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Dexamethasone (Systemic)

Medically reviewed by Drugs.com. Last updated on Dec 22, 2019.

Pronunciation

(deks a METH a sone)

Index Terms

  • Decadron
  • Dexamethasone Sod Phosphate
  • Dexamethasone Sodium Phosphate
  • Hemady

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Concentrate, Oral:

Dexamethasone Intensol: 1 mg/mL (30 mL) [contains alcohol, usp; unflavored flavor]

Elixir, Oral:

Decadron: 0.5 mg/5 mL (237 mL [DSC]) [contains alcohol, usp, benzoic acid, fd&c red #40, propylene glycol]

Generic: 0.5 mg/5 mL (237 mL)

Kit, Injection, as sodium phosphate:

ReadySharp Dexamethasone: 10 mg/mL [contains benzyl alcohol, sodium sulfite]

TopiDex: 10 mg/mL [contains benzyl alcohol]

Kit, Injection, as sodium phosphate [preservative free]:

Active Injection D: 10 mg/mL

DoubleDex: 10 mg/mL

MAS Care-Pak: 10 mg/mL

Solution, Oral:

Generic: 0.5 mg/5 mL (240 mL, 500 mL)

Solution, Injection, as sodium phosphate:

Generic: 4 mg/mL (1 mL); 20 mg/5 mL (5 mL); 120 mg/30 mL (30 mL); 10 mg/mL (1 mL); 100 mg/10 mL (10 mL)

Solution, Injection, as sodium phosphate [preservative free]:

Generic: 4 mg/mL (1 mL); 10 mg/mL (1 mL)

Solution Prefilled Syringe, Injection, as sodium phosphate [preservative free]:

Generic: 10 mg/mL (1 mL)

Tablet, Oral:

Decadron: 0.5 mg [scored; contains fd&c yellow #10 (quinoline yellow), tartrazine (fd&c yellow #5)]

Decadron: 0.75 mg [scored; contains brilliant blue fcf (fd&c blue #1), fd&c yellow #10 (quinoline yellow)]

Decadron: 4 mg, 6 mg [scored]

Generic: 0.5 mg, 0.75 mg, 1 mg, 1.5 mg, 2 mg, 4 mg, 6 mg

Tablet Therapy Pack, Oral:

DexPak 10 Day: 1.5 mg (35 ea) [scored; contains fd&c red #40 aluminum lake]

DexPak 13 Day: 1.5 mg (51 ea) [scored; contains fd&c red #40 aluminum lake]

DexPak 6 Day: 1.5 mg (21 ea) [scored; contains fd&c red #40 aluminum lake]

Dxevo 11-Day: 1.5 mg (39 ea)

Dxevo 11-Day: 1.5 mg (39 ea) [scored]

HiDex 6-Day: 1.5 mg (21 ea) [scored; contains fd&c red #40]

LoCort 11-Day: 1.5 mg (41 ea [DSC]) [scored; contains fd&c red #40]

LoCort 7-Day: 1.5 mg (27 ea [DSC]) [scored; contains fd&c red #40]

TaperDex 12-Day: 1.5 mg (49 ea) [contains fd&c red #40]

TaperDex 6-Day: 1.5 mg (21 ea) [contains fd&c red #40 aluminum lake]

TaperDex 7-Day: 1.5 mg (27 ea) [scored; contains fd&c red #40]

Zodex 12-Day: 1.5 mg (49 ea [DSC]) [scored; contains fd&c red #40]

Zodex 6-Day: 1.5 mg (21 ea [DSC]) [scored; contains fd&c red #40 aluminum lake]

ZonaCort 11 Day: 1.5 mg (41 ea [DSC]) [scored; contains fd&c red #40]

ZonaCort 7 Day: 1.5 mg (27 ea [DSC]) [scored; contains fd&c red #40]

Generic: 1.5 mg (21 ea, 35 ea, 51 ea)

Brand Names: U.S.

  • Active Injection D
  • Decadron
  • Dexamethasone Intensol
  • DexPak 10 Day
  • DexPak 13 Day
  • DexPak 6 Day
  • DoubleDex
  • Dxevo 11-Day
  • HiDex 6-Day
  • LoCort 11-Day [DSC]
  • LoCort 7-Day [DSC]
  • MAS Care-Pak
  • ReadySharp Dexamethasone
  • TaperDex 12-Day
  • TaperDex 6-Day
  • TaperDex 7-Day
  • TopiDex
  • Zodex 12-Day [DSC]
  • Zodex 6-Day [DSC]
  • ZonaCort 11 Day [DSC]
  • ZonaCort 7 Day [DSC]

Pharmacologic Category

  • Anti-inflammatory Agent
  • Antiemetic
  • Corticosteroid, Systemic

Pharmacology

Dexamethasone is a long acting corticosteroid with minimal sodium-retaining potential. It decreases inflammation by suppression of neutrophil migration, decreased production of inflammatory mediators, and reversal of increased capillary permeability; suppresses normal immune response. Dexamethasone's mechanism of antiemetic activity is unknown.

Absorption

Oral: 61% to 86% (Czock 2005).

Metabolism

Hepatic.

Excretion

Urine (~10%) (Duggan 1975; Miyabo 1981).

Onset of Action

Acetate: IV: Rapid.

Immune thrombocytopenia: Oral: Initial response: 2 to 14 days; Peak response: 4 to 28 days (Neunert 2011).

Time to Peak

Serum: Oral: 1 to 2 hours (Czock 2005); IM: ~30 to 120 minutes (Egerman 1997; Hochhaus 2001); IV: 5 to 10 minutes (free dexamethasone) (Miyabo 1981; Rohdewald 1987).

Duration of Action

IV: Short.

Half-Life Elimination

Extremely low birth-weight infants with BPD: 9.26 ± 3.34 hours (range: 5.85 to 16.1 hours) (Charles 1993).

Children 4 months to 16 years: 4.34 ± 4.14 hours (range: 2.33 to 9.54 hours) (Richter 1983).

Adults: Oral: 4 ± 0.9 hours (Czock 2005); IV: ~1 to 5 hours (Hochhaus 2001; Miyabo 1981; Rohdewald 1987; Tóth 1999).

Use: Labeled Indications

Oral, IV, or IM injection: Anti-inflammatory or immunosuppressant agent in the treatment of a variety of diseases, including those of allergic, hematologic (eg, immune thrombocytopenia), dermatologic, neoplastic, rheumatic, autoimmune, nervous system, renal, and respiratory origin; primary or secondary adrenocorticoid deficiency (not first line); management of shock, cerebral edema, and as a diagnostic agent.

Intra-articular or soft tissue injection: As adjunctive therapy for short-term administration in synovitis of osteoarthritis, rheumatoid arthritis, acute and subacute bursitis, acute gouty arthritis, epicondylitis, acute nonspecific tenosynovitis, and posttraumatic osteoarthritis.

Intralesional injection: Keloids; localized hypertrophic, infiltrated, inflammatory lesions of lichen planus, psoriatic plaques, granuloma annulare, and lichen simplex chronicus (neurodermatitis); discoid lupus erythematosus; necrobiosis lipoidica diabeticorum; alopecia areata; and cystic tumors of an aponeurosis or tendon (ganglia).

Off Label Uses

Acute mountain sickness/high-altitude cerebral edema

Based on the Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness, the use of dexamethasone is effective and recommended for the prevention or treatment of acute altitude illnesses, including acute mountain sickness and cerebral edema [Luks 2014].

Antiemetic regimens: Chemotherapy-associated nausea and vomiting, prevention

Based on guidelines from the American Society of Clinical Oncology (ASCO) and the Multinational Association of Supportive Care in Cancer (MASCC), dexamethasone is recommended as a component of antiemetic regimens for the prevention of nausea and vomiting associated with chemotherapy [ASCO [Hesketh 2017]], [MASCC/ESMO [Roila 2016]].

Antiemetic regimens: Radiation therapy-associated nausea and vomiting, prevention

Based on guidelines from ASCO and MASCC, dexamethasone is recommended as a component of antiemetic regimens for the prevention of nausea and vomiting associated with radiation [ASCO [Hesketh 2017]], [MASCC/ESMO [Roila 2016]].

Asthma, acute exacerbation

Data from one randomized, single-center study suggest that the use of dexamethasone for acute asthma exacerbations is as effective as prednisone and prevents relapse [Kravitz 2011].

Based on the Global Initiative for Asthma global strategy for asthma management and prevention, dexamethasone is recommended as an alternative to prednisone for the treatment of patients with acute asthma exacerbations presenting to the emergency department [GINA 2018].

