, resulting in decreased plasma concentration. [8844] Inebilizumab: (Moderate) Concomitant usage of inebilizumab with immunosuppressant drugs, including systemic corticosteroids, may increase the risk of infection. Consider the risk of additive immune system effects when coadministering therapies that cause immunosuppression with inebilizumab. [65576] Infliximab: (Moderate) Many serious infections during infliximab therapy have occurred in patients who received concurrent immunosuppressives that, in addition to their underlying Crohn's disease or rheumatoid arthritis, predisposed patients to infections. The impact of concurrent infliximab therapy and immunosuppression on the development of malignancies is unknown. In clinical trials, the use of concomitant immunosuppressant agents appeared to reduce the frequency of antibodies to infliximab and appeared to reduce infusion reactions. [4711] Insulin Degludec; Liraglutide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Insulin Glargine; Lixisenatide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Insulins: (Moderate) Monitor patients receiving insulin closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Interferon Alfa-2a: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Interferon Alfa-2b: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Interferon Alfa-2b; Ribavirin: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Iohexol: (Major) Serious adverse events, including death, have been observed during intrathecal administration of both corticosteroids (i.e., dexamethasone) and radiopaque contrast agents (i.e., iohexol); therefore, concurrent use of these medications via the intrathecal route is contraindicated. Cases of cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been temporally associated (i.e., within minutes to 48 hours after injection) with epidural administration of injectable corticosteroids. In addition, patients inadvertently administered iohexol formulations not indicated for intrathecal use have experienced seizures, convulsions, cerebral hemorrhages, brain edema, and death. Administering these medications together via the intrathecal route may increase the risk for serious adverse events. [28963] [57053] Iopamidol: (Severe) Because both intrathecal corticosteroids (i.e., dexamethasone) and intrathecal radiopaque contrast agents (i.e., iopamidoll) can increase the risk of seizures, the intrathecal administration of corticosteroids with intrathecal radiopaque contrast agents is contraindicated. [5442] Isavuconazonium: (Major) Avoid concurrent use of dexamethasone with isavuconazonium. An alternative corticosteroid should be considered. Dexamethasone is a substrate and inducer of the hepatic isoenzyme CYP3A4 and a substrate of the drug transporter P-glycoprotein (P-gp); isavuconazole, the active moiety of isavuconazonium, is a sensitive substrate and moderate inhibitor of CYP3A4 and an inhibitor of P-gp. Concurrent use may result in significant decreases in the plasma concentrations of isavuconazole, leading to a reduction of antifungal efficacy and the potential for treatment failure. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. [34477] [54286] [59042] Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] Isoniazid, INH; Rifampin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] Isoproterenol: (Moderate) The risk of cardiac toxicity with isoproterenol in asthma patients appears to be increased with the coadministration of corticosteroids. Intravenous infusions of isoproterenol in refractory asthmatic children at rates of 0.05 to 2.7 mcg/kg/min have caused clinical deterioration, myocardial infarction (necrosis), congestive heart failure and death. [28004] Isotretinoin: (Minor) Both isotretinoin and corticosteroids can cause osteoporosis during chronic use. Patients receiving systemic corticosteroids should receive isotretinoin therapy with caution. [5283] Itraconazole: (Moderate) Monitor for corticosteroid-related adverse effects and altered response to itraconazole if coadminsitration is necessary. Itraconazole is a strong CYP3A4 inhibitor and substrate; dexamethasone is a moderate CYP3A4 inducer and substrate. Another strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. The clearance of itraconazole may also be increased, resulting in decreased plasma concentrations. [27983] [30011] [40233] Ivabradine: (Major) Avoid coadministration of ivabradine and dexamethasone. Ivabradine is primarily metabolized by CYP3A4; dexamethasone is an inducer of CYP3A4. Coadministration may decrease the plasma concentrations of ivabradine resulting in the potential for treatment failure. [34477] [59430] Ixabepilone: (Major) Ixabepilone is a CYP3A4 substrate and concomitant use with strong CYP3A4 inducers such as dexamethasone may lead to reduced and subtherapeutic concentrations of ixabepilone. Caution should be utilized when CYP3A4 inducers are coadministered with ixabepilone, and alternative therapies with low enzyme induction potential should be considered. [10415] [4718] Ketoconazole: (Moderate) Coadministration may result in increased exposure to dexamethasone and increased corticosteroid-related adverse effects. Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%. In addition, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal. [27982] [28001] [28279] [28761] [34535] Lansoprazole: (Minor) Monitor for decreased efficacy of lansoprazole if coadministration with dexamethasone is necessary. Lansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased lansoprazole plasma concentrations. [40596] [54286] Lansoprazole; Naproxen: (Minor) Monitor for decreased efficacy of lansoprazole if coadministration with dexamethasone is necessary. Lansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased lansoprazole plasma concentrations. [40596] [54286] Lapatinib: (Major) Avoid coadministration of lapatinib with dexamethasone due to decreased plasma concentrations of lapatinib. If concomitant use is unavoidable, gradually titrate the dose of lapatinib from 1,250 mg per day to 4,500 mg per day in patients receiving concomitant capecitabine (HER2-positive metastatic breast cancer), and from 1,500 mg per day to 5,500 mg per day in patients receiving concomitant aromatase inhibitor therapy (HR-positive, HER2-positive breast cancer) based on tolerability. If dexamethasone is discontinued, reduce lapatinib to the indicated dose. Lapatinib is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Concomitant use with a strong CYP3A4 inducer decreased lapatinib exposure by 72%. [33192] L-Asparaginase Escherichia coli: (Moderate) Concomitant use of L-asparaginase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions. [55362] Ledipasvir; Sofosbuvir: (Moderate) Caution and close monitoring of dexamethasone-associated adverse reactions is advised with concomitant administration of ledipasvir. Dexamethasone is a substrate of the drug transporter P-glycoprotein (P-gp); ledipasvir is a P-gp inhibitor. Taking these drugs together may increase dexamethasone plasma concentrations. [34477] [58167] Lefamulin: (Major) Avoid coadministration of lefamulin with dexamethasone unless the benefits outweigh the risks as concurrent use may decrease lefamulin exposure and efficacy. Lefamulin is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. [54286] [64576] Lemborexant: (Major) Avoid coadministration of lemborexant and dexamethasone as concurrent use may decrease lemborexant exposure which may reduce efficacy. Lemborexant is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. [54286] [64870] Letermovir: (Moderate) An increase in the plasma concentration of dexamethasone may occur if given with letermovir. In patients who are also receiving treatment with cyclosporine, the magnitude of this interaction may be amplified. Dexamethasone is a CYP3A4 substrate. Letermovir is a moderate CYP3A4 inhibitor; however, when given with cyclosporine, the combined effect on CYP3A4 substrates may be similar to a strong CYP3A4 inhibitor. In a drug interaction study, concurrent administration of certain corticosteroids with another potent CYP3A4 inhibitor significantly decreased the corticosteroid metabolism (up to 60% reduction). [54286] [62611] Levetiracetam: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Levomethadyl: (Major) Caution is advised when using levomethadyl in combination with other agents, such as corticosteroids, that may lead to electrolyte abnormalities, especially hypokalemia or hypomagnesemia. [3085] Lidocaine: (Moderate) Concomitant use of systemic lidocaine and dexamethasone may decrease lidocaine plasma concentrations. Higher lidocaine doses may be required; titrate to effect. Lidocaine is a CYP3A4 and CYP1A2 substrate; dexamethasone induces CYP3A4. [32857] [54286] Lidocaine; Prilocaine: (Moderate) Concomitant use of systemic lidocaine and dexamethasone may decrease lidocaine plasma concentrations. Higher lidocaine doses may be required; titrate to effect. Lidocaine is a CYP3A4 and CYP1A2 substrate; dexamethasone induces CYP3A4. [32857] [54286] Linagliptin; Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Liraglutide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Live Vaccines: (Severe) Live vaccines should generally not be administered to an immunosuppressed patient. Live vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live vaccines. Patients on corticosteroid treatment for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to live vaccine administration may be sufficient. Live vaccines should not be given to individuals who are considered to be immunocompromised until more information is available. [43236] [54286] Lixisenatide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Lomustine, CCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [5946] [7714] [7944] Loop diuretics: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia and/or hypomagnesemia. While glucocorticoids with mineralocorticoid activity (e.g., cortisone, hydrocortisone) can cause sodium and fluid retention. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly. [26417] [28429] [29779] Loperamide: (Moderate) The plasma concentration and efficacy of loperamide may be reduced when administered concurrently with dexamethasone. Loperamide is metabolized by the hepatic enzyme CYP3A4; dexamethasone is an inducer of this enzyme. [30106] [34477] [54286] Loperamide; Simethicone: (Moderate) The plasma concentration and efficacy of loperamide may be reduced when administered concurrently with dexamethasone. Loperamide is metabolized by the hepatic enzyme CYP3A4; dexamethasone is an inducer of this enzyme. [30106] [34477] [54286] Lopinavir; Ritonavir: (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate. [4718] [5070] [5206] (Moderate) Decreased lopinavir plasma concentrations are seen when dexamethasone and lopinavir are coadministered. Consider use of an alternative corticosteroid. If these drugs are used together, carefully monitor for decreased clinical efficacy of lopinavir. [28341] Lorlatinib: (Major) Avoid coadministration of lorlatinib with dexamethasone due to the risk of severe hepatotoxicity as well as decreased lorlatinib exposure which may reduce its efficacy; dexamethasone plasma concentrations may also decrease. If concomitant use is unavoidable, monitor ALT, AST, and bilirubin 48 hours after initiating concomitant therapy and at least 3 times during the first week of treatment. If persistent grade 2 or higher hepatotoxicity occurs, discontinue either lorlatinib or dexamethasone. A dose adjustment of systemic dexamethasone may be necessary if lorlatinib is initiated or withdrawn during therapy. Both drugs are CYP3A substrates and moderate inducers. Coadministration with a strong CYP3A inducer decreased lorlatinib exposure by 85% and caused severe (grade 3 or 4) hepatotoxicity in 83% of patients. The effect of the concomitant use of moderate CYP3A inducers on lorlatinib pharmacokinetics or the risk of hepatotoxicity is unknown. [34477] [54286] [63732] Lumacaftor; Ivacaftor: (Moderate) Concomitant use of dexamethasone and lumacaftor; ivacaftor may alter dexamethasone exposure. If used together, dexamethasone dosages may need to be adjusted to achieve desired therapeutic effects. Dexamethasone is a substrate and moderate inducer of CYP3A and a substrate of the P-glycoprotein (P-gp) drug transporter. Ivacaftor is a sensitive CYP3A substrate and lumacaftor is a strong CYP3A inducer; in vitro data suggests lumacaftor; ivacaftor may also induce and/or inhibit P-gp. Although induction of dexamethasone through the CYP3A pathway may lead to decreased drug efficacy, the net effect of lumacaftor; ivacaftor on P-gp transport is not clear. Monitor the patient for decreased corticosteroid efficacy or increased or prolonged therapeutic effects and adverse events. Additionally, ivacaftor exposure could theoretically be further decreased when given with another CYP3A inducer; however, ivacaftor; lumacaftor dosage adjustments are not recommended with concomitant use of a moderate CYP3A inducer such as dexamethasone. [30676] [34477] [54286] [59891] Lumateperone: (Major) Avoid coadministration of lumateperone and dexamethasone as concurrent use may decrease lumateperone exposure which may reduce efficacy. Lumateperone is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. [54286] [64885] Lurasidone: (Moderate) Because lurasidone is primarily metabolized by CYP3A4, decreased plasma concentrations of lurasidone may occur when the drug is co-administered with inducers of CYP3A4. Decreased plasma concentrations of lurasidone may lead to a decrease in efficacy of lurasidone. If lurasidone is used with a moderate CYP3A4 inducer, it may be necessary to increase the lurasidone dose after chronic treatment (7 days or more). [30011] [42227] Lurbinectedin: (Minor) Although there may be an interaction, these drugs may be used together. The manufacturer of lurbinectedin, a CYP3A substrate, recommends avoiding coadministration with moderate CYP3A inducers like dexamethasone due to the risk of decreased lurbinectedin exposure which may reduce its efficacy. However, the manufacturer specifically recommends administration of dexamethasone as a premedication for lurbinectedin to prevent chemotherapy-induced nausea and vomiting. [54286] [65593] Macimorelin: (Major) Avoid use of macimorelin with drugs that directly affect pituitary growth hormone secretion, such as corticosteroids. Healthcare providers are advised to discontinue corticosteroid therapy and observe a sufficient washout period before administering macimorelin. Use of these medications together may impact the accuracy of the macimorelin growth hormone test. [62723] Magnesium Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Mannitol: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia. Also, corticotropin may cause calcium loss and sodium and fluid retention. Mannitol itself can cause hypernatremia. