Version October 2024
Dosage guidance:
Safety: Only the methylprednisolone succinate formulation (Solu-Medrol) may be given IV. Methylprednisolone acetate suspension (Depo-Medrol) is intended for IM or intra-articular administration only; do not administer the acetate preparation IV (Ref).
Dosing: Individualize glucocorticoid dosing and use the minimum effective dose/duration. Evidence to support an optimal dose and duration is lacking for most indications; recommendations provided are general guidelines only.
Clinical considerations: HPA-axis suppression is likely in any adult receiving >20 mg/day (daytime dosing) or ≥5 mg per 24 hours (evening or night dosing) for >2 weeks or with Cushingoid appearance (although HPA suppression may occur with lower doses or briefer exposure in some patients); do not abruptly discontinue treatment; dose tapering may be necessary (Ref).
Usual dosage range:
IV (succinate): 40 to 125 mg/day given in a single daily dose or in divided doses; rarely, for certain conditions, may go up to 1 to 2 mg/kg/day.
Initial high-dose “pulse” therapy for select indications (eg, severe systemic rheumatic disorders): 7 to 15 mg/kg/dose (or 500 mg to 1 g/dose) given once daily for 3 to 5 days.
Oral: 16 to 64 mg/day once daily or in divided doses.
The following dose taper example is from the commercially available tapered-dosage product:
Day 1: 24 mg on day 1 administered as 8 mg before breakfast, 4 mg after lunch, 4 mg after supper, and 8 mg at bedtime or 24 mg as a single dose or divided into 2 or 3 doses upon initiation (regardless of time of day).
Day 2: 20 mg on day 2 administered as 4 mg before breakfast, 4 mg after lunch, 4 mg after supper, and 8 mg at bedtime.
Day 3: 16 mg on day 3 administered as 4 mg before breakfast, 4 mg after lunch, 4 mg after supper, and 4 mg at bedtime.
Day 4: 12 mg on day 4 administered as 4 mg before breakfast, 4 mg after lunch, and 4 mg at bedtime.
Day 5: 8 mg on day 5 administered as 4 mg before breakfast and 4 mg at bedtime.
Day 6: 4 mg on day 6 administered as 4 mg before breakfast.
IM (acetate or succinate): 40 to 60 mg as a single dose.
Intra-articular (acetate suspension): Note: Dose ranges per manufacturer's labeling. Specific dose is determined based upon joint size, severity of inflammation, amount of articular fluid present, and clinician judgment.
Larger joint (eg, knee, shoulder, hip): 20 to 80 mg.
Medium joint (eg, wrist, ankle, elbow): 10 to 40 mg.
Small joint (eg, toe, finger): 4 to 10 mg.
Intralesional (acetate) (alternative agent): Note: Other agents (eg, triamcinolone acetonide) may be more commonly employed (Ref).
Usual dosage range: 20 to 60 mg; for large lesions, it may be necessary to distribute doses ranging from 20 to 40 mg by repeated local injections; 1 to 4 injections are usually employed with intervals between injections varying with the type of lesion being treated and clinical response.
Acute respiratory distress syndrome, moderate to severe (off-label use): Note: May consider in most patients with persistent or refractory, moderate to severe acute respiratory distress syndrome, who are relatively early in the disease course (within 14 days) (Ref). Use ideal body weight to calculate dose. If patient is extubated between days 1 to 14, advance to day 15 of therapy and taper according to the following schedule. Do not abruptly discontinue since this may cause deterioration due to inflammatory response (Ref).
Example regimen (Ref):
IV (succinate): Loading dose of 1 mg/kg over 30 minutes, followed by a gradual taper:
Days 1 to 14: 1 mg/kg/day in divided doses.
Days 15 to 21: 0.5 mg/kg/day in divided doses.
Days 22 to 25: 0.25 mg/kg/day in divided doses.
Days 26 to 28: 0.125 mg/kg/day in divided doses.
Allergic conditions:
Anaphylaxis, secondary treatment during emergency management (adjunct to epinephrine): Note : Do not use for initial or sole treatment of anaphylaxis because corticosteroids do not result in the prompt relief of upper or lower airway obstruction or shock and do not prevent biphasic anaphylaxis (Ref). Some experts limit use of corticosteroids to patients with severe or persistent steroid-responsive symptoms (eg, bronchospasm in patients with asthma) (Ref).
IV (succinate): 1 to 2 mg/kg once; may consider a repeat dose after 24 hours based on clinical response; maximum daily dose: 125 mg per day (Ref).
Angioedema (acute allergic) and/or new-onset urticaria: Note: For moderate to severe symptoms without signs of anaphylaxis. Use epinephrine if anaphylaxis symptoms (eg, risk of airway or cardiovascular compromise) are present (Ref). In patients with new-onset urticaria, reserve use for those with significant angioedema or with symptoms that are unresponsive to antihistamines (Ref). The optimal dosing strategy has not been defined (Ref).