Fetal lung maturation, acceleration of

Data from systematic reviews of randomized, controlled trials using betamethasone or dexamethasone support the use of a single course of antenatal corticosteroids to accelerate fetal lung maturation in women at risk for preterm delivery, with no clear advantages found regarding use of one corticosteroid over another [Brownfoot 2013], [Roberts 2017]. Some experts prefer betamethasone due to lack of superiority and need for fewer injections compared to dexamethasone [Lee 2019].

Based on the American College of Obstetricians and Gynecologists (ACOG) practice bulletins for the management of prelabor rupture of membranes or preterm labor, the antenatal use of corticosteroids (eg, dexamethasone) to accelerate fetal lung maturation is effective and recommended [ACOG 171 2016], [ACOG 713 2017], [ACOG 188 2018].

Meningitis (bacterial), prevention of neurologic complications

Data from a prospective, randomized, double-blind, multicenter trial suggest that early use of dexamethasone improves clinical outcomes in patients with bacterial meningitis in the developed world [de Gans 2002].

Data from a prospective, randomized, double-blind, placebo-controlled trial suggest that early use of dexamethasone improves clinical outcomes in patients with microbiologically proven bacterial meningitis in the developing world [Nguyen 2007].

Based on the Infectious Diseases Society of America guidelines for the management of bacterial meningitis and the Society of Critical Care Medicine and European Society of Intensive Care Medicine guidelines for the diagnosis and management of critical illness-related corticosteroid insufficiency in critically ill patients, dexamethasone is recommended in patients with suspected or proven bacterial meningitis.

Multiple myeloma

Data from large randomized, phase 3 studies support the use of dexamethasone (in various combination regimens) in the treatment of newly diagnosed and relapsed or refractory multiple myeloma [Chari 2017], [Dimopoulos 2016a], [Dimopoulos 2016b], [Dimopoulos 2018], [Facon 2019], [Lonial 2015], [Moreau 2015], [Moreau 2018], [Palumbo 2016], [Rajkumar 2010], [San Miguel 2013], [Sonneveld 2012], [Stewart 2015].

Contraindications

Hypersensitivity to dexamethasone or any component of the formulation; systemic fungal infections

Documentation of allergenic cross-reactivity for corticosteroids is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.

Dosing: Adult

Note: Dosing: Evidence to support an optimal dose and duration is lacking for most indications; recommendations provided are general guidelines only and primarily based on expert opinion. In general, glucocorticoid dosing should be individualized and the minimum effective dose/duration should be used. For select indications with weight-based dosing, consider using ideal body weight in obese patients, especially with longer durations of therapy (Erstad 2004; Furst 2019a). Hypothalamic-pituitary-adrenal (HPA) suppression: Although some patients may become hypothalamic-pituitary-adrenal (HPA) suppressed with lower doses or briefer exposure, some experts consider HPA-axis suppression likely in any adult receiving >3 mg/day (daytime dosing) or ≥0.75 mg per 24 hours (evening or night dosing) for >3 weeks or with Cushingoid appearance (Furst 2019b; Joseph 2016); do not abruptly discontinue treatment in these patients; dose tapering may be necessary (Cooper 2003).

Usual dosage range: Oral, IV, IM: 4 to 20 mg/day given in a single daily dose or in 2 to 4 divided doses; High dose: 0.4 to 0.8 mg/kg/day (usually not to exceed 40 mg/day).

Indication-specific dosing:

Acute mountain sickness/high-altitude cerebral edema (off-label use):

Prevention, moderate- to high-risk situations(alternative agent): Note: Use in addition to gradual ascent and start the day of ascent.

Oral: 2 mg every 6 hours or 4 mg every 12 hours; may be discontinued after staying at the same elevation for 2 to 4 days or if descent is initiated. Due to adverse effects, limit duration to ≤10 days (Luks 2014); some experts limit to ≤7 days (Gallagher 2019). In situations of rapid ascent to altitudes >3,500 meters (eg, rescue or military operations), 4 mg every 6 hours may be considered (Luks 2014).

Treatment:

Acute mountain sickness (moderate to severe): Note: Dexamethasone does not facilitate acclimatization; further ascent should be delayed until patient is asymptomatic off medication (Gallagher 2019; Luks 2014).

Oral, IM, IV: 4 mg every 6 hours, continue until 24 hours after symptoms resolve or descent completed (not longer than 7 days total) (Gallagher 2019; Luks 2014).

High-altitude cerebral edema: Oral, IM, IV: 8 mg as a single dose, followed by 4 mg every 6 hours until descent is complete and symptoms resolve (Luks 2014).

Adrenal insufficiency (adrenal crisis) (alternative agent): Note: Dexamethasone should only be used if hydrocortisone is unavailable. Corticosteroid therapy should be combined with adequate fluid resuscitation in patients with primary adrenal insufficiency (ES [Bornstein 2016]).

IV: 4 mg every 12 hours; transition to hydrocortisone as soon as possible (ES [Bornstein 2016]; Nieman 2019).

Antiemetic regimens: Chemotherapy-associated nausea and vomiting, prevention (off-label use): Note: When dexamethasone is given with rolapitant in a prechemotherapy regimen, the oral route for both is generally used.

Single-day IV chemotherapy regimens:

Highly emetogenic chemotherapy (>90% risk of emesis): Cisplatin and other highly emetogenic single agents:

Dexamethasone dose depends on specific neurokinin 1 (NK1) receptor antagonist (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]):

Day of chemotherapy: Administer prior to chemotherapy and in combination with a NK1 receptor antagonist, and a 5-HT3 receptor antagonist, with or without olanzapine (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]).

In combination with aprepitant, fosaprepitant, netupitant/palonosetron (NEPA), or fosnetupitant/palonosetron: Oral, IV: 12 mg.

In combination with rolapitant: Oral, IV: 20 mg.

If NK1 receptor antagonist not used: Oral, IV: 20 mg.

Postchemotherapy days:

If aprepitant given: Oral, IV: 8 mg once daily on days 2 to 4 (ASCO [Hesketh 2017]).

If fosaprepitant given: Oral, IV: 8 mg once on day 2, followed by 8 mg twice daily on days 3 and 4 (ASCO [Hesketh 2017]).

If NEPA or fosnetupitant/palonosetron given: Prophylaxis with dexamethasone on subsequent days is not needed unless regimen contained cisplatin: Oral, IV: 8 mg once daily on days 2 to 4 (Hesketh 2019).

If rolapitant given: Oral, IV: 8 mg twice daily on days 2 to 4 (ASCO [Hesketh 2017]).

If NK1 receptor antagonist not used: Oral, IV: 8 mg twice daily on days 2 to 4 (ASCO [Hesketh 2017]).

Highly emetogenic chemotherapy (>90% risk of emesis): Breast cancer regimens that include an anthracycline combined with cyclophosphamide:

Dexamethasone dose depends on specific NK1 receptor antagonist [ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]):

Day of chemotherapy: Administer prior to chemotherapy and in combination with a NK1 receptor antagonist, and a 5-HT3 receptor antagonist, with or without olanzapine (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]).

In combination with aprepitant, fosaprepitant, NEPA, fosnetupitant/palonosetron: Oral, IV: 12 mg (ASCO [Hesketh 2017]; Hesketh 2019).

In combination with rolapitant: Oral, IV: 20 mg (ASCO [Hesketh 2017]).

If NK1 receptor antagonist not used: Oral, IV: 20 mg (ASCO [Hesketh 2017]).

Postchemotherapy days: Dexamethasone use is not recommended (an alternative agent or agents is/are recommended) (ASCO [Hesketh 2017]; Hesketh 2019).

Moderately emetogenic chemotherapy (30% to 90% risk of emesis): Carboplatin-based regimens:

Dexamethasone dose depends on specific NK1 receptor antagonist (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]):

Day of chemotherapy: Administer prior to chemotherapy and in combination with a NK1 receptor antagonist and a 5-HT3 receptor antagonist (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]).

In combination with aprepitant, fosaprepitant, NEPA, or fosnetupitant/palonosetron: Oral, IV: 12 mg (ASCO [Hesketh 2017]; Hesketh 2019).

In combination with rolapitant: Oral, IV: 20 mg (ASCO [Hesketh 2017]).

Postchemotherapy days: Prophylaxis is not necessary on subsequent days (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]).

Moderately emetogenic chemotherapy (30% to 90% risk of emesis): Non-carboplatin-based regimens:

Day of chemotherapy: Administer prior to chemotherapy and in combination with a 5-HT3 receptor antagonist: Oral, IV: 8 mg (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]).