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly. [6524] Maraviroc: (Moderate) Use caution if coadministration of maraviroc with dexamethasone is necessary, due to a possible decrease in maraviroc exposure. Maraviroc is a CYP3A substrate and dexamethasone is a CYP3A4 inducer. Monitor for a decrease in maraviroc efficacy with concomitant use. [33473] [54286] Mecasermin rinfabate: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored. [8314] [8315] Mecasermin, Recombinant, rh-IGF-1: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored. [8314] [8315] Mefloquine: (Moderate) Mefloquine is metabolized by CYP3A4. Dexamethasone is an inducer of CYP3A4, and may increase the metabolism of mefloquine and reduce mefloquine plasma concentrations if coadministered. [4718] [5213] [8888] Meglitinides: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Melphalan: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] [7943] [7944] Mepenzolate: (Minor) Anticholinergics, such as mepenzolate, antagonize the effects of antiglaucoma agents. Mepenzolate is contraindicated in patients with glaucoma and therefore should not be coadministered with medications being prescribed for the treatment of glaucoma. In addition, anticholinergic drugs taken concurrently with corticosteroids in the presence of increased intraocular pressure may be hazardous. [42281] Mephobarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Mephobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Metformin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Metformin; Pioglitazone: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Metformin; Repaglinide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Metformin; Rosiglitazone: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Metformin; Saxagliptin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Metformin; Sitagliptin: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [28550] [30585] [51002] [62853] Methazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with methazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy. The chronic use of corticosteroids may augment calcium excretion with methazolamide leading to increased risk for hypocalcemia and/or osteoporosis. [5023] Methenamine; Sodium Acid Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] Methenamine; Sodium Acid Phosphate; Methylene Blue; Hyoscyamine: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] Methoxsalen: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Methyclothiazide: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Metolazone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Metyrapone: (Severe) Medications which affect pituitary or adrenocortical function, including all corticosteroid therapy, should be discontinued prior to and during testing with metyrapone. Patients taking inadvertent doses of corticosteroids on the test day may exhibit abnormally high basal plasma cortisol levels and a decreased response to the test. Although systemic absorption of ocular, inhaled and topical corticosteroids is minimal, temporary discontinuation of these products should be considered if possible to reduce the potential for interference with the test results. [33528] Micafungin: (Moderate) Leukopenia, neutropenia, anemia, and thrombocytopenia have been associated with micafungin. Patients who are taking immunosuppressives such as the corticosteroids with micafungin concomitantly may have additive risks for infection or other side effects. In a pharmacokinetic trial, micafungin had no effect on the pharmacokinetics of prednisolone. Acute intravascular hemolysis and hemoglobinuria was seen in a healthy volunteer during infusion of micafungin (200 mg) and oral prednisolone (20 mg). This reaction was transient, and the subject did not develop significant anemia. [44913] Mifepristone: (Major) Mifepristone for termination of pregnancy is contraindicated in patients on long-term corticosteroid therapy and mifepristone for Cushing's disease or other chronic conditions is contraindicated in patients who require concomitant treatment with systemic corticosteroids for life-saving purposes, such as serious medical conditions or illnesses (e.g., immunosuppression after organ transplantation). For other situations where corticosteroids are used for treating non-life threatening conditions, mifepristone may lead to reduced corticosteroid efficacy and exacerbation or deterioration of such conditions. This is because mifepristone exhibits antiglucocorticoid activity that may antagonize corticosteroid therapy and the stabilization of the underlying corticosteroid-treated illness. Mifepristone may also cause adrenal insufficiency, so patients receiving corticosteroids for non life-threatening illness require close monitoring. Because serum cortisol levels remain elevated and may even increase during treatment with mifepristone, serum cortisol levels do not provide an accurate assessment of hypoadrenalism. Patients should be closely monitored for signs and symptoms of adrenal insufficiency, If adrenal insufficiency occurs, stop mifepristone treatment and administer systemic glucocorticoids without delay; high doses may be needed to treat these events. Factors considered in deciding on the duration of glucocorticoid treatment should include the long half-life of mifepristone (85 hours). [28003] [48697] Mitotane: (Major) Use caution if mitotane and dexamethasone are used concomitantly, and monitor for decreased efficacy of dexamethasone and a possible change in dosage requirements. Mitotane is a strong CYP3A4 inducer and dexamethasone is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of dexamethasone. [34477] [41934] [54286] Mitoxantrone: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Mivacurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Modafinil: (Minor) Drugs that exhibit significant induction of the hepatic microsomal CYP3A4 isoenzyme, such as dexamethasone, may potentially increase the metabolism of modafinil. Decreased serum levels of modafinil could potentially result in decreased efficacy of modafinil. [5259] Moxifloxacin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Muromonab-CD3: (Major) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. While therapy is designed to take advantage of this effect, patients may be predisposed to over-immunosuppression resulting in an increased risk for the development of severe infections. Close clinical monitoring is advised with concurrent use; in the presence of serious infections, continuation of the corticosteroid or immunosuppressive agent may be necessary but should be accompanied by appropriate antimicrobial therapies as indicated. [7714] Nanoparticle Albumin-Bound Paclitaxel: (Moderate) Monitor for decreased efficacy of nab-paclitaxel or increased paclitaxel-related adverse reactions if coadministration of nab-paclitaxel with dexamethasone is necessary. Nab-paclitaxel is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer; plasma concentrations of dexamethasone may decrease. In vitro however, the metabolism of paclitaxel is inhibited by dexamethasone at concentrations that exceed those found in vivo following normal therapeutic doses. [30742] [54286] Natalizumab: (Major) Ordinarily, patients receiving chronic immunosuppressant therapy should not be treated with natalizumab. Treatment recommendations for combined corticosteroid therapy are dependent on the underlying indication for natalizumab therapy. Corticosteroids should be tapered in those patients with Crohn's disease who are on chronic corticosteroids when they start natalizumab therapy, as soon as a therapeutic benefit has occurred. If the patient cannot discontinue systemic corticosteroids within 6 months, discontinue natalizumab. The concomitant use of natalizumab and corticosteroids may further increase the risk of serious infections, including progressive multifocal leukoencephalopathy, over the risk observed with use of natalizumab alone. In multiple sclerosis (MS) clinical trials, an increase in infections was seen in patients concurrently receiving short courses of corticosteroids. However, the increase in infections in natalizumab-treated patients who received steroids was similar to the increase in placebo-treated patients who received steroids. Short courses of steroid use during natalizumab, such as when they are needed for MS relapse treatment, appear to be acceptable for use concurrently. [30470] [62264] Nateglinide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Nelarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Neostigmine: (Moderate) Concomitant use of anticholinesterase agents, such as neostigmine, and systemic corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating systemic corticosteroid therapy. [29779] [30015] [30028] [31123] [54891] [56146] [64165] Neratinib: (Major) Avoid concomitant use dexamethasone with neratinib due to decreased efficacy of neratinib. Neratinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Simulations using physiologically based pharmacokinetic (PBPK) models suggest that another moderate CYP3A4 inducer may decrease neratinib exposure by 52%. [34477] [54286] [62127] Netupitant, Fosnetupitant; Palonosetron: (Moderate) Netupitant is a moderate inhibitor of CYP3A4 and should be used with caution in patients receiving concomitant medications that are primarily metabolized through CYP3A4, such as dexamethasone. The plasma concentrations of CYP3A4 substrates can increase when co-administered with netupitant. The inhibitory effect on CYP3A4 can last for multiple days. A two-fold increase in the systemic exposure of dexamethasone was observed 4 days after single dose of netupitant. The duration of the effect was not studied beyond 4 days. If coadministration is necessary, decrease the dose of dexamethasone. [58171] Neuromuscular blockers: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Nicardipine: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Nilotinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of nilotinib with dexamethasone is necessary due to increased dexamethasone exposure. Dexamethasone is a CYP3A4 substrate and nilotinib is a moderate CYP3A4 inhibitor. A strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, increasing the risk of corticosteroid-related side effects. [54286] [58766] Nisoldipine: (Major) Avoid coadministration of nisoldipine with dexamethasone due to decreased plasma concentrations of nisoldipine. Alternative antihypertensive therapy should be considered. Nisoldipine is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a strong CYP3A4 inducer lowered nisoldipine plasma concentrations to undetectable levels. [29088] [54286] Nonsteroidal antiinflammatory drugs: (Moderate) Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged concomitant administration should be avoided. Concomitant use of corticosteroids appears to increase the risk of adverse GI events due to NSAIDs. Corticosteroids can have profound effects on sodium-potassium balance; NSAIDs also can affect sodium and fluid balance. Monitor serum potassium concentrations; potassium supplementation may be necessary. In addition, NSAIDs may mask fever, pain, swelling and other signs and symptoms of an infection; use NSAIDs with caution in patients receiving immunosuppressant dosages of corticosteroids. The Beers criteria recommends that this drug combination be avoided in older adults; if coadministration cannot be avoided, provide gastrointestinal protection. [24574] [29890] [63923] Ocrelizumab: (Moderate) Ocrelizumab has not been studied in combination with other immunosuppressive or immune modulating therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids. Concomitant use of ocrelizumab with any of these therapies may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection. [61838] Olaparib: (Major) Avoid coadministration of olaparib with dexamethasone due to the risk of decreasing the efficacy of olaparib. Olaparib is a CYP3A substrate and dexamethasone is a moderate CYP3A4 inducer; concomitant use may decrease olaparib exposure. Coadministration with a moderate CYP3A inducer is predicted to decrease the olaparib Cmax by 31% and the AUC by 60%. [34477] [54286] [58662] Ombitasvir; Paritaprevir; Ritonavir: (Severe) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir or ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. [34477] [54286] [58664] (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate. [4718] [5070] [5206] Omeprazole: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29564] [54286] Omeprazole; Amoxicillin; Rifabutin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29564] [54286] Omeprazole; Sodium Bicarbonate: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. [29564] [54286] Ondansetron: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Oritavancin: (Minor) Dexamethasone is metabolized by CYP3A4; oritavancin is a weak CYP3A4 inducer. Plasma concentrations and efficacy of dexamethasone may be reduced if these drugs are administered concurrently. Dosages of dexamethasone may require adjustment if oritavancin is initiated or withdrawn during dexamethasone therapy. [34477] [54557] [57741] Oxycodone: (Moderate) Monitor for reduced efficacy of oxycodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of oxycodone as needed. If dexamethasone is discontinued, consider a dose reduction of oxycodone and frequently monitor for signs of respiratory depression and sedation. Oxycodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease oxycodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. [39926] [54286] Oxymetholone: (Moderate) Concomitant use of oxymetholone with corticosteroids or corticotropin, ACTH may cause increased edema. Manage edema with diuretic and/or digitalis therapy. [48342] Ozanimod: (Moderate) Concomitant use of ozanimod with dexamethasone may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection. Ozanimod has not been studied in combination with other immunosuppressive or immune modulating therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids. [65169] Pancuronium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Pazopanib: (Major) Avoid administering pazopanib in patients who require chronic treatment with a strong CYP3A4 inducer, such as dexamethasone. The concomitant use of pazopanib, a weak CYP3A4 inhibitor and a substrate for CYP3A4 and P-glycoprotein (P-gp), and dexamethasone, a strong CYP3A4 inducer and a CYP3A4and P-gp substrate, may result in altered pazopanib and/or dexamethasone concentrations. In addition, because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with antineoplastic agents. While therapy is designed to take advantage of this effect, patients may be predisposed to over-immunosuppression resulting in an increased risk for the development of severe infections. Close clinical monitoring is advised with concurrent use; in the presence of serious infections, continuation of the corticosteroid or immunosuppressive agent may be necessary but should be accompanied by appropriate antimicrobial therapies as indicated. [49829] [6759] [7714] Pegaspargase: (Moderate) Concomitant use of pegaspargase with corticosteroids can result in additive hyperglycemia. Insulin therapy may be required in some cases. [55362] Peginterferon Alfa-2a: (Moderate) Additive myelosuppressive effects may be seen when alpha interferons are given concurrently with other myelosuppressive agents, such as antineoplastic agents or immunosuppressives. [6161] Pemigatinib: (Major) Avoid coadministration of pemigatinib and dexamethasone due to the risk of decreased pemigatinib exposure which may reduce its efficacy. Pemigatinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a moderate CYP3A4 inducer is predicted to decrease pemigatinib exposure by more than 50%. [54286] [65307] Penicillamine: (Major) Agents such as immunosuppressives have adverse reactions similar to those of penicillamine. Concomitant use of penicillamine with these agents is contraindicated because of the increased risk of developing severe hematologic and renal toxicity. [5567] Perampanel: (Major) Start perampanel at a higher initial dose of 4 mg once daily at bedtime when using concurrently with dexamethasone due to a potential reduction in perampanel plasma concentration. If introduction or withdrawal of dexamethasone occurs during perampanel therapy, closely monitor patient response; a dosage adjustment may be necessary. Dexamethasone is a moderate CYP3A4 inducer, and perampanel is a CYP3A4 substrate. [52140] [54286] Perindopril; Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased. [34477] [35588] [54286] Phenobarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Phenobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Phenylephrine; Promethazine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly. [54374] [57578] Photosensitizing agents (topical): (Minor) Corticosteroids administered prior to or concomitantly with photosensitizing agents used in photodynamic therapy may decrease the efficacy of the treatment. [6625] Physostigmine: (Moderate) Concomitant use of anticholinesterase agents. such as physostigmine, and systemic corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, withdraw anticholinesterase inhibitors at least 24 hours before initiating corticosteroid therapy. [29779] [30015] [30028] [31123] [56146] [64165] Pimavanserin: (Major) Because pimavanserin is primarily metabolized by CYP3A4 and CYP3A5, the manufacturer recommends