Postchemotherapy days: Note: Consider single-agent dexamethasone use for regimens containing agents with known potential to induce delayed emesis (eg, oxaliplatin, cyclophosphamide, doxorubicin) (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]); however, if a first-generation 5-HT3 antagonist was used on day 1 rather than palonosetron, some experts suggest the first-generation 5-HT3 receptor antagonist be continued for postchemotherapy emetic prophylaxis on days 2 and 3 (Hesketh 2019).

Oral, IV: 8 mg on days 2 and 3 (ASCO [Hesketh 2017]; MASCC/ESMO [Roila 2016]).

Low emetogenic risk (10% to 30% risk of emesis): Oral, IV: 4 to 8 mg administered as a single agent in a single dose prior to chemotherapy; prophylaxis is not necessary on subsequent days (ASCO [Hesketh 2017]; Hesketh 2019; MASCC/ESMO [Roila 2016]).

Antiemetic regimens: Radiation therapy-associated nausea and vomiting, prevention (off-label use):

High emetogenic risk radiation therapy (total body irradiation):

Radiation day(s): Oral, IV: 4 mg once daily prior to each fraction of radiation; give in combination with a 5-HT3 receptor antagonist (ASCO [Hesketh 2017]).

Postradiation days: Oral, IV: The appropriate duration of therapy following radiotherapy days is not well defined; ASCO guidelines recommend continuing dexamethasone 4 mg once on the day after each day of radiation if radiation is not planned for that day (ASCO [Hesketh 2017]).

Moderate emetogenic risk radiation therapy (upper abdomen, craniospinal irradiation):

Radiation day(s): Oral, IV: 4 mg once daily prior to each of the first 5 fractions of radiation; give in combination with a 5-HT3 receptor antagonist (ASCO [Hesketh 2017]).

Asthma, acute exacerbation (alternative agent) (off-label use): Note: Alternative to a longer course of other corticosteroids in mild to moderate exacerbations or in patients who do not respond promptly and completely to short-acting beta-agonists; administer within 1 hour of presentation to emergency department (GINA 2018; NAEPP 2007).

Oral: 16 mg daily for 2 days only (Kravitz 2011); longer treatment at this dose may be associated with metabolic adverse effects (GINA 2018).

Cerebral (vasogenic) edema associated with brain tumor:

Moderate to severe symptoms (eg, lowered consciousness/brainstem dysfunction):

Initial: IV: 10 mg once followed by maintenance dosing (Vecht 1994).

Maintenance: IV, Oral: 4 mg every 6 hours (Chang 2019; Vecht 1994). Note: Consider taper after 7 days of therapy; taper slowly over several weeks (Ryken 2010; Vecht 1994).

Mild symptoms: IV, Oral: 4 to 8 mg/day in 1 to 4 divided doses (Chang 2019; Vecht 1994). Note: Consider taper after 7 days of therapy; taper slowly over several weeks (Ryken 2010; Vecht 1994).

Cushing syndrome, diagnosis: Note: Interpretation requires evaluation of one or more of the following: serum cortisol concentration, serum dexamethasone concentration, urinary cortisol excretion, or 17-hydroxycorticosteroid excretion; consultation with a clinical endocrinologist is recommended (ES [Nieman 2008]).

Initial testing:

Overnight 1 mg dexamethasone suppression test: Oral: 1 mg given once between 11 PM and 12 AM (ES [Nieman 2008]).

Longer low-dose dexamethasone suppression test (2 mg/day for 48 hours): Note: May be preferred in patients with depression, anxiety, obsessive-compulsive disorder, morbid obesity, alcoholism, or diabetes mellitus (ES [Nieman 2008]).

Oral: 0.5 mg every 6 hours for 48 hours for a total of 8 doses; start time varies (eg, 9 AM or 12 PM) (ES [Nieman 2008]; Yanovski 1993).

Fetal lung maturation, acceleration of (maternal administration) (alternative to preferred agent [ie, betamethasone]) (off-label use): Note: Generally, for women between 24 and 34 weeks of gestation, including those with ruptured membranes or multiple gestations, who are at risk of delivering within 7 days. A single course may be appropriate in some women beginning at 23 weeks' gestation or late preterm (between 34 0/7 weeks' and 36 6/7 weeks' gestation) who are at risk of delivering within 7 days.

IM: 6 mg every 12 hours for a total of 4 doses. May repeat course in select patients (eg, women with pregnancies up to 34 weeks' gestation at risk for delivery within 7 days and >14 days have elapsed since initial course of antenatal corticosteroids) (ACOG 171 2016; ACOG 713 2017; ACOG 188 2018; Lee 2019).

Immune thrombocytopenia (initial therapy): Note: Goal of therapy is to provide a safe platelet count to prevent clinically important bleeding rather than normalization of the platelet count (Arnold 2019).

Oral, IV: 40 mg once daily for 4 days and then stop (no taper); may repeat if inadequate response (ASH [Neunert 2011]; Mazzucconi 2007; Provan 2010; Wei 2016). For severe bleeding with thrombocytopenia, give in combination with other therapies (Arnold 2019).

Iodinated contrast media allergic-like reaction, prevention (alternative agent): Note: Generally for patients with a prior allergic-like or unknown-type iodinated contrast reaction who will be receiving another iodinated contrast agent. Nonurgent premedication with an oral corticosteroid (eg, prednisone) is generally preferred when contrast administration is scheduled to begin in ≥12 hours; however, consider an urgent (accelerated) regimen with an IV corticosteroid for those requiring contrast in <12 hours (ACR 2018).

Urgent (accelerated) regimen: IV: 7.5 mg every 4 hours until contrast medium administration in combination with IV diphenhydramine 50 mg (administered 1 hour prior to contrast) (ACR 2018).

Meningitis (bacterial), prevention of neurologic complications (off-label use): Note: Administer first dose of dexamethasone shortly before or at the same time as the first dose of antibacterials. If antibacterials have already been administered, do not administer dexamethasone. In patients with pneumococcal meningitis who receive dexamethasone, some experts recommend adding rifampin to the standard initial antibacterial regimen or adding rifampin if susceptibility tests, once available, show intermediate susceptibility (MIC ≥2 mcg/mL) to ceftriaxone and cefotaxime (IDSA [Tunkel 2004]; Sexton 2019).

Developed world (suspected or confirmed pneumococcal meningitis): IV: 0.15 mg/kg/dose or 10 mg every 6 hours for 4 days; discontinue if culture data reveal non-pneumococcal etiology (de Gans 2002; IDSA [Tunkel 2004]; SCCM/ESICM [Pastores 2018]; Sexton 2019).

Developing world (strongly suspected or confirmed bacterial meningitis): IV: 0.4 mg/kg/dose every 12 hours for 4 days; discontinue if culture data reveal non-pneumococcal etiology; not recommended in regions with high rates of HIV infection and/or malnutrition or in cases of delayed clinical presentation (Nguyen 2007; Sexton 2019).

Multiple myeloma (off-label use): Note: Multiple dexamethasone-containing regimens are available. Refer to literature/guidelines for additional details. For many regimens, dexamethasone is continued until disease progression or unacceptable toxicity. When administered weekly, dexamethasone is reduced to 20 mg once weekly for frail patients (eg, >75 years of age, BMI <18.5, poorly controlled diabetes, corticosteroid intolerance) (Dimopoulos 2016b; Palumbo 2016).

Combination regimens that do not include a monoclonal antibody:

Oral:

40 mg once weekly on days 1, 8, 15, and 22 every 28 days in combination with lenalidomide (Rajkumar 2010), pomalidomide (San Miguel 2013), ixazomib and lenalidomide (Moreau 2015), carfilzomib and lenalidomide (Stewart 2015), or bortezomib and lenalidomide (Rajkumar 2011) or 40 mg once weekly on days 1, 8, 15, and 22 every 28 days in cycles 1 to 9, and then 40 mg once weekly on days 1, 8, and 15 every 28 days beginning at cycle 10 (in combination with carfilzomib) (Moreau 2018).

or

20 mg on days 1, 2, 8, 9, 15, 16, 22, and 23 every 28 days (in combination with carfilzomib) (Dimopoulos 2016a).

or

20 mg on days 1 and 3 of each week (in combination with selinexor) (Chari 2019).

or

40 mg once daily on days 1 to 4, 9 to 12, and 17 to 20 in combination with bortezomib and doxorubicin for 3 cycles as induction (Sonneveld 2012). Note: Some experts reserve this dosing (for 1 cycle, followed by 40 mg once weekly thereafter) for patients with an aggressive disease presentation or acute renal failure from light chain cast nephropathy (Rajkumar 2019).

Combination regimens that include a monoclonal antibody:

Oral, IV:

40 mg weekly in combination with daratumumab and pomalidomide (Chari 2017) or daratumumab and lenalidomide (Dimopoulos 2016b; Facon 2019) or 20 mg once daily on days 1, 2, 4, 5, 8, 9, 11, and 12 in combination with daratumumab and bortezomib (Palumbo 2016). Note: In some studies, the dexamethasone dose is split over 2 days (20 mg before daratumumab and 20 mg the day after daratumumab infusion).

or

40 mg weekly, except on days elotuzumab is administered (administer dexamethasone 28 mg orally [8 mg orally in patients >75 years of age] plus 8 mg IV prior to elotuzumab) in combination with elotuzumab and pomalidomide (Dimopoulos 2018) or elotuzumab and lenalidomide (Lonial 2015).

Neoplastic epidural spinal cord compression, symptomatic: Note: As an adjunct to definitive treatment (radiotherapy or surgery), particularly in patients with neurologic deficits (Loblaw 2012; NICE 2008).

IV (initial dose): 10 or 16 mg followed by oral dosing (Loblaw 2012; NICE 2008).

Oral (after IV dose): 16 mg/day (usually given in 2 to 4 divided doses). Once definitive treatment is underway, taper gradually over 1 to 2 weeks until discontinuation (George 2015; Kumar 2017; Loblaw 2012; NICE 2008).

Tuberculosis, central nervous system: Note: In general, steroids are indicated for patients with established or suspected tuberculous meningitis, regardless of HIV status (HHS [OI adult 2019]; WHO 2017).

IV: Initial dose: 0.3 to 0.4 mg/kg/day for 2 weeks, then 0.2 mg/kg/day for week 3, then 0.1 mg/kg/day for week 4, followed by oral therapy (Leonard 2019; Thwaites 2004).

Oral: Starting week 5 of treatment: 4 mg/day, then taper by 1 mg of the daily dose each week; total combined IV/oral therapy duration: ~8 weeks (Leonard 2019; Thwaites 2004).

Dosing: Geriatric

Refer to adult dosing. Use cautiously in the elderly at the lowest possible dose.

Dosing: Pediatric

Acute mountain sickness (AMS) (moderate)/high altitude cerebral edema (HACE); treatment: Limited data available: Infants, Children, and Adolescents: Oral, IM, IV: 0.15 mg/kg/dose every 6 hours; maximum dose: 4 mg/dose; consider using for high altitude pulmonary edema because of associated HACE with this condition (Luks 2010; Pollard 2001)

Airway edema or extubation: Limited data available: Infants, Children, and Adolescents: Oral, IM, IV: 0.5 mg/kg/dose (maximum dose: 10 mg/dose) administered 6 to 12 hours prior to extubation then every 6 hours for 6 doses (total dexamethasone dose: 3 mg/kg) (Anene 1996; Khemani 2009; Tellez 1991)

Anti-inflammatory: Infants, Children, and Adolescents: Oral, IM, IV: Initial dose range: 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day in divided doses every 6 to 12 hours; dose depends upon condition being treated and response of patient; dosage for infants and children should be based on disease severity and patient response; usual adult daily dose range: 0.75 to 9 mg/day

Asthma exacerbation: Limited data available: Infants, Children, and Adolescents: Oral, IM, IV: 0.6 mg/kg once daily as a single dose or once daily for 2 days; maximum dose: 16 mg/dose (AAP [Hegenbarth 2008]; Keeney 2014; Qureshi 2001); single dose regimens as low as 0.3 mg/kg/dose and as high as 1.7 mg/kg/dose have also been reported (Keeney 2014; Qureshi 2001; Shefrin 2009). Note: Duration >2 days is not recommended due to increased risk of metabolic effects (GINA 2014).

Bacterial meningitis (H. influenzae type b): Limited data available: Infants >6 weeks and Children: IV: 0.15 mg/kg/dose every 6 hours for the first 2 to 4 days of antibiotic treatment; start dexamethasone 10 to 20 minutes before or with the first dose of antibiotic; if antibiotics have already been administered, dexamethasone use has not been shown to improve patient outcome and is not recommended (IDSA [Tunkel 2004]). Note: For pneumococcal meningitis, data has not shown clear benefit from dexamethasone administration; risk and benefits should be considered prior to use (Red Book [AAP 2012]).

Cerebral edema: Infants, Children, and Adolescents: Oral, IM, IV: Loading dose: 1 to 2 mg/kg/dose as a single dose; maintenance: 1 to 1.5 mg/kg/day in divided doses every 4 to 6 hours; maximum daily dose: 16 mg/day (Kliegman 2007)

Chemotherapy-induced nausea and vomiting, prevention: Refer to individual protocols and emetogenic potential: Infants, Children, and Adolescents:

POGO recommendations (Dupuis 2013): Note: Reduce dose by 50% if administered concomitantly with aprepitant:

Highly/severely emetogenic chemotherapy: Oral, IV: 6 mg/m2/dose every 6 hours

Moderately emetogenic chemotherapy: Oral, IV:

BSA ≤0.6 m2: 2 mg every 12 hours

BSA >0.6 m2: 4 mg every 12 hours

Alternate dosing: Highly/severely emetogenic chemotherapy: IV: Usual: 10 mg/m2/dose once daily on days of chemotherapy; some patients may require every 12-hour dosing; usual range: 8 to 14 mg/m2/dose (Holdsworth 2006; Jordan 2010; Phillips 2010); others have used: Initial: 10 mg/m2/dose prior to chemotherapy (maximum dose: 20 mg) then 5 mg/m2/dose every 6 hours (Kliegman 2007)

Congenital adrenal hyperplasia: Adolescents (fully grown): Oral: 0.25 to 0.5 mg once daily; use of a liquid dosage form may be preferable to allow for better dose titration (AAP 2010; Speiser 2010). Note: For younger patients who are still growing, hydrocortisone or fludrocortisone are preferred.

Croup (laryngotracheobronchitis): Limited data available; dosing regimens variable: Infants and Children: Oral, IM, IV: 0.6 mg/kg once; reported maximum dose highly variable; usual maximum dose: 16 mg/dose (AAP [Hegenbarth 2008]); in trials, maximum doses of 10 to 20 mg/dose have been reported with similar efficacy findings for mild to moderate croup. The majority of reported experience in infants are those ≥3 months of age; data available in <3 months of age is very limited (AAP [Hegenbarth 2008]; Bjornson 2004; Cruz 1995; Petrocheilou 2014; Russell 2011). In one evaluation of 22 children >2 years of age, a maximum dose of 12 mg/dose (at 0.6 mg/kg/dose) did not decrease endogenous glucocorticoid levels (Gill 2017). A single oral dose of 0.15 mg/kg has also been shown effective in infants ≥3 months and children with mild to moderate croup (Russell 2004; Sparrow 2006).

Physiologic replacement: Infants, Children, and Adolescents: Oral, IM, IV: 0.03 to 0.15 mg/kg/day in divided doses every 6 to 12 hours (Kliegman 2007) or Initial: 0.2 to 0.25 mg/m2/day administered once daily; some patients may require 0.3 mg/m2/day (Gupta 2008)

Reconstitution

IV: May be given undiluted or further diluted in NS or D5W.

Administration

Oral: Administer with meals to help prevent GI upset. May administer antacids between meals to help prevent peptic ulcers.

Oral concentrate: Use only the calibrated dropper provided. Draw dose into dropper; squeeze dropper contents into a liquid or semi-solid food (water, juice, soda or soda-like beverage, applesauce, pudding). Gently stir for a few seconds. Administer the entire mixture immediately. Do not store for future use.

IV: May administer 4 mg/mL or 10 mg/mL concentration undiluted over ≤1 minute (Gahart 2015). Rapid administration may be associated with perineal irritation (especially with higher doses); consider further dilution and administration by IV intermittent infusion over 5 to 15 minutes (Allan 1986; Neff 2002; Perron 2003; Singh 2011).

IM: Administer 4 mg/mL or 10 mg/mL concentration by deep IM injection.