avoiding concomitant use of pimavanserin with moderate CYP3A4 inducers, such as dexamethasone. Moderate inducers of CYP3A4 can reduce pimavanserin exposure, potentially decreasing the effectiveness of pimavanserin. [54286] [60748] Pimozide: (Moderate) According to the manufacturer of pimozide, the drug should not be coadministered with drugs known to cause electrolyte imbalances, such as high-dose, systemic corticosteroid therapy. Pimozide is associated with a well-established risk of QT prolongation and torsade de pointes (TdP), and electrolyte imbalances (e.g., hypokalemia, hypocalcemia, hypomagnesemia) may increase the risk of life-threatening arrhythmias. Pimozide is contraindicated in patients with known hypokalemia or hypomagnesemia. Topical corticosteroids are less likely to interact. [28225] [43463] Posaconazole: (Moderate) Posaconazole and dexamethasone should be coadministered with caution due to an increased potential for adverse events. Posaconazole is a potent inhibitor of CYP3A4, an isoenzyme partially responsible for the metabolism of dexamethasone. Further, both dexamethasone and posaconazole are substrates of the drug efflux protein, P-glycoprotein, which when administered together may increase the absorption or decrease the clearance of the other drug. This complex interaction may cause alterations in the plasma concentrations of both posaconazole and dexamethasone, ultimately resulting in an increased risk of adverse events. [11334] [32723] [6759] Potassium Chloride: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Potassium Phosphate; Sodium Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] Potassium: (Moderate) Corticotropin can cause alterations in serum potassium levels. The use of potassium salts or supplements would be expected to alter the effects of corticotropin on serum potassium levels. Also, there have been reports of generalized tonic-clonic seizures and/or loss of consciousness associated with use of bowel preparation products in patients with no prior history of seizure disorder. Therefore, magnesium sulfate; potassium sulfate; sodium sulfate should be administered with caution during concurrent use of medications that lower the seizure threshold such as systemic corticosteroids. [30015] [41573] Potassium-sparing diuretics: (Minor) The manufacturer of spironolactone lists corticosteroids as a potential drug that interacts with spironolactone. Intensified electrolyte depletion, particularly hypokalemia, may occur. However, potassium-sparing diuretics such as spironolactone do not induce hypokalemia. In fact, hypokalemia is one of the indications for potassium-sparing diuretic therapy. Therefore, drugs that induce potassium loss, such as corticosteroids, could counter the hyperkalemic effects of potassium-sparing diuretics. [26417] [29016] [30011] Pramlintide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Prasterone, Dehydroepiandrosterone, DHEA (Dietary Supplements): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations. [2460] Prasterone, Dehydroepiandrosterone, DHEA (FDA-approved): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations. [2460] Praziquantel: (Moderate) Drugs that induce hepatic metabolism via the microsomal CYP450 enzyme system decrease the bioavailability of praziquantel. Plasma levels of praziquantel have been reported to be 50% lower when dexamethasone was given simultaneously, presumably due to CYP induction by dexamethasone. [4558] Primidone: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Primidone is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. [28001] Propranolol: (Moderate) Patients receiving corticosteroids during propranolol therapy may be at increased risk of hypoglycemia due to the loss of counter-regulatory cortisol response. This effect may be more pronounced in infants and young children. If concurrent use is necessary, carefully monitor vital signs and blood glucose concentrations as clinically indicated. [56853] Purine analogs: (Minor) Concurrent use of purine analogs with other agents which cause bone marrow or immune suppression such as other antineoplastic agents or immunosuppressives may result in additive effects. [5504] Pyridostigmine: (Moderate) Concomitant use of anticholinesterase agents. such as pyridostigmine, and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. [29779] [30015] [30028] [31123] [34253] [56146] [64002] [64165] Quetiapine: (Moderate) Use caution when administering quetiapine with corticosteroids. QT prolongation has occurred during concurrent use of quetiapine and medications known to cause electrolyte imbalance (i.e. corticosteroids). [26417] [29118] Quinidine: (Moderate) Quinidine is a substrate of the CYP3A4 isoenzyme. Inducers of CYP3A4 such as dexamethasone may increase hepatic elimination of quinidine with the potential for reduced efficacy of quinidine. [10571] [6759] Quinolones: (Moderate) Quinolones have been associated with an increased risk of tendon rupture requiring surgical repair or resulting in prolonged disability; this risk is further increased in those receiving concomitant corticosteroids. Discontinue quinolone therapy at the first sign of tendon inflammation or tendon pain, as these are symptoms that may precede rupture of the tendon. [28423] [28424] [28764] [29818] [30738] [62028] [65562] Rapacuronium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Regular Insulin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Remdesivir: (Moderate) Theoretically, the systemic exposure to remdesivir may be reduced when administered concurrently with dexamethasone; close monitoring for reduced remdesivir efficacy is advised if these drugs are used together. Although an interaction may occur, the manufacturer expects minimal to no reduction in remdesivir exposure when administered with dexamethasone. In vitro data show remdesivir is a substrate for CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. [54286] [65210] [65314] [65365] Repaglinide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Ribociclib: (Moderate) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with ribociclib is necessary. Dexamethasone is a CYP3A4 substrate and ribociclib is a strong CYP3A4 inhibitor. [54286] [61816] Ribociclib; Letrozole: (Moderate) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with ribociclib is necessary. Dexamethasone is a CYP3A4 substrate and ribociclib is a strong CYP3A4 inhibitor. [54286] [61816] Rifabutin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] Rifampin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] Rifamycins: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] Rifapentine: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate [28483] [28818] [29210] [30011] [34477] Rilonacept: (Moderate) Patients receiving immunosuppressives along with rilonacept may be at a greater risk of developing an infection. [10690] Rilpivirine: (Severe) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine. [44376] [54286] Rimegepant: (Major) Avoid coadministration of rimegepant with dexamethasone; concurrent use may significantly decrease rimegepant exposure which may result in loss of efficacy. Rimegepant is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [54286] [65052] Ritodrine: (Major) Ritodrine has caused maternal pulmonary edema, which appears more often in patients treated concomitantly with corticosteroids. Patients so treated should be closely monitored in the hospital. [7110] [7111] [7572] Ritonavir: (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate. [4718] [5070] [5206] Rituximab: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy. [30943] [49773] [56233] Rituximab; Hyaluronidase: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy. [30943] [49773] [56233] Rivaroxaban: (Minor) Coadministration of rivaroxaban and dexamethasone may result in decreased rivaroxaban exposure and may decrease the efficacy of rivaroxaban. Dexamethasone is an inducer of CYP3A4, and rivaroxaban is a substrate of CYP3A4. If these drugs are administered concurrently, monitor the patient for signs of lack of efficacy of rivaroxaban. [11334] [44854] Rocuronium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Roflumilast: (Major) Coadminister dexamethasone and roflumilast cautiously as this may lead to reduced systemic exposure to roflumilast. Dexamethasone induces CYP3A4 and roflumilast is a CYP3A4 substrate. In pharmacokinetic study, administration of a single dose of roflumilast in patients receiving another CYP3A4 inducer, rifampin, resulted in decreased roflumilast Cmax and AUC, as well as increased Cmax and decreased AUC of the active metabolite roflumilast N-oxide. [43551] [6759] Romidepsin: (Major) The concomitant use of romidepsin, a CYP3A4 substrate, and dexamethasone, a strong CYP3A4 inducer, may result in significantly altered romidepsin plasma exposure. Therefore, avoid using romidepsin with potent CYP3A4 inducers if possible. [37292] [6759] Ruxolitinib: (Moderate) Ruxolitinib is a CYP3A4 substrate. When used with drugs that are CYP3A4 inducers such as dexamethasone, a dose adjustment is not necessary, but closely monitor patients and titrate the ruxolitinib dose based on safety and efficacy. The Cmax and AUC of a single 50 mg dose of ruxolitinib was decreased by 32% and 61%, respectively, after rifampin 600 mg once daily was administered for 10 days. The relative exposure to ruxolitinib's active metabolites increased by about 100%, which may partially explain the reported disproportionate 10% reduction in the pharmacodynamic marker pSTAT3 inhibition. [11334] [46782] [6759] Salicylates: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Salsalate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. [24574] [28502] Sapropterin: (Moderate) Caution is advised with the concomitant use of sapropterin and dexamethasone as coadministration may result in increased systemic exposure of dexamethasone. Dexamethasone is a substrate for the drug transporter P-glycoprotein (P-gp); in vitro data show that sapropterin may inhibit P-gp. If these drugs are used together, closely monitor for increased side effects of dexamethasone. [33635] [34477] [54286] Saquinavir: (Major) Avoid concurrent administration of dexamethasone and saquinavir boosted with ritonavir. Dexamethasone is may induce the CYP3A4 metabolism of saquinavir, resulting in reduced saquinavir plasma concentrations. Decreased saquinavir plasma concentrations could lead to HIV treatment failures or the development of viral-resistance. If used concomitantly, the patient should be observed for changes in the clinical efficacy and concentrations of the antiretroviral regimen. [28995] Sargramostim, GM-CSF: (Major) Avoid the concomitant use of sargramostim and systemic corticosteroid agents due to the risk of additive myeloproliferative effects. If coadministration of these drugs is required, frequently monitor patients for clinical and laboratory signs of excess myeloproliferative effects (e.g., leukocytosis). Sargramostim is a recombinant human granulocyte-macrophage colony-stimulating factor that works by promoting proliferation and differentiation of hematopoietic progenitor cells. [61087] Selpercatinib: (Major) Avoid coadministration of selpercatinib and dexamethasone due to the risk of decreased selpercatinib exposure which may reduce its efficacy. Selpercatinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with other moderate CYP3A4 inducers is predicted to decrease selpercatinib exposure by 40% to 70%. [54286] [65387] Selumetinib: (Major) Avoid coadministration of selumetinib and dexamethasone due to the risk of decreased selumetinib exposure which may reduce its efficacy. Selumetinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a moderate CYP3A4 inducer is predicted to decrease selumetinib exposure by 38%. [54286] [65246] Semaglutide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] SGLT2 Inhibitors: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Sildenafil: (Minor) Sildenafil is metabolized principally by CYP3A4. It can be expected that concomitant administration of sildenafil with CYP3A4 enzyme inducers like dexamethasone will decrease plasma concentrations of sildenafil. [28001] [28199] Simeprevir: (Major) Avoid concurrent use of simeprevir and systemic dexamethasone. Induction of CYP3A4 by dexamethasone may reduce the plasma concentrations of simeprevir, resulting in treatment failure. [56471] Siponimod: (Moderate) Concomitant use of siponimod and dexamethasone is not recommended for patients with CYP2C9*1/*3 and *2/*3 genotypes due to a significant decrease in siponimod exposure. Siponimod is a CYP2C9 and CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Across different CYP2C9 genotypes, a moderate CYP3A4 inducer decreased the exposure of siponimod by up to 52% according to in silico evaluation. Additonally, monitor patients carefully for signs and symptoms of infection if coadministration is necessary, as concomitant use may increase the risk of immunosuppression. Siponimod has not been studied in combination with other immunosuppressive therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids. [54286] [64031] Sipuleucel-T: (Major) Concomitant use of sipuleucel-T and immunosuppressives should be avoided. Concurrent administration of immunosuppressives with the leukapheresis procedure that occurs prior to sipuleucel-T infusion has not been studied. Sipuleucel-T stimulates the immune system and patients receiving immunosuppressives may have a diminished response to sipuleucel-T. When appropriate, consider discontinuing or reducing the dose of immunosuppressives prior to initiating therapy with sipuleucel-T. [40277] Sirolimus: (Major) Dexamethasone is an inducer of CYP3A4. Sirolimus is extensively metabolized by CYP3A4 in the gut and liver. Concurrent use of sirolimus with dexamethasone may decrease patient exposure to sirolimus. Consider alternative steroid therapy. Use sirolimus and dexamethasone with caution, if at all, and monitor patients closely. [4718] [5341] Sodium Benzoate; Sodium Phenylacetate: (Moderate) Corticosteroids may cause protein breakdown, which could lead to elevated blood ammonia concentrations, especially in patients with an impaired ability to form urea. Corticosteroids should be used with caution in patients receiving treatment for hyperammonemia. [8083] Sodium Chloride: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Sodium Phenylbutyrate: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids. [57685] Sodium Phosphate Monobasic Monohydrate; Sodium Phosphate Dibasic Anhydrous: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] Sofosbuvir; Velpatasvir: (Major) Avoid coadministration of velpatasvir with dexamethasone. Taking these drugs together may significantly decrease velpatasvir plasma concentrations, potentially resulting in loss of antiviral efficacy. Velpatasvir is a CYP3A4 substrate; dexamethasone a moderate inducer of CYP3A4. Additionally, velpatasvir is an inhibitor of the drug transporter P-glycoprotein (P-gp). Coadministration with substrates of this transporter, such as dexamethasone, may increase their exposure. [34477] [54286] [60911] Sofosbuvir; Velpatasvir; Voxilaprevir: (Major) Avoid coadministration of velpatasvir with dexamethasone. Taking these drugs together may significantly decrease velpatasvir plasma concentrations, potentially resulting in loss of antiviral efficacy. Velpatasvir is a CYP3A4 substrate; dexamethasone a moderate inducer of CYP3A4. Additionally, velpatasvir is an inhibitor of the drug transporter P-glycoprotein (P-gp). Coadministration with substrates of this transporter, such as dexamethasone, may increase their exposure. [34477] [54286] [60911] (Major) Avoid coadministration of voxilaprevir (a CYP3A4 substrate) with moderate to strong inducers of CYP3A4, such as dexamethasone. Taking these drugs together may significantly decrease voxilaprevir plasma concentrations, potentially resulting in loss of antiviral efficacy. In addition, voxilaprevir, a P-glycoprotein (P-gp) inhibitor, may alter concentrations of dexamethasone, a P-gp substrate. [34477] [54286] [62131] Somatropin, rh-GH: (Moderate) Corticosteroids can retard bone growth and therefore, can