Intra-articular or soft tissue injection: Note: Dexamethasone sodium phosphate (a short-acting solution) in the 4 mg/mL concentration is the only formulation available for intra-articular or soft tissue injections. Dexamethasone acetate (a long-acting suspension) is not available in the United States or Canada. Therefore, other glucocorticoids, such as triamcinolone acetonide or methylprednisolone acetate, are used more commonly for intra-articular or soft-tissue injection (Centeno 1994; Roberts 2019).

Intra-articular: Administer into affected joint using the 4 mg/mL concentration only.

Soft tissue: Administer into affected tissue using the 4 mg/mL concentration only.

Intralesional injection: Note: Dexamethasone sodium phosphate (a short-acting solution) in the 4 mg/mL concentration is the only formulation available for intralesional injections. Another glucocorticoid, triamcinolone acetonide, is used more commonly for intralesional injection (Mathes 2019).

Intralesional: Administer into affected area using the 4 mg/mL concentration only.

Dietary Considerations

May be taken with meals to decrease GI upset. May need diet with increased potassium, pyridoxine, vitamin C, vitamin D, folate, calcium, and phosphorus.

Storage

Elixir: Store at 15°C to 30°C (59°F to 86°F); avoid freezing.

Injection: Store intact vials at 20°C to 25°C (68°F to 77°F). Protect from light, heat, and freezing. Do not autoclave. Diluted solutions should be used within 24 hours.

Oral concentrated solution (Intensol): Store at 20°C to 25°C (68°F to 77°F); do not freeze; do not use if precipitate is present; dispense only in original bottle and only with manufacturer-supplied calibrated dropper; discard open bottle after 90 days.

Oral solution, tablets: Store at 20°C to 25°C (68°F to 77°F); protect from moisture.

Drug Interactions

Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Monitor therapy

Aldesleukin: Corticosteroids may diminish the antineoplastic effect of Aldesleukin. Avoid combination

Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Monitor therapy

Androgens: Corticosteroids (Systemic) may enhance the fluid-retaining effect of Androgens. Monitor therapy

Antacids: May decrease the bioavailability of Corticosteroids (Oral). Management: Consider separating doses by 2 or more hours. Budesonide enteric coated tablets could dissolve prematurely if given with drugs that lower gastric acid, with unknown impact on budesonide therapeutic effects. Consider therapy modification

Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Monitor therapy

Aprepitant: May increase the serum concentration of Corticosteroids (Systemic). Management: No dose adjustment is needed for single 40 mg aprepitant doses. For other regimens, reduce oral dexamethasone or methylprednisolone doses by 50%, and IV methylprednisolone doses by 25%. Antiemetic regimens containing dexamethasone reflect this adjustment. Consider therapy modification

Asparaginase (E. coli): May increase the serum concentration of DexAMETHasone (Systemic). This is thought to be due to an asparaginase-related decrease in hepatic proteins responsible for dexamethasone metabolism. Monitor therapy

Asparaginase (Erwinia): May increase the serum concentration of DexAMETHasone (Systemic). This is thought to be due to an asparaginase-related decrease in hepatic proteins responsible for dexamethasone metabolism. Monitor therapy

Axicabtagene Ciloleucel: Corticosteroids (Systemic) may diminish the therapeutic effect of Axicabtagene Ciloleucel. Management: Avoid use of corticosteroids as premedication before axicabtagene ciloleucel. Corticosteroids may, however, be required for treatment of cytokine release syndrome or neurologic toxicity. Consider therapy modification

Baricitinib: Immunosuppressants may enhance the immunosuppressive effect of Baricitinib. Management: Use of baricitinib in combination with potent immunosuppressants such as azathioprine or cyclosporine is not recommended. Concurrent use with antirheumatic doses of methotrexate or nonbiologic disease modifying antirheumatic drugs (DMARDs) is permitted. Consider therapy modification

BCG (Intravesical): Immunosuppressants may diminish the therapeutic effect of BCG (Intravesical). Avoid combination

Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Monitor therapy

Bosentan: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Calcitriol (Systemic): Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol (Systemic). Monitor therapy

Caspofungin: Inducers of Drug Clearance may decrease the serum concentration of Caspofungin. Management: Consider using an increased caspofungin dose of 70 mg daily in adults (or 70 mg/m2, up to a maximum of 70 mg, daily in pediatric patients) when coadministered with known inducers of drug clearance. Consider therapy modification

Cladribine: May enhance the immunosuppressive effect of Immunosuppressants. Avoid combination

Clofazimine: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Monitor therapy

CloZAPine: CYP3A4 Inducers (Weak) may decrease the serum concentration of CloZAPine. Monitor therapy

Cobicistat: DexAMETHasone (Systemic) may decrease the serum concentration of Cobicistat. Dexamethasone (Systemic) may also counteract the boosting effects of Cobicistat on some agents. Management: Consider an alternative corticosteroid. Monitor patients receiving this combination closely for evidence of diminished response to the antiviral regimen. Consider therapy modification

Coccidioides immitis Skin Test: Immunosuppressants may diminish the diagnostic effect of Coccidioides immitis Skin Test. Monitor therapy

Conivaptan: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Avoid combination

Corticorelin: Corticosteroids may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Monitor therapy

Cosyntropin: Corticosteroids (Systemic) may diminish the diagnostic effect of Cosyntropin. Monitor therapy

CycloSPORINE (Systemic): DexAMETHasone (Systemic) may decrease the serum concentration of CycloSPORINE (Systemic). DexAMETHasone (Systemic) may increase the serum concentration of CycloSPORINE (Systemic). CycloSPORINE (Systemic) may increase the serum concentration of DexAMETHasone (Systemic). Monitor therapy

CYP3A4 Inducers (Moderate): May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

CYP3A4 Inducers (Strong): May decrease the serum concentration of DexAMETHasone (Systemic). Management: Consider dexamethasone dose increases in patients receiving strong CYP3A4 inducers and monitor closely for reduced dexamethasone efficacy. Consider avoiding this combination when treating life threatening conditions (ie, multiple myeloma). Consider therapy modification

CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates (High risk with Inhibitors). Monitor therapy

CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates (High risk with Inhibitors). Consider therapy modification

Dabrafenib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Seek alternatives to the CYP3A4 substrate when possible. If concomitant therapy cannot be avoided, monitor clinical effects of the substrate closely (particularly therapeutic effects). Consider therapy modification

Daclatasvir: DexAMETHasone (Systemic) may decrease the serum concentration of Daclatasvir. Management: US labeling recommends increasing the daclatasvir dose to 90 mg once daily if used with dexamethasone. Canadian labeling states that the combination of daclatasvir and dexamethasone is contraindicated. Consider therapy modification

Dasatinib: DexAMETHasone (Systemic) may decrease the serum concentration of Dasatinib. Management: Avoid when possible. If such a combination cannot be avoided, consider increasing dasatinib dose and monitoring clinical response and toxicity closely. Consider therapy modification

Deferasirox: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Deferasirox: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Monitor therapy

Deferasirox: Corticosteroids may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Monitor therapy

Denosumab: May enhance the adverse/toxic effect of Immunosuppressants. Specifically, the risk for serious infections may be increased. Monitor therapy

Desirudin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Desirudin. More specifically, corticosteroids may increase hemorrhagic risk during desirudin treatment. Management: Discontinue treatment with systemic corticosteroids prior to desirudin initiation. If concomitant use cannot be avoided, monitor patients receiving these combinations closely for clinical and laboratory evidence of excessive anticoagulation. Consider therapy modification

Desmopressin: Corticosteroids (Systemic) may enhance the hyponatremic effect of Desmopressin. Avoid combination

DilTIAZem: May increase the serum concentration of Corticosteroids (Systemic). Monitor therapy

Duvelisib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Monitor therapy

Echinacea: May diminish the therapeutic effect of Immunosuppressants. Consider therapy modification

Elvitegravir: DexAMETHasone (Systemic) may decrease the serum concentration of Elvitegravir. Management: Consider using an alternative corticosteroid. Monitor patients receiving these agents in combination for diminished antiviral response. Consider therapy modification

Enzalutamide: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Concurrent use of enzalutamide with CYP3A4 substrates that have a narrow therapeutic index should be avoided. Use of enzalutamide and any other CYP3A4 substrate should be performed with caution and close monitoring. Consider therapy modification

Erdafitinib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Erdafitinib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Monitor therapy

Erdafitinib: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. Monitor therapy

Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Monitor therapy

Fexinidazole [INT]: Corticosteroids (Systemic) may enhance the arrhythmogenic effect of Fexinidazole [INT]. Avoid combination

Fingolimod: Immunosuppressants may enhance the immunosuppressive effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and other immunosuppressants when possible. If combined, monitor patients closely for additive immunosuppressant effects (eg, infections). Consider therapy modification

Fosamprenavir: DexAMETHasone (Systemic) may decrease the serum concentration of Fosamprenavir. Fosamprenavir may increase the serum concentration of DexAMETHasone (Systemic). Monitor therapy

Fosaprepitant: May increase the serum concentration of Corticosteroids (Systemic). The active metabolite aprepitant is likely responsible for this effect. Consider therapy modification

Fosnetupitant: May increase the serum concentration of DexAMETHasone (Systemic). Management: Decrease dexamethasone doses to 12 mg on day 1, and if needed based on the emetic potential of the regimen, 8 mg daily on days 2 to 4 of chemotherapy when administered with fosnetupitant. Consider therapy modification

Fosphenytoin: May decrease the serum concentration of DexAMETHasone (Systemic). DexAMETHasone (Systemic) may decrease the serum concentration of Fosphenytoin. DexAMETHasone (Systemic) may increase the serum concentration of Fosphenytoin. Management: Consider dexamethasone dose increases when combined with fosphenytoin and monitor closely for reduced steroid efficacy. Monitor phenytoin levels closely, both increased and decreased phenytoin levels have been reported. Consider therapy modification

Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Avoid combination

Hyaluronidase: Corticosteroids may diminish the therapeutic effect of Hyaluronidase. Management: Patients receiving corticosteroids (particularly at larger doses) may not experience the desired clinical response to standard doses of hyaluronidase. Larger doses of hyaluronidase may be required. Consider therapy modification

Idelalisib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Avoid combination

Imatinib: DexAMETHasone (Systemic) may decrease the serum concentration of Imatinib. Management: Avoid concurrent use of imatinib with dexamethasone when possible. If such a combination must be used, increase imatinib dose by at least 50% and monitor clinical response closely. Consider therapy modification

Indacaterol: May enhance the hypokalemic effect of Corticosteroids (Systemic). Monitor therapy

Indium 111 Capromab Pendetide: Corticosteroids (Systemic) may diminish the diagnostic effect of Indium 111 Capromab Pendetide. Avoid combination

Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Monitor therapy

Ivosidenib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Ixabepilone: DexAMETHasone (Systemic) may decrease the serum concentration of Ixabepilone. Management: Avoid this combination whenever possible. If this combination must be used, a gradual increase in ixabepilone dose from 40 mg/m2 to 60 mg/m2 (given as a 4-hour infusion), as tolerated, should be considered. Consider therapy modification

Lapatinib: DexAMETHasone (Systemic) may decrease the serum concentration of Lapatinib. Management: If therapy overlap cannot be avoided, consider titrating lapatinib gradually from 1,250 mg/day up to 4,500 mg/day (HER2 positive metastatic breast cancer) or 1,500 mg/day up to 5,500 mg/day (hormone receptor/HER2 positive breast cancer) as tolerated. Avoid combination

Larotrectinib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Monitor therapy

Lasmiditan: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. Avoid combination

Leflunomide: Immunosuppressants may enhance the adverse/toxic effect of Leflunomide. Specifically, the risk for hematologic toxicity such as pancytopenia, agranulocytosis, and/or thrombocytopenia may be increased. Management: Consider not using a leflunomide loading dose in patients receiving other immunosuppressants. Patients receiving both leflunomide and another immunosuppressant should be monitored for bone marrow suppression at least monthly. Consider therapy modification

Lenalidomide: DexAMETHasone (Systemic) may enhance the thrombogenic effect of Lenalidomide. Consider therapy modification

Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Monitor therapy

Lorlatinib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Avoid concurrent use of lorlatinib with any CYP3A4 substrates for which a minimal decrease in serum concentrations of the CYP3A4 substrate could lead to therapeutic failure and serious clinical consequences. Consider therapy modification

Macimorelin: Corticosteroids (Systemic) may diminish the diagnostic effect of Macimorelin. Avoid combination

Mifamurtide: Corticosteroids (Systemic) may diminish the therapeutic effect of Mifamurtide. Avoid combination

MiFEPRIStone: May diminish the therapeutic effect of Corticosteroids (Systemic). MiFEPRIStone may increase the serum concentration of Corticosteroids (Systemic). Management: Avoid mifepristone in patients who require long-term corticosteroid treatment of serious illnesses or conditions (e.g., for immunosuppression following transplantation). Corticosteroid effects may be reduced by mifepristone treatment. Avoid combination

Mitotane: May decrease the serum concentration of Corticosteroids (Systemic). Consider therapy modification

Mitotane: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Doses of CYP3A4 substrates may need to be adjusted substantially when used in patients being treated with mitotane. Consider therapy modification

Nalmefene: DexAMETHasone (Systemic) may decrease the serum concentration of Nalmefene. Monitor therapy

Natalizumab: Immunosuppressants may enhance the adverse/toxic effect of Natalizumab. Specifically, the risk of concurrent infection may be increased. Avoid combination

Netupitant: May increase the serum concentration of DexAMETHasone (Systemic). Management: Decrease dexamethasone doses to 12 mg on day 1, and if needed based on the emetic potential of the regimen, 8 mg daily on days 2 to 4 of chemotherapy when administered with netupitant. Consider therapy modification

Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse neuromuscular effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Consider therapy modification

Nicorandil: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nicorandil. Gastrointestinal perforation has been reported in association with this combination. Monitor therapy

NiMODipine: CYP3A4 Inducers (Weak) may decrease the serum concentration of NiMODipine. Monitor therapy

Nivolumab: Immunosuppressants may diminish the therapeutic effect of Nivolumab. Consider therapy modification

Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective). Monitor therapy

Nonsteroidal Anti-Inflammatory Agents (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Monitor therapy

Ocrelizumab: May enhance the immunosuppressive effect of Immunosuppressants. Monitor therapy

Palbociclib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Monitor therapy

P-glycoprotein/ABCB1 Inducers: May decrease the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Monitor therapy

P-glycoprotein/ABCB1 Inhibitors: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Monitor therapy

Phenytoin: May decrease the serum concentration of DexAMETHasone (Systemic). DexAMETHasone (Systemic) may decrease the serum concentration of Phenytoin. DexAMETHasone (Systemic) may increase the serum concentration of Phenytoin. Management: Consider dexamethasone dose increases when combined with phenytoin and monitor closely for reduced steroid efficacy. Monitor phenytoin levels closely when combined with dexamethasone, both increased and decreased phenytoin levels have been reported. Consider therapy modification

Pidotimod: Immunosuppressants may diminish the therapeutic effect of Pidotimod. Monitor therapy

Pimecrolimus: May enhance the adverse/toxic effect of Immunosuppressants. Avoid combination

Quinolones: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolones. Specifically, the risk of tendonitis and tendon rupture may be increased. Monitor therapy

Ranolazine: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. Monitor therapy

Rilpivirine: DexAMETHasone (Systemic) may decrease the serum concentration of Rilpivirine. Avoid combination

Ritodrine: Corticosteroids may enhance the adverse/toxic effect of Ritodrine. Monitor therapy

Roflumilast: May enhance the immunosuppressive effect of Immunosuppressants. Consider therapy modification

Salicylates: May enhance the adverse/toxic effect of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease the serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Monitor therapy

Sargramostim: Corticosteroids (Systemic) may enhance the therapeutic effect of Sargramostim. Specifically, corticosteroids may enhance the myeloproliferative effects of sargramostim. Monitor therapy

Sarilumab: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Siltuximab: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Simeprevir: DexAMETHasone (Systemic) may decrease the serum concentration of Simeprevir. Avoid combination

Siponimod: Immunosuppressants may enhance the immunosuppressive effect of Siponimod. Monitor therapy

Sipuleucel-T: Immunosuppressants may diminish the therapeutic effect of Sipuleucel-T. Management: Evaluate patients to see if it is medically appropriate to reduce or discontinue therapy with immunosuppressants prior to initiating sipuleucel-T therapy. Consider therapy modification

Somatropin: Corticosteroids (Systemic) may diminish the therapeutic effect of Somatropin. Monitor therapy

Stiripentol: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Management: Use of stiripentol with CYP3A4 substrates that are considered to have a narrow therapeutic index should be avoided due to the increased risk for adverse effects and toxicity. Any CYP3A4 substrate used with stiripentol requires closer monitoring. Consider therapy modification

Tacrolimus (Systemic): Corticosteroids (Systemic) may decrease the serum concentration of Tacrolimus (Systemic). Conversely, when discontinuing corticosteroid therapy, tacrolimus concentrations may increase. Monitor therapy