inhibit the growth-promoting effects of somatropin. If corticosteroid therapy is required, the corticosteroid dose should be carefully adjusted. [6807] Sonidegib: (Major) Avoid the concomitant use of sonidegib and dexamethasone; sonidegib levels may be significantly decreased and its efficacy reduced. Sonidegib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Physiologic-based pharmacokinetics (PBPK) simulations indicate that a moderate CYP3A4 inducer would decrease the sonidegib AUC by 56% if administered for 14 days and by 69% if the moderate CYP3A inducer is administered for more than 14 days. [54286] [60000] Sorafenib: (Major) Avoid coadministration of sorafenib with dexamethasone due to decreased plasma concentrations of sorafenib. Sorafenib is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Concomitant use with another strong CYP3A4 inducer decreased sorafenib exposure by 37%. [31832] Succinylcholine: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Sufentanil: (Moderate) Because the dose of the sufentanil sublingual tablets cannot be titrated, consider an alternate opiate if dexamethasone must be administered. Monitor for reduced efficacy of sufentanil injection and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of sufentanil injection as needed. If dexamethasone is discontinued, consider a dose reduction of sufentanil injection and frequently monitor for signs or respiratory depression and sedation. Sufentanil is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease sufentanil concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. [30966] [54286] [63731] Sulfonylureas: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Sunitinib: (Major) Avoid coadministration of dexamethasone with sunitinib if possible due to decreased exposure to sunitinib which could decrease efficacy. If concomitant use is unavoidable, consider increasing the dose of sunitinib in 12.5 mg increments based on individual safety and tolerability to a maximum of 87.5 mg (GIST and RCC) or 62.5 mg (pNET) daily; monitor carefully for toxicity. The maximum daily dose administered in the pNET study was 50 mg. Sunitinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [31970] [54286] Tadalafil: (Minor) Tadalafil is metabolized principally by cytochrome P450 3A4. Studies have shown that concomitant administration of CYP3A4 enzyme-inducers, such as dexamethasone, will decrease plasma levels of tadalafil. [4946] Tasimelteon: (Moderate) Caution is recommended during concurrent use of tasimelteon and dexamethasone. Because tasimelteon is partially metabolized via CYP3A4, use with CYP3A4 inducers, such as dexamethasone, may reduce the efficacy of tasimelteon. [56665] Tazemetostat: (Major) Avoid coadministration of tazemetostat with dexamethasone as concurrent use may decrease tazemetostat exposure, which may reduce its efficacy. Tazemetostat is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. [54286] [64952] Telaprevir: (Moderate) Coadministration of dexamethasone and telaprevir is not recommended. If coadministered, close clinical monitoring for increased dexamethasone-related adverse events and for decreased telaprevir efficacy is advised. If dexamethasone dose adjustments are made, re-adjust the dose upon completion of telaprevir treatment. Predictions about the interaction can be made based on the metabolic pathways of dexamethasone and telaprevir. Dexamethasone is an inducer and substrate of the hepatic isoenzyme CYP3A4; telaprevir is an inhibitor and substrate of this isoenzyme. Additionally, both dexamethasone and telaprevir are substrates for the drug efflux transporter P-glycoprotein (PGP). When used in combination, the plasma concentrations of dexamethasone may be elevated and the plasma concentration of telaprevir may be deceased, resulting in an increased potential for dexamethasone-related adverse events and telaprevir treatment failure. [44393] [6759] Telbivudine: (Moderate) The risk of myopathy may be increased if corticosteroids are coadministered with telbivudine. Monitor patients for any signs or symptoms of unexplained muscle pain, tenderness, or weakness, particularly during periods of upward dosage titration. [9671] Telithromycin: (Major) Concentrations of dexamethasone may be increased and concentrations of telithromycin may be decreased with coadministration. Dexamethasone is a CYP3A4 and P-glycoprotein (PGP) substrate and telithromycin is a strong CYP3A4 inhibitor and potential PGP inhibitor. Additionally, dexamethasone is a CYP3A4 inducer, while telithromycin is CYP3A4 substrate. [11334] [28156] [34329] [6759] Telotristat Ethyl: (Moderate) Use caution if coadministration of telotristat ethyl and dexamethasone is necessary, as the systemic exposure of dexamethasone may be decreased resulting in reduced efficacy. If these drugs are used together, monitor patients for suboptimal efficacy of dexamethasone; consider increasing the dose of dexamethasone if necessary. Dexamethasone is a CYP3A4 substrate. The mean Cmax and AUC of another sensitive CYP3A4 substrate was decreased by 25% and 48%, respectively, when coadministered with telotristat ethyl; the mechanism of this interaction appears to be that telotristat ethyl increases the glucuronidation of the CYP3A4 substrate. [34477] [54286] [61795] Temsirolimus: (Major) Avoid coadministration of temsirolimus with dexamethasone due to the risk of decreased plasma concentrations of the primary active metabolite of temsirolimus (sirolimus). If concomitant use is unavoidable, consider increasing the dose of temsirolimus from 25 mg per week up to 50 mg per week. If dexamethasone is discontinued, decrease the dose of temsirolimus to the dose used before initiation of dexamethasone. Temsirolimus is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Coadministration with another strong CYP3A4 inducer had no significant effect on the AUC or Cmax of temsirolimus, but decreased the AUC and Cmax of the active metabolite, sirolimus, by 56% and 65%, respectively. [50586] Terbinafine: (Moderate) Due to the risk for breakthrough fungal infections, caution is advised when administering terbinafine with dexamethasone. Although this interaction has not been studied by the manufacturer, and published literature suggests the potential for interactions to be low, taking these drugs together may decrease the systemic exposure of terbinafine. Predictions about the interaction can be made based on the metabolic pathways of both drugs. Terbinafine is metabolized by at least 7 CYP isoenyzmes, with major contributions coming from CYP3A4; dexamethasone induces this enzyme. Monitor patients for breakthrough fungal infections. [11334] [37590] [43880] [43881] [56538] [6759] Testosterone: (Moderate) Coadministration of corticosteroids and testosterone may increase the risk of edema, especially in patients with underlying cardiac or hepatic disease. Corticosteroids with greater mineralocorticoid activity, such as fludrocortisone, may be more likely to cause edema. Administer these drugs in combination with caution. [33698] Thalidomide: (Moderate) Coadministration of dexamethasone with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use. [8844] Thiazide diuretics: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. [26417] [54246] Thiazolidinediones: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Thyroid hormones: (Moderate) The metabolism of corticosteroids is increased in hyperthyroidism and decreased in hypothyroidism. Dosage adjustments may be necessary when initiating, changing or discontinuing thyroid hormones or antithyroid agents. [29779] [30015] [43942] Ticagrelor: (Moderate) Coadministration of ticagrelor with dexamethasone may result in decreased concentrations of ticagrelor. Use combination with caution and monitor for decreased efficacy of ticagrelor. Ticagrelor is a substrate of CYP3A4/5 and dexamethasone is a moderate CYP3A4 inducer. [44951] Tobramycin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Tolazamide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Tolbutamide: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. [28032] [30585] [51002] [62853] Tolvaptan: (Major) Tolvaptan is metabolized by CYP3A4. Dexamethasone is an inducer of CYP3A4. Coadministration of CYP3A4 inducers, such as dexamethasone, with tolvaptan may result in reduced plasma concentration and subsequent reduced effectiveness of tolvaptan therapy and should be avoided. If coadministration is unavoidable, an increase in the tolvaptan dose may be necessary and patients should be monitored for decreased effectiveness of tolvaptan. Additionally, the potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including diuretics. Serum potassium levels should be monitored in patients receiving these drugs concomitantly. [35780] [6759] Toremifene: (Major) Avoid coadministration of dexamethasone with toremifene due to decreased plasma concentrations of toremifene which may result in decreased efficacy. Toremifene is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Coadministration with strong CYP3A4 inducers lowers steady-state serum concentrations of toremifene. [28822] Tositumomab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Tranexamic Acid: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Tretinoin, ATRA: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. [7714] Tuberculin Purified Protein Derivative, PPD: (Moderate) Immunosuppressives may decrease the immunological response to tuberculin purified protein derivative, PPD. This suppressed reactivity can persist for up to 6 weeks after treatment discontinuation. Consider deferring the skin test until completion of the immunosuppressive therapy. [43298] [43299] Tubocurarine: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Tucatinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of tucatinib with dexamethasone is necessary, due to increased dexamethasone exposure; Cushing's syndrome and adrenal suppression could potentially occur with long-term use. Consider the use of corticosteroids such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, especially for long-term use. Tucatinib is a strong CYP3A4 inhibitor and dexamethasone is primarily metabolized by CYP3A4. Another strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. [54286] [65295] Ubrogepant: (Major) Increase the initial and second dose of ubrogepant to 100 mg if coadministered with dexamethasone as concurrent use may decrease ubrogepant exposure and reduce its efficacy. Ubrogepant is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. [54286] [64874] Ulipristal: (Major) Avoid administration of ulipristal with drugs that induce CYP3A4. Ulipristal is a substrate of CYP3A4 and dexamethasone is a CYP3A4 inducer. Concomitant use may decrease the plasma concentration and effectiveness of ulipristal. [41569] [48201] [50623] Vancomycin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. [54506] Vecuronium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years. [41361] [41961] [42031] [43319] [54278] [60760] [61750] [61937] Vemurafenib: (Major) Concomitant use of vemurafenib and dexamethasone may result in altered concentrations of dexamethasone and decreased concentrations vemurafenib. Vemurafenib is a substrate/inducer of CYP3A4 and a substrate/inhibitor of P-glycoprotein (P-gp). Dexamethasone is a substrate/inducer of CYP3A4 and a substrate of P-gp. Avoid using these agents together if possible. [11334] [45335] [6759] Venetoclax: (Major) Avoid the concomitant use of venetoclax and dexamethasone; venetoclax levels may be decreased and its efficacy reduced. Venetoclax is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Consider alternative agents. In a drug interaction study (n = 11), the venetoclax Cmax and AUC values were decreased by 42% and 71%, respectively, following the co-administration of multiple doses of a strong CYP3A4 inducer. Use of venetoclax with a moderate CYP3A4 inducer has not been evaluated. [34477] [54286] [60706] Vigabatrin: (Major) Vigabatrin should not be used with corticosteroids, which are associated with serious ophthalmic effects (e.g., retinopathy or glaucoma) unless the benefit of treatment clearly outweighs the risks. [36250] Vincristine Liposomal: (Moderate) Avoid the concomitant use of dexamethasone and vincristine. Vincristine is a substrate for cytochrome P450 (CYP) 3A4. Agents that induce CYP 3A4 such as dexamethasone may increase the metabolism of vincristine and decrease the efficacy of drug. [4718] [51432] (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. [57713] [57714] [57715] Vincristine: (Moderate) Avoid the concomitant use of dexamethasone and vincristine. Vincristine is a substrate for cytochrome P450 (CYP) 3A4. Agents that induce CYP 3A4 such as dexamethasone may increase the metabolism of vincristine and decrease the efficacy of drug. [4718] [51432] Vorapaxar: (Moderate) Use caution during concurrent use of vorapaxar and dexamethasone. Decreased serum concentrations of vorapaxar and thus decreased efficacy are possible when vorapaxar, a CYP3A4 substrate, is coadministered with dexamethasone, a CYP3A inducer. [57151] [6759] Voriconazole: (Moderate) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with voriconazole is necessary. Dexamethasone is a CYP3A4 substrate and voriconazole is a strong CYP3A4 inhibitor. [28158] [54286] Vorinostat: (Moderate) Use vorinostat and corticosteroids together with caution; the risk of QT prolongation and arrhythmias may be increased if electrolyte abnormalities occur. Corticosteroids may cause electrolyte imbalances; hypomagnesemia, hypokalemia, or hypocalcemia and may increase the risk of QT prolongation with vorinostat. Frequently monitor serum electrolytes if concomitant use of these drugs is necessary. [26417] [32789] Voxelotor: (Major) Avoid coadministration of voxelotor and dexamethasone as concurrent use may decrease voxelotor exposure and lead to reduced efficacy. If coadministration is unavoidable, increase voxelotor dosage to 2,500 mg PO once daily. Voxelotor is a substrate of CYP3A4; dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer is predicted to decrease voxelotor exposure by up to 60%. [54286] [64778] Warfarin: (Moderate) The effect of corticosteroids on oral anticoagulants (e.g., warfarin) is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids; however, limited published data exist, and the mechanism of the interaction is not well described. High-dose corticosteroids appear to pose a greater risk for increased anticoagulant effect. In addition, corticosteroids have been associated with a risk of peptic ulcer and gastrointestinal bleeding. Thus corticosteroids should be used cautiously and with appropriate clinical monitoring in patients receiving oral anticoagulants; coagulation indices (e.g., INR, etc.) should be monitored to maintain the desired anticoagulant effect. During high-dose corticosteroid administration, daily laboratory monitoring may be desirable. [28549] [29779] Zafirlukast: (Minor) Zafirlukast inhibits the CYP3A4 isoenzymes and should be used cautiously in patients stabilized on drugs metabolized by CYP3A4, such as corticosteroids. [4718] [4948] Zanubrutinib: (Major) Avoid the concomitant use of zanubrutinib and dexamethasone. Coadministration may result in decreased zanubrutinib exposure and reduced efficacy. Zanubrutinib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. The AUC of zanubrutinib is predicted to decrease by 60% when coadministered with another moderate CYP3A4 inducer. [54286] [64748] Zolpidem: (Moderate) It is advisable to closely monitor for reductions in zolpidem efficacy during co-administration of moderate CYP3A4 inducers, such as dexamethasone. CYP3A4 is the primary isoenzyme responsible for zolpidem metabolism, and there is evidence of significant decreases in systemic exposure and pharmacodynamic effects of zolpidem during co-administration of rifampin, a potent CYP3A4 inducer. [48902] [57789] Zonisamide: (Minor) Zonisamide is metabolized by hepatic cytochrome P450 enzyme 3A4. Inducers of CYP3A4, such as dexamethasone, can reduce the systemic exposure to zonisamide by increasing the metabolism of the drug. [4718]
    Revision Date: 08/07/2020, 02:26:00 AM

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Milford, PA: Serenity Pharmaceuticals LLC; 2017 Mar.61816 - Kisqali (ribociclib) tablets package insert. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2020 July.61838 - Ocrevus (ocrelizumab) injection package insert. South San Francisco, CA: Genentech, Inc.; 2020 May.61902 - Stimpel M, Proksch A, Wagner H, et al. Macrophage activation and induction of macrophage cytotoxicity by purified polysaccharide fractions from the plant Echinacea purpurea. Infect Immun 1984;46:845-961905 - Chavez ML, Jordan MA, Chavez PI. Evidence-based drug-herbal interactions. Life Sci 2006;78:2146-57.61909 - Alunbrig (brigatinib) tablet package insert. Cambridge, MA: Ariad Pharmaceuticals Inc.; 2020 May.61937 - Millipred (prednisolone) oral tablet package insert. Research Triangle Park, NC: Zylera Pharmaceuticals, LLC; 2015 Nov.62028 - Baxdela (delafloxacin) package insert. Lincolnshire, IL: Melinta Therapeutics, Inc.; 2019 Oct.62127 - Nerlynx (neratinib) package insert. 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New York, NY: Pfizer Labs; 2018 Nov.63777 - Daurismo (glasdegib) tablets package insert. New York, NY: Pfizer Labs; 2020 Mar.63790 - Firdapse (amifampridine) tablets package insert. Coral Gables, FL: Catalyst Pharmaceuticals, Inc.; 2018 Nov.63923 - The American Geriatrics Society 2019 Beers Criteria Update Expert Panel. American Geriatrics Society 2019 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2019;00:1-21.64002 - Pyridostigmine Bromide oral solution package insert. East Windsor, NJ: Novitium Pharma LLC; 2019 Mar.64031 - Mayzent (siponimod) tablets package insert. East Hanover, NJ: Novartis Pharmaceutical Corporation; 2019 Mar.64064 - Balversa (erdafitinib) tablets package insert. Horsham, PA: Janssen Products, LP; 2019 April.64165 - Dexamethasone (Decadron) tablets package insert. Whitehouse Station, NJ: Merck & Co., Inc.; 2019 May.64567 - Rozlytrek (entrectinib) package insert. 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    Monitoring Parameters