Tacrolimus (Topical): May enhance the adverse/toxic effect of Immunosuppressants. Avoid combination

Temsirolimus: DexAMETHasone (Systemic) may decrease serum concentrations of the active metabolite(s) of Temsirolimus. Monitor therapy

Tertomotide: Immunosuppressants may diminish the therapeutic effect of Tertomotide. Monitor therapy

Thalidomide: DexAMETHasone (Systemic) may enhance the dermatologic adverse effect of Thalidomide. DexAMETHasone (Systemic) may enhance the thrombogenic effect of Thalidomide. Consider therapy modification

Thiazide and Thiazide-Like Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. Monitor therapy

Tisagenlecleucel: Corticosteroids (Systemic) may diminish the therapeutic effect of Tisagenlecleucel. Management: Avoid use of corticosteroids as premedication or at any time during treatment with tisagenlecleucel, except in the case of life-threatening emergency (such as resistant cytokine release syndrome). Consider therapy modification

Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Monitor therapy

Tofacitinib: Immunosuppressants may enhance the immunosuppressive effect of Tofacitinib. Management: Concurrent use with antirheumatic doses of methotrexate or nonbiologic disease modifying antirheumatic drugs (DMARDs) is permitted, and this warning seems particularly focused on more potent immunosuppressants. Consider therapy modification

Trastuzumab: May enhance the neutropenic effect of Immunosuppressants. Monitor therapy

Triazolam: DexAMETHasone (Systemic) may decrease the serum concentration of Triazolam. Monitor therapy

Ubrogepant: CYP3A4 Inducers (Weak) may decrease the serum concentration of Ubrogepant. Management: Use an initial ubrogepant dose of 100 mg and second dose (if needed) of 100 mg when used with a weak CYP3A4 inducer. Consider therapy modification

Upadacitinib: Immunosuppressants may enhance the immunosuppressive effect of Upadacitinib. Avoid combination

Urea Cycle Disorder Agents: Corticosteroids (Systemic) may diminish the therapeutic effect of Urea Cycle Disorder Agents. More specifically, Corticosteroids (Systemic) may increase protein catabolism and plasma ammonia concentrations, thereby increasing the doses of Urea Cycle Disorder Agents needed to maintain these concentrations in the target range. Monitor therapy

Vaccines (Inactivated): Immunosuppressants may diminish the therapeutic effect of Vaccines (Inactivated). Management: Vaccine efficacy may be reduced. Complete all age-appropriate vaccinations at least 2 weeks prior to starting an immunosuppressant. If vaccinated during immunosuppressant therapy, revaccinate at least 3 months after immunosuppressant discontinuation. Consider therapy modification

Vaccines (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Vaccines (Live). Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Live). Management: Doses equivalent to less than 2 mg/kg or 20 mg per day of prednisone administered for less than 2 weeks are not considered sufficiently immunosuppressive to create vaccine safety concerns. Higher doses and longer durations should be avoided. Consider therapy modification

Voriconazole: DexAMETHasone (Systemic) may decrease the serum concentration of Voriconazole. Monitor therapy

Warfarin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Warfarin. Monitor therapy

Test Interactions

May suppress the wheal and flare reactions to skin test antigens

Adverse Reactions

Some reactions listed are based on reports for other agents in this same pharmacologic class and may not be specifically reported for dexamethasone.

Frequency not defined:

Cardiovascular: Bradycardia, cardiac arrhythmia, cardiac failure, cardiomegaly, circulatory shock, edema, embolism (fat), hypertension, hypertrophic cardiomyopathy (premature infants), myocardial rupture (post-MI), syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis

Central nervous system: Depression, emotional lability, euphoria, headache, increased intracranial pressure, insomnia, malaise, myasthenia, neuritis, neuropathy, paresthesia, personality changes, pseudotumor cerebri (usually following discontinuation), psychic disorder, seizure, vertigo

Dermatologic: Acne vulgaris, allergic dermatitis, alopecia, atrophic striae, diaphoresis, ecchymoses, erythema, facial erythema, fragile skin, hyperpigmentation, hypertrichosis, hypopigmentation, perianal skin irritation (itching, burning, tingling; following IV injection), petechiae, skin atrophy, skin rash, subcutaneous atrophy, suppression of skin test reaction, urticaria, xeroderma

Endocrine & metabolic: Adrenal suppression, carbohydrate intolerance, Cushing syndrome, decreased glucose tolerance, decreased serum potassium, diabetes mellitus, fluid retention, glycosuria, growth suppression (children), hirsutism, HPA-axis suppression, hyperglycemia, hypokalemic alkalosis, menstrual disease, moon face, negative nitrogen balance, protein catabolism, redistribution of body fat, sodium retention, weight gain

Gastrointestinal: Abdominal distention, gastrointestinal hemorrhage, gastrointestinal perforation, hiccups, increased appetite, nausea, pancreatitis, peptic ulcer, pruritus ani (following IV injection), ulcerative esophagitis

Genitourinary: Defective (increased or decreased) spermatogenesis

Hematologic & oncologic: Kaposi sarcoma, petechial, tumor lysis syndrome

Hepatic: Hepatomegaly, increased serum transaminases

Hypersensitivity: Anaphylactoid reaction, anaphylaxis, angioedema, hypersensitivity

Infection: Infection, sterile abscess

Local: Postinjection flare (intra-articular use)

Neuromuscular & skeletal: Amyotrophy, aseptic necrosis of bones (femoral and humoral heads), bone fractures, Charcot-like arthropathy, myasthenia, myopathy (particularly in conjunction with neuromuscular disease or neuromuscular-blocking agents), osteoporosis, rupture of tendon, steroid myopathy, vertebral compression fracture

Ophthalmic: Exophthalmos, glaucoma, increased intraocular pressure, subcapsular posterior cataract

Respiratory: Pulmonary edema

Miscellaneous: Wound healing impairment

Warnings/Precautions

Concerns related to adverse effects:

• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children or in patients receiving high doses for prolonged periods. HPA axis suppression may lead to adrenal crisis. Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully. Particular care is required when patients are transferred from systemic corticosteroids to inhaled products due to possible adrenal insufficiency or withdrawal from steroids, including an increase in allergic symptoms. Adult patients receiving >20 mg per day of prednisone (or equivalent) may be most susceptible. Fatalities have occurred due to adrenal insufficiency in asthmatic patients during and after transfer from systemic corticosteroids to aerosol steroids; aerosol steroids do not provide the systemic steroid needed to treat patients having trauma, surgery, or infections.

• Anaphylactoid reactions: Rare cases of anaphylactoid reactions have been observed in patients receiving corticosteroids.

• Immunosuppression: Prolonged use of corticosteroids may increase the incidence of secondary infection, cause activation of latent infections, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to killed or inactivated vaccines. Exposure to chickenpox or measles should be avoided; corticosteroids should not be used to treat ocular herpes simplex. Corticosteroids should not be used for cerebral malaria, fungal infections, or viral hepatitis. Close observation is required in patients with latent tuberculosis and/or TB reactivity; restrict use in active TB (only fulminating or disseminated TB in conjunction with antituberculosis treatment). Amebiasis should be ruled out in any patient with recent travel to tropic climates or unexplained diarrhea prior to initiation of corticosteroids. Use with extreme caution in patients with Strongyloides infections; hyperinfection, dissemination and fatalities have occurred.

• Kaposi sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi sarcoma (case reports); if noted, discontinuation of therapy should be considered (Goedert 2002).

• Myopathy: Acute myopathy has been reported with high-dose corticosteroids, usually in patients with neuromuscular transmission disorders; may involve ocular and/or respiratory muscles; monitor creatine kinase; recovery may be delayed.

• Perineal irritation: Perineal burning, tingling, pain and pruritus have been reported with IV administration. May occur more commonly in females, with higher doses, and with rapid administration. Symptom onset is sudden and usually resolves in <1 minute (Allan 1986; Neff 2002; Perron 2003; Singh 2011).

• Psychiatric disturbances: Corticosteroid use may cause psychiatric disturbances, including depression, euphoria, insomnia, mood swings, personality changes, severe depression to psychotic manifestations. Preexisting psychiatric conditions may be exacerbated by corticosteroid use.

Disease-related concerns:

• Adrenal insufficiency: Dexamethasone does not provide any mineralocorticoid activity in adrenal insufficiency (may be employed as a single dose while cortisol assays are performed). In the management/prevention of adrenal crisis in patients with known primary adrenal insufficiency, the Endocrine Society practice guidelines state dexamethasone (intravenous) is the least preferred alternative agent and should be used only if no other glucocorticoid is available. For the treatment of chronic primary adrenal insufficiency (ie, physiologic replacement), dexamethasone (oral) is not recommended due to the risk of Cushingoid side effects (ES [Bornstein 2016]).

• Cardiovascular disease: Use with caution in patients with heart failure and/or hypertension; use has been associated with fluid retention, electrolyte disturbances, and hypertension. Use with caution following acute myocardial infarction; corticosteroids have been associated with myocardial rupture.

• Diabetes: Use corticosteroids with caution in patients with diabetes mellitus; may alter glucose production/regulation leading to hyperglycemia.

• Gastrointestinal disease: Use with caution in patients with GI diseases (diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, ulcerative colitis, abscess or other pyogenic infection) due to perforation risk.

• Head injury: Increased mortality was observed in patients receiving high-dose IV methylprednisolone. High-dose corticosteroids should not be used for the management of head injury (BTF [Carney 2016]).

• Hepatic impairment: Use with caution in patients with hepatic impairment, including cirrhosis; long-term use has been associated with fluid retention.

• Myasthenia gravis: Use with caution in patients with myasthenia gravis; exacerbation of symptoms has occurred especially during initial treatment with corticosteroids.

• Ocular disease: Use with caution in patients with cataracts and/or glaucoma; increased intraocular pressure, open-angle glaucoma, and cataracts have occurred with prolonged use. Use with caution in patients with a history of ocular herpes simplex; corneal perforation has occurred; do not use in active ocular herpes simplex. Not recommended for the treatment of optic neuritis; may increase frequency of new episodes. Consider routine eye exams in chronic users.

• Osteoporosis: Use with caution in patients with osteoporosis; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures.

• Renal impairment: Use with caution in patients with renal impairment; fluid retention may occur.

• Seizure disorders: Use corticosteroids with caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis.

• Systemic sclerosis (scleroderma): Use of higher dose corticosteroid therapy (in adults, ≥15 mg/day of prednisone or equivalent) in patients with systemic sclerosis may increase the risk of scleroderma renal crisis; avoid use when possible (Steen 1998; Trang 2012).

• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid ones.

Concurrent drug therapy issues:

• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

Special populations:

• Elderly: Use with caution in the elderly with the smallest possible effective dose for the shortest duration.

• Pediatric: May affect growth velocity; growth should be routinely monitored in pediatric patients.

Dosage form specific issues:

• Benzyl alcohol and derivatives: Some dosage forms may contain sodium benzoate/benzoic acid; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol derivative with caution in neonates. See manufacturer's labeling.

• Propylene glycol: Some dosage forms may contain propylene glycol; large amounts are potentially toxic and have been associated hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP ["Inactive" 1997]; Zar 2007).

• Sulfite: Some products may contain sodium sulfite, a sulfite that may cause allergic-type reactions including anaphylaxis and life-threatening or less severe asthmatic episodes in susceptible patients.

Other warnings/precautions:

• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.

• Epidural injection: Corticosteroids are not approved for epidural injection. Serious neurologic events (eg, spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke), some resulting in death, have been reported with epidural injection of corticosteroids, with and without use of fluoroscopy.

• Intra-articular injection: May produce systemic as well as local effects. Appropriate examination of any joint fluid present is necessary to exclude a septic process. Avoid injection into an infected site. Do not inject into unstable joints. Patients should not overuse joints in which symptomatic benefit has been obtained as long as the inflammatory process remains active. Frequent intra-articular injection may result in damage to joint tissues.

• Stress: Patients may require higher doses when subject to stress (ie, trauma, surgery, severe infection).

Monitoring Parameters

Hemoglobin, occult blood loss, blood pressure, serum potassium, glucose, bone mineral density; IOP with systemic use >6 weeks; weight and height in children; HPA axis suppression

Pregnancy Risk Factor

C

Pregnancy Considerations

Adverse events have been observed with corticosteroids in animal reproduction studies. Dexamethasone crosses the placenta (Brownfoot 2013); and is partially metabolized by placental enzymes to an inactive metabolite (Murphy 2007). Some studies have shown an association between first trimester systemic corticosteroid use and oral clefts or decreased birth weight; however, information is conflicting and may be influenced by maternal dose/indication for use (Lunghi 2010; Park-Wyllie 2000; Pradat 2003). Hypoadrenalism may occur in newborns following maternal use of corticosteroids during pregnancy; monitor.

Because antenatal corticosteroid administration may reduce the incidence of intraventricular hemorrhage, necrotizing enterocolitis, neonatal mortality, and respiratory distress syndrome, the injection is often used for antenatal fetal lung maturation in patients with preterm premature rupture of membranes or preterm labor who are at risk of preterm delivery (most data is available for betamethasone). A single course of corticosteroids is recommended for women between 24 and 34 weeks' gestation who are at risk of delivering within 7 days, including those with ruptured membranes or multiple gestations. A single course of corticosteroids may be considered for women beginning at 23 weeks' gestation, who are at risk of delivering within 7 days, in consultation with the family. In addition, a single course of corticosteroids may be given to women between 34 0/7 weeks and 36 6/7 weeks who are at risk of preterm delivery within 7 days and who have not previously received corticosteroids; use of concomitant tocolytics is not currently recommended and administration of late preterm corticosteroids has not been evaluated in women with intrauterine infection, multiple gestations, pregestational diabetes, or women who delivered previously by cesarean section at term. Multiple repeat courses are not recommended. However, in women with pregnancies less than 34 weeks' gestation at risk for delivery within 7 days and who had a course of antenatal corticosteroids >14 days prior, a single repeat course may be considered; use of a repeat course in women with premature rupture of membranes is controversial (ACOG 171 2016; ACOG 713 2017; ACOG 188 2018).

When systemic corticosteroids are needed in pregnancy, it is generally recommended to use the lowest effective dose for the shortest duration of time, avoiding high doses during the first trimester (Leachman 2006; Lunghi 2010; Makol 2011; Østensen 2009). Dexamethasone should not be used to treat primary adrenal insufficiency or congenital adrenal hyperplasia in pregnant women (ES [Bornstein 2016]; ES [Speiser 2018]).

Patient Education

What is this drug used for?

• It is used for many health problems like allergy signs, asthma, adrenal gland problems, blood problems, skin rashes, or swelling problems.

• This is not a list of all health problems that this drug may be used for. Talk with the doctor.

Frequently reported side effects of this drug

• Nausea

• Vomiting

• Trouble sleeping

• Agitation

• Increased hunger

• Hiccups

Other side effects of this drug: Talk with your doctor right away if you have any of these signs of:

• Infection

• High blood sugar like confusion, fatigue, increased thirst, increased hunger, passing a lot of urine, flushing, fast breathing, or breath that smells like fruit.

• Skin changes like acne, stretch marks, slow healing, or hair growth.

• Low potassium like muscle pain or weakness, muscle cramps, or an abnormal heartbeat.

• Pancreatitis like severe abdominal pain, severe back pain, severe nausea, or vomiting.

• Adrenal gland problems like severe nausea, vomiting, severe dizziness, passing out, muscle weakness, severe fatigue, mood changes, lack of appetite, or weight loss.

• Cushings disease like weight gain in upper back or abdomen; moon face; severe headache; or slow healing.

• Tumor lysis syndrome like fast heartbeat or abnormal heartbeat; any passing out; unable to pass urine; muscle weakness or cramps; nausea, vomiting, diarrhea or lack of appetite; or feeling sluggish.

• DVT like edema, warmth, numbness, change in color, or pain in the extremities.

• Severe loss of strength and energy

• Irritability

• Tremors

• Fast heartbeat

• Confusion

• Sweating a lot

• Dizziness

• Shortness of breath

• Excessive weight gain

• Swelling of arms or legs

• Buffalo hump

• Severe headache

• Passing out

• Slow heartbeat

• Abnormal heartbeat

• Chest pain

• Menstrual changes

• Bone pain

• Joint pain

• Vision changes

• Behavioral changes

• Depression

• Seizures

• Burning or numbness feeling

• Bruising

• Bleeding

• Severe abdominal pain

• Black, tarry, or bloody stools

• Vomiting blood

• Injection site irritation

• Signs of a significant reaction like wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat.

Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.

Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a brief summary of general information about this medicine. It does NOT include all information about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not specific medical advice and does not replace information you receive from the healthcare provider. You must talk with the healthcare provider for complete information about the risks and benefits of using this medicine.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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