    • blood glucose
    • blood pressure
    • intraocular pressure
    • ophthalmologic exam
    • pulmonary function tests (PFTs)
    • serum cortisol
    • serum potassium

    US Drug Names

    • AK-Dex
    • Baycadron
    • Dalalone
    • Dalalone D.P
    • Dalalone L.A
    • Decadron
    • Decadron-LA
    • Dexabliss
    • Dexacort PH Turbinaire
    • Dexacort Respihaler
    • DexPak Jr TaperPak
    • DexPak TaperPak
    • Dextenza
    • DEXYCU
    • DoubleDex
    • Dxevo
    • HiDex
    • Maxidex
    • Ocu-Dex
    • Ozurdex
    • Simplist Dexamethasone
    • Solurex
    • TaperDex
    • ZCORT
    • Zema-Pak
    • ZoDex
    • ZonaCort 11 Day
    • ZonaCort 7 Day

    Global Drug names

    Argentina

    • Decadron - (Sidus)
    • Degabina - (Rivero)
    • Dexabion - (Merck)
    • Dexafarm - (ICN)
    • Dexalaf - (Lafedar)
    • Dexalergin - (Ivax)
    • Dexameral - (Raymos)
    • Dexa-Rhinospray N - (Boehringer Ingelheim)
    • Dexatotal - (Ariston)
    • Duo-Decadron - (Sidus)
    • Fadametasona - (Fada)
    • Ingedex - (Ingens)
    • Isopto Maxidex - (Alcon)
    • Lormine - (Northia)
    • Nexadron - (Klonal)
    • Rapi-Dexacort - (Cassara)
    • Rupedex - (Duncan)
    • Sedesterol - (Poen)
    • Trofinan - (Biol)

    Australia

    • Decadron - (MSD)
    • Dexmethsone - (Aspen)
    • Maxidex - (Novartis)
    • Oradexon - (Organon)
    • Otodex - (Sanofi-Aventis)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)
    • Tobispray - (Boehringer Ingelheim)

    Austria

    • Decadron - (MSD)
    • Dexabene - (Ratiopharm)
    • Fortecortin - (Merck)
    • Infectodexakrupp - (Infectopharm)
    • Monodex - (Thea)
    • Ozurdex - (Allergan)

    Belgium

    • Aacidexam - (Organon)
    • Decadron - (MSD)
    • Dexamgel - (Bausch & Lomb)
    • Dexa-Rhinospray - (Boehringer Ingelheim)
    • Dexa-Sine - (Alcon)
    • Dexa-Sol - (Hoechst Marion Roussel)
    • Dexa-Sol Soframycine - (Hoechst Marion Roussel)
    • Frakidex - (Bausch & Lomb)
    • Maxidex - (Novartis)
    • Oradexon - (Organon)
    • Ozurdex - (Allergan)
    • Percutalgine - (Besins)

    Brazil

    • Bexeton - (Geolab)
    • Cetadex - (Geolab)
    • Cortidex - (Pharlab)
    • Cortitop - (Multilab)
    • Decadron - (Ache)
    • Decadronal - (Ache)
    • Deflaren - (Sanval)
    • Dexacilin - (Prodotti)
    • Dexaden - (Cifarma)
    • Dexadermil - (Legrand)
    • Dexaflan - (Hebron)
    • Dexaglos - (Belfar)
    • Dexagreen - (Greenpharma)
    • Dexameson - (Cristalia)
    • Dexametax - (Hertz)
    • Dexametonal - (Sandoz)
    • Dexametrat - (Globo)
    • Dexamex - (Vitamedic)
    • Dexaminor - (Allergan)
    • Dexanil - (Neo Quimica)
    • Dexanom - (Uniao Quimica)
    • Dexason - (Teuto)
    • Dexazen - (Luper)
    • Dexazona - (Bunker)
    • Dexmene - (Biofarma)
    • Dextasona - (Blausiegel)
    • Duo-Decadron - (Ache)
    • Koidexa - (Momenta)
    • Lisoderme - (Belfar)
    • Maxidex - (Alcon)
    • Metadex - (Osorio de Moraes)
    • Metaxon - (Ariston)
    • Minidex - (Alcon)
    • Neodex - (Neo Quimica)
    • Netazon - (Neckerman)
    • Ozurdex - (Allergan)
    • Topidexa - (Kinder)
    • Uni Dexa - (Uniao Quimica)
    • Vibetrat Dexa - (Cimed)
    • Vitatonus Dexa - (Bunker)

    Canada

    • AK-Dex - (Akorn)
    • Cresophene - (Septodont)
    • Decadron - (Merck Frosst)
    • Deronil - (Schering)
    • Dexasone - (Valeant)
    • Diodex - (Dioptic)
    • Hexadrol - (Organon Teknika)
    • Maxidex - (Alcon)
    • Ocudex - (Charton)
    • Opticort - (Sandoz)
    • Oradexon - (Organon)
    • Ozurdex - (Allergan)
    • RO-Dexsone - (Richmond Ophthalmics)
    • Sofracort - (Sanofi-Aventis)
    • Spersadex - (Ciba Vision)

    Chile

    • Cortyk - (Pasteur)
    • Maxidex - (Alcon)
    • Oradexon - (Schering-Plough)
    • Ozurdex - (Allergan)

    China

    • 999 Piyanping - (SanJiu)
    • Di Da - (Di Ao)
    • Duo Li Sheng - (Mitsubishi)
    • Duo Ta Ke Mei - (Fengyuan)
    • Ge Da Li - (Tiantaishan)
    • Limethason - (Mitsubishi)
    • Ozurdex - (Allergan)
    • Surodex - (Zizhu)
    • Xi Luo An - (Lai Mei)
    • Yi Ke Tie - (Taitai)
    • You Nuo Ping - (SanJiu)
    • Zhong Yi Mei Song - (Guang Da)

    Czech Republic

    • Dexa - (Merckle)
    • Dexaltin - (Kayaku)
    • Dexamed - (Medochemie)
    • Dexapos - (Ursapharm)
    • Dexason - (ICN)
    • Dexona - (Cadila)
    • Fortecortin - (Merck)
    • Maxidex - (Alcon)
    • Otobacid N - (Chiesi)
    • Ozurdex - (Allergan)
    • Sofradex - (Aventis)

    Denmark

    • Decadron - (MSD)
    • Dexavital - (Vital)
    • Maxidex - (Alcon)
    • Monopex - (Thea)
    • Neofordex - (Medical Need)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)

    Finland

    • Decadron - (MSD)
    • Dexliq - (CTRS)
    • Käärmepakkaus - (Lyocentre)
    • Monopex - (Thea)
    • Neofordex - (Medical Need)
    • Oftan Dexa - (Santen)
    • Oradexon - (Aspen)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)

    France

    • Auxisone - (Boehringer Ingelheim)
    • Cébédex - (Chauvin)
    • Corticétine - (Chauvin)
    • Cresophene - (Septodont)
    • Décadron - (MSD-Chibret)
    • Dectancyl - (Sanofi-Aventis)
    • Désocort - (Chauvin)
    • Dexafree - (Thea)
    • Dexane - (Alcon)
    • Eucaryl - (Zizine)
    • Frakidex - (Chauvin)
    • Maxidex - (Alcon)
    • Mepacyl - (Pierre Rolland)
    • Neodex - (CTRS)
    • Ozurdex - (Allergan)
    • Percutalgine - (Besins)
    • Soludecadron - (MSD-Chibret)

    Germany

    • afpred-DEXA - (Riemser)
    • Anemul mono - (Medopharm)
    • Auxiloson - (Boehringer Ingelheim)
    • Axidexa - (Apocare)
    • Cortidexason - (Dermapharm)
    • Cortisumman - (Winzer)
    • Decadron - (Chibret)
    • Decadron Phosphat - (MSD)
    • Dexa - (Mibe)
    • Dexa Biciron - (Alcon)
    • Dexa in der Ophtiole - (Mann)
    • Dexa Loscon - (Basotherm)
    • Dexa Loscon mono - (Galderma)
    • Dexa Siozwo - (Febena)
    • Dexa-Allvoran - (TAD)
    • Dexabene - (Recordati)
    • Dexabeta - (Betapharm)
    • Dexa-Brachialin N - (Steigerwald)
    • dexa-clinit - (Hormosan)
    • DexaEDO - (Mann)
    • Dexa-Effekton - (Teofarma)
    • Dexaflam - (Lichtenstein)
    • Dexaflam - (Winthrop)
    • Dexafluid - (Mibe)
    • Dexagalen - (Galen)
    • Dexagel - (Mann)
    • Dexahexal - (Hexal)
    • Dexa-Injekt - (Kettelhack Riker)
    • Dexamed - (Medice)
    • Dexamonozon - (Medice)
    • Dexamonozon N - (Medice)
    • Dexa-Ophtal - (Winzer)
    • Dexapos - (Ursapharm)
    • Dexa-ratiopharm - (Ratiopharm)
    • Dexa-Rhinospray Mono - (Mann)
    • Dexa-Rhinospray N - (Mann)
    • Dexa-sine - (Alcon)
    • Ell-Cranell dexa - (Galderma)
    • Fortecortin - (Merck Serono)
    • InfectoDexaKrupp - (Infectopharm)
    • Isopto Dex - (Alcon)
    • Lipotalon - (Recordati)
    • Lokalison-F - (Dorsch)
    • Lokalison-universale - (Dorsch)
    • Millicorten-Vioform - (Novartis)
    • Monodex - (Thea)
    • Otobacid N - (Chiesi)
    • Ozurdex - (Allergan)
    • Predni-F-Tablinen - (Sanorania)
    • Rheumasit - (Medice)
    • Sokaral - (Allergan)
    • Solupen - (Winzer)
    • Solutio Cordes Dexa N - (Ichthyol)
    • Spersadex - (OmniVision)
    • Spondy-Dexa - (Efeka)
    • Totocortin - (Winzer)
    • Tuttozem N - (Strathmann)

    Greece

    • Decadron - (IFET)
    • Dexacollyre - (Cooper (Κοπερ))
    • Dexafar - (Faran)
    • Dexafree - (Thea)
    • Dexamed - (Anpharm (Ανφαρμ))
    • Dexa-Rhinaspray-N - (Boehringer Ingelheim)
    • Dexa-Sine - (IFET)
    • Dexaton - (Vianex (Βιανεξ))
    • Dexatopic - (Organon)
    • Maxidex - (Alcon)
    • Oradexon - (Organon (Οργανον))
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)
    • Soldesanil - (Diapit)
    • Suomi - (Verisfield)
    • Thilodexine - (Pharmex (Φαρμεξ))
    • Thiloxedine - (Pharmex (Φαρμεξ))

    Hong Kong

    • Acolon - (Wings)
    • Anatondex - (Europharm)
    • Arthrodex - (Vickmans)
    • Atrofin Adex - (Europharm)
    • Bufforidex - (Europharm)
    • Cassuliedex - (Europharm)
    • Cervicondex - (Europharm)
    • CP-Dexa - (Christo)
    • Deca - (Hitpharm)
    • Decadron - (MSD)
    • Dexa-B - (Vickmans)
    • Dexalocal - (Medinova)
    • Dexaltin - (Kayaku)
    • Dexamed - (Medochemie)
    • Dexasone - (Atlantic)
    • Dexatab - (HealthCare PharmaScience)
    • Dexmetha - (Synco)
    • Dexmethsone - (Aspen)
    • Dexone - (Quality)
    • Difomindex - (Europharm)
    • Donapaindex - (Europharm)
    • Etrofindex - (Europharm)
    • Euromethasone - (Europharm)
    • Flucloxdex - (Europharm)
    • Frakidex - (Chauvin)
    • Goldisdex - (Europharm)
    • Gopainlindex - (Europharm)
    • Hi-Methasone - (Lanway)
    • Kovin Tong - (Hitpharm)
    • Limethason - (Green Cross)
    • Logifuldex - (Europharm)
    • Marrinisdex - (Europharm)
    • Maxidex - (Alcon)
    • Medexone - (Medipharma)
    • Ozurdex - (Allergan)
    • Parasone - (Vida)
    • Parloviadex - (Europharm)
    • Phildaxdex - (Europharm)
    • Raposiddex - (Europharm)
    • Rocolone - (Weijian)
    • Rolessdex - (Europharm)
    • Sanroxdex - (Europharm)
    • Scandexon - (Hang Lung)
    • Sofradex - (Sanofi-Aventis)
    • Sonimindex - (Europharm)
    • Spersadex - (Novartis)
    • Stamforddex - (Europharm)
    • Sumitondex - (Europharm)
    • Trabit - (Mepha)
    • Trankaldex - (Europharm)
    • Turoska-Edex - (Europharm)
    • Vesonicdex - (Europharm)
    • Wationaldex - (Europharm)
    • Wharnisdex - (Europharm)
    • Zotex - (Deltapharm)

    Hungary

    • Dexa - (Teva)
    • Maxidex - (Alcon)
    • Oradexon - (Organon)
    • Ozurdex - (Allergan)

    India

    • Decdak - (Wockhardt)
    • Decdan - (Wockhardt)
    • Decolite - (Intas)
    • Decrina - (Intra-Labs)
    • Dedron - (Sanjivani)
    • Deksa - (Intas)
    • Demisone - (Cadila)
    • Deosone - (PC India)
    • Dex - (Neon)
    • Dexaject - (Sterkem)
    • Dexalab - (Laborate)
    • Dexamac - (Mac)
    • Dexamag - (Shalaks)
    • Dexamine - (Baroda)
    • Dexane - (Samarth)
    • Dexaquin - (Cadila)
    • Dexar - (Rass)
    • Dexariv - (East African)
    • Dexasia - (Willow)
    • Dexasone - (Cadila)
    • Dexona - (Zydus)
    • Dex-V - (Vensat)
    • Idizone - (Indian Drugs)
    • Intradex - (Intra-Labs)
    • Losone - (Cadila)
    • Low-Dex - (Syntho)
    • Mexa - (Hauz)
    • Millicortenol - (Novartis)
    • Millicorten-Vioform - (Novartis)
    • Sofracort - (Sanofi-Aventis)
    • Sofradex - (Sanofi-Aventis)
    • Wymesone - (Wyeth)

    Indonesia

    • Blecidex - (Sanbe Vision)
    • Camidexon - (Global Health)
    • Cetadexon - (Soho)
    • Corsona - (Phapros)
    • Cortidex - (Sanbe)
    • Danasone - (Hexpharm)
    • Decilone - (Westmont)
    • Dellamethasone - (Darya-Varia)
    • Dexaharsen - (Harsen)
    • Dexa-M - (Dexa)
    • Etason - (Otto)
    • Fortecortin - (Merck)
    • Indexon - (Interbat)
    • Inthesa-5 - (Fahrenheit)
    • Kalmethasone - (Hexpharm)
    • Lanadexon - (Landson)
    • Licodexon - (Berlico Mulia)
    • Metsocrim - (Tropica Mas)
    • Molacort - (Molex Ayus)
    • Nufadex - (Nufarindo)
    • Oradexon - (MSD)
    • Prodexon - (Meprofarm)
    • Pycameth - (Tropica Mas)
    • Pyradexon - (Pyridam)
    • Scandexon - (Tempo Scan Pacific)
    • Sofradex - (Sanofi-Aventis)

    Ireland

    • Decadron - (MSD)
    • Dexafree - (Thea)
    • Dexa-Rhinaspray Duo - (Boehringer Ingelheim)
    • Dexsol - (Rosemont)
    • Dropodex - (Rayner)
    • Maxidex - (Novartis)
    • Neofordex - (CTRS)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)

    Israel

    • Cresophene - (Septodont)
    • Dexacort - (Teva)
    • Dexsol - (Perrigo)
    • Maxidex - (Alcon)
    • Ozurdex - (Allergan)
    • Sterodex - (Fischer)

    Italy

    • Antimicotico - (IFI)
    • Capital - (Krugher)
    • Corti-Arscolloid - (SIT)
    • Decadron - (Visufarma)
    • Decofluor - (Salfa)
    • Dermadex - (Teofarma)
    • Dermadex Chinolinico - (SmithKline Beecham)
    • Desalark - (Farmacologico Milanese)
    • Desalfa - (INTES)
    • Deseronil - (Essex)
    • Dexamono - (Thea)
    • Etacortilen - (SIFI)
    • Firmalone - (FIRMA)
    • Luxazone - (Allergan)
    • Meclocil Desa - (Esseti)
    • Megacort - (Farma 1)
    • Netildex - (SIFI)
    • Rinedrone - (Deca)
    • Situalin - (Formenti)
    • Situalin Antibiotico - (Formenti)
    • Soldesam - (Farmacologico Milanese)
    • Usoldec - (Genetic)
    • Visumetazone - (Visufarma)

    Japan

    • Decadron - (Nichi-Iko)
    • LenaDex - (Celgene)
    • Limethason - (Mitsubishi Tanabe)
    • Methaderm - (Taiho)
    • Voalla - (Maruho)

    Malaysia

    • Cortidax - (Raza)
    • Decadron - (MSD)
    • Decan - (YSP)
    • Dexalone - (CCM)
    • Dexaltin - (Kayaku)
    • Dexasone - (Atlantic)
    • Limethason - (Mitsubishi)
    • Maxidex - (Alcon)
    • Penatone - (CCM)
    • Roximeth - (CCM)
    • Sofradex - (Sanofi-Aventis)
    • Vextasone - (YSP)

    Mexico

    • Adrecort - (Allen)
    • Alin - (Chinoin)
    • Arecort-I - (Allen)
    • Azona - (Keton)
    • Beamoken A - (Kendrick)
    • Beminex - (Sons)
    • Bexine - (Collins)
    • Brulin - (Bruluart)
    • Butisel - (Diba)
    • Cortidex - (Rayere)
    • Cryometasona - (Cryopharma)
    • Daxafrin - (Sophia)
    • Decadron - (MSD)
    • Decadronal - (MSD)
    • Decorex - (Pisa)
    • Dexadutil - (Parggon)
    • Dexafrin - (Sophia)
    • Dexagrin - (Grin)
    • Dexal - (Marcel)
    • Dexamilan - (Parggon)
    • Dexatam - (Euromex)
    • Dexicar - (Provit)
    • Dexilal - (Silanes)
    • Dexona - (Jofrain)
    • Dibasona - (Diba)
    • Dibutasona - (Diba)
    • Etacortilen - (SIFI)
    • Examsa - (Antibioticos)
    • Indarzona-N - (Streger)
    • Lergosin - (Degorts)
    • Maxidex - (Alcon)
    • Metax - (Sons)
    • Mexona - (Orthos)
    • Migradexan - (Collins)
    • Pardex - (Parggon)
    • Reusan - (Reuffer)
    • Taprodex - (Provit)
    • Taxyl - (Solfran)
    • Vericort - (Maver)
    • Wiserdex - (Advaita)

    Netherlands

    • Decadron - (MSD)
    • Decadron Depot - (MSD)
    • Dexamgel - (Bausch & Lomb)
    • Dexa-POS - (Ursapharm)
    • Dexsol - (Rosemont)
    • Maxidex - (Alcon)
    • Neofordex - (CTRS)
    • Oradexon - (Aspen)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)

    New Zealand

    • Decadron - (MSD)
    • Dexmethsone - (Healthcare Logistics)
    • Maxidex - (Pharmaco)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)

    Norway

    • Decadron - (MSD)
    • Isopto Maxidex - (Novartis)
    • Monopex - (Thea)
    • Neofordex - (CTRS)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)
    • Spersadex - (Blumont)

    Philippines

    • Adrecort - (Tai Yu)
    • Cordex - (Steril-Gene)
    • Dabrin - (Pasteur)
    • Decan - (Yung Shin)
    • Decilone - (Westmont)
    • Dexamet - (Daewon)
    • Dexavit - (Pan-Ject)
    • Dexicort - (Basic)
    • Dexticort - (LBS)
    • Doxam - (Syncom)
    • Drenex - (Unilab)
    • Isodexam - (Sensomed)
    • Maxidex - (Alcon)
    • Metacort - (Ruixin)
    • Midexone - (SM)
    • Ondex - (Mercury)
    • Oradexon - (Aspen)
    • Penodex - (Rotexmedica)
    • Santeson - (Santen)
    • Scancortin - (Oriental)
    • Vexamet - (Vamsler)
    • Vherdex - (Vhermann)

    Poland

    • Demezon - (Sun-Farm)
    • Dexafree - (Thea)
    • Dexapolcort - (Polfa Tarchomin)
    • Dexaven - (PharmaSwiss)
    • Neofordex - (CTRS)
    • Ozurdex - (Allergan)

    Portugal

    • Atria - (Gide)
    • Decadron - (Medinfar)
    • Dexafree - (Thea)
    • Dexaval - (Tecnifar)
    • Dexaval V - (Tecnifar)
    • Eko - (Edol)
    • Frakidex - (Bausch & Lomb)
    • Oradexon - (Aspen)
    • Ozurdex - (Allergan)
    • Ronic - (Edol)

    Russian Federation

    • Detametazon - (Dalkhimfarm)
    • Dexacort - (Darou Pakhsh)
    • Dexafar - (Faran)
    • Dexamed - (Medochemie)
    • Dexapos - (Ursapharm)
    • Dexason - (Galenika)
    • Dexaven - (Jelfa)
    • Dexona - (Cadila)
    • Dexophthan - (Slavic)
    • Maxidex - (Alcon)
    • Megadexan - (Ozon)
    • Oftan Dexamethason - (Santen)
    • Ozurdex - (Allergan)
    • Percutalgine - (Besins)
    • Sofradex - (Sanofi-Aventis)

    Singapore

    • Decan - (Yung Shin)
    • Decordex - (Nida)
    • Dexaltin - (Kayaku)
    • Dexamed - (Medochemie)
    • Dexasone - (Atlantic)
    • Dexmetha - (Synco)
    • Dextrasone - (Xepa-Soul Pattinson)
    • Erladexone - (Malaysia Chemist)
    • Frakidex - (Bausch & Lomb)
    • Limethason - (Welfide)
    • Maxidex - (Alcon)
    • Mexasone - (Malayan)
    • Ozurdex - (Allergan)
    • Roximeth - (Duopharma)
    • Sofradex - (Sanofi-Aventis)
    • SP-Cordexa - (Sunward)
    • SW-Dexasone - (Sunward)

    South Africa

    • Decadron - (MSD)
    • Decasone - (Aspen)
    • Dexagel - (Bausch & Lomb)
    • Dexona - (Zydus)
    • Maxidex - (Alcon)
    • Oradexon - (Donmed)
    • Sofradex - (Sanofi-Aventis)
    • Spersadex - (Adcock Ingram)

    Spain

    • Amplidermis - (Medea)
    • Aqua Dexa - (Sarget)
    • Artrosone - (Belmac)
    • Dalamon Inyectable - (Alter)
    • Decadran - (MSD)
    • Dexafree - (Thea)
    • Dexamiso - (Oftalmiso)
    • Dexaplast - (Llorens)
    • Fortecortin - (Merck)
    • Fosfodexa - (Llorens)
    • Hemidexa - (Llorens)
    • Linoderm - (Sigma-Tau)
    • Maxidex - (Alcon Cusi)
    • Neurocatavin Dexa - (Llorente)
    • Neurodavur Plus - (Davur)
    • Neurosido - (Knoll)
    • Ozopulmin Antiasmatico - (Wasserman)
    • Ozurdex - (Allergan)
    • Percutalin - (Almirall)
    • Rectolmin Bronquial - (Frumtost)
    • Solone - (Boots)

    Sweden

    • Decadron - (MSD)
    • Dexacortal - (MSD)
    • Dexafree - (Thea)
    • Isopto Maxidex - (Alcon)
    • Neofordex - (Medical Need)
    • Opnol - (CCS)
    • Ozurdex - (Allergan)
    • Sofradex - (Hoechst Marion Roussel)

    Switzerland

    • Chronocorte - (Streuli)
    • Corticetine - (Bausch & Lomb)
    • Cresophene - (Septodont)
    • Decadron - (MSD)
    • Dexacortin - (Streuli)
    • Dexacortin-K - (Streuli)
    • Dexafree - (Thea)
    • Dexa-Helvacort - (Helvepharm)
    • Dexalocal - (Medinova)
    • Dexalocal-F - (Medinova)
    • Fortecortin - (Merck)
    • Frakidex - (Bausch & Lomb)
    • Maxidex - (Alcon)
    • Mephamésone - (Mepha)
    • Millicortene - (Novartis)
    • Oradexon - (Organon)
    • Ozurdex - (Allergan)
    • Sofradex - (Sanofi-Aventis)
    • Spersadex - (OmniVision)

    Thailand

    • B Dexol - (Central)
    • Decadron - (M & H)
    • Dexa - (Utopian)
    • Dexa ANB - (ANB)
    • Dexacortisone - (ANB)
    • Dexagel - (Bausch & Lomb)
    • Dexaltin - (ANB)
    • Dexano - (Milano)
    • Dexa-O - (Chinta)
    • Dexa-P - (PP Lab)
    • Dexapro - (Medicine Products)
    • Dexasone - (Atlantic)
    • Dexa-Y - (Chinta)
    • Dexion - (Umeda)
    • Dexon - (General Drugs)
    • Dexone - (The Forty-Two)
    • Dexthasol - (Olan-Kemed)
    • Dexthasone - (Utopian)
    • Dexton - (TP)
    • Limethason - (Mitsubishi)
    • Lodexa - (LBS)
    • Oradexon - (MSD)
    • Ozurdex - (Allergan)
    • Percutalgine - (Piette)
    • Phenodex - (Vesco)
    • Sofradex - (Sanofi-Aventis)
    • Trabit - (Mepha)

    Turkey

    • Cebedex - (Abdi)
    • Dekort - (Deva)
    • Deksalon - (Sanli)
    • Deksamet - (Osel)
    • Dexa-Sine - (Liba)
    • Dexoject - (Tum)
    • Gadexon - (Avicenna)
    • Kordexa - (Kocak)
    • Maxidex - (Alcon)
    • Netildex - (Teka)
    • Onadron - (Ulagay)
    • Ozurdex - (Allergan)
    • Spersadex - (Novartis)

    Ukraine

    • Dexagel - (Bausch & Lomb)
    • Farmadex - (Farmak)
    • Maxidex - (Alcon)
    • Medexol - (World Medicine)
    • Ozurdex - (Allergan)
    • Percutalgine - (Besins)
    • Sofradex - (Sanofi-Aventis)

    United Kingdom

    • Decadron - (MSD)
    • Dexafree - (Spectrum)
    • Dexa-Rhinaspray Duo - (Boehringer Ingelheim)
    • Dexsol - (Rosemont)
    • Dropodex - (Moorfields)
    • Glensoludex - (Glenmark)
    • Martapan - (Martindale Pharmaceuticals)
    • Maxidex - (Alcon)
    • Neofordex - (Aspire)
    • Oradexon - (Organon)
    • Ozurdex - (Allergan)
    • Sofradex - (Florizel)

    Venezuela

    • Decadron - (MSD)
    • Decalona - (Biotech)
    • Decobel - (Ronava)
    • Dexacort - (Behrens)
    • Dexamin - (Vivax Optipharm)
    • Kanasone - (Leti)
    • Maradex - (Oftalmi)
    • Metalexina - (Rowe-Fleming)