IV (succinate): Initial: 60 to 80 mg; switch to an oral corticosteroid as soon as possible, tapering the dose for a total treatment duration of ≤10 days (Ref).
Oral: Note: Dose is based on prednisone equivalency. An example regimen is 16 to 48 mg daily initially, followed by a taper over 5 to 7 days (Ref). The total treatment duration should not exceed 10 days (Ref).
Asthma, acute exacerbation: Note: For moderate to severe 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 (Ref).
Oral , IV (succinate): 40 to 60 mg/day in 1 or 2 divided doses for 5 to 7 days (Ref); doses up to 60 to 80 mg every 6 to 12 hours have been used in critically ill patients (Ref). If symptoms do not resolve and peak expiratory flow is not at least 70% of personal best, then longer treatment may be required (Ref).
Chronic obstructive pulmonary disease, acute exacerbation (off-label use): Note: In patients with severe but not life-threatening exacerbations, oral regimens are recommended. Use IV route in patients who cannot tolerate oral therapy (eg, shock, mechanically ventilated) (Ref).
Oral; IV (succinate): 40 to 60 mg daily for 5 to 14 days (Ref). Doses up to 60 mg every 6 hours have been used in critically ill patients, although outcome data are limited. Note: Dose is based on an equivalent dose of prednisone; optimal dose has not been established. If patient improves with therapy, may discontinue without taper. If patient does not improve, a longer duration of therapy may be indicated (Ref).
COVID-19, hospitalized patients (alternative agent) (off-label use):
Note: Methylprednisolone is recommended for treatment of COVID-19 in hospitalized patients requiring supplemental oxygen or ventilatory support when dexamethasone is not available or there are specific indications for methylprednisolone. Dosing is extrapolated from a study that used dexamethasone; the equivalent dose of methylprednisolone (or other glucocorticoid) may be substituted if necessary (Ref).
Oral; IV (succinate): 32 mg once daily or 16 mg twice daily for up to 10 days (or until discharge, if sooner) as part of an appropriate combination regimen (Ref).
Deceased organ donor management (hormonal resuscitation for the deceased organ donor) (off-label use): Note: Data supporting benefit are conflicting; if given, it should be administered after blood has been collected for tissue typing (Ref).
IV (succinate): Regimens include: 1 g (as an IV infusion) or 15 mg/kg (as an IV infusion) or 250 mg (as an IV bolus) followed by a continuous infusion at 100 mg/hour; usually given as part of combination hormone therapy (Ref).
Giant cell arteritis, treatment: Note: Due to the rapidly progressive nature of the disease, start treatment immediately once diagnosis is highly suspected (Ref). In patients presenting without threatened/evolving vision loss, an oral glucocorticoid is suggested as initial therapy rather than IV methylprednisolone (Ref).
Initial pulse therapy in patients presenting with threatened/evolving vision loss: IV (succinate): 500 mg to 1 g daily for 3 days, followed by an oral glucocorticoid (eg, prednisone) (Ref).
Gout, treatment, acute flares:
Note: Avoid use in patients with known or suspected septic arthritis (Ref).
Intra-articular (acetate): Note: Consider in patients with gout flare limited to 1 or 2 affected joints; clinicians must have sufficient expertise to perform arthrocentesis and injection (Ref). May mix with an equal volume of local anesthetic (Ref). Dose is individualized based on joint size, disease severity, and clinician judgment (Ref). Typical doses are:
Large joint (eg, knee): 40 mg as a single dose (Ref).
Medium joint (eg, wrist, ankle, elbow): 30 mg as a single dose (Ref).
Small joint (eg, toe, finger): 10 mg as a single dose (Ref).
Oral: Note: Dose is based on an equivalent dose of prednisone.
24 to 32 mg/day given once daily or in 2 divided doses until symptom improvement (usually 2 to 5 days), then taper gradually as tolerated (typically over 7 to 10 days); a slower taper (eg, over 14 to 21 days) may be required, particularly in patients with multiple recent flares (Ref).
IM (acetate or succinate) (alternative route): Note: Reserve for patients who are not candidates for oral therapies or intra-articular glucocorticoid administration.
Initial: 40 to 60 mg as a single dose; may repeat at ≥48-hour intervals if benefit fades or there is no flare resolution (Ref).
IV (succinate) (alternative route): Note: Reserve for patients who are not candidates for oral therapies or intra-articular glucocorticoid administration.
Initial: 20 mg twice daily until clinical improvement (usually 2 to 5 days), then taper gradually as tolerated (typically over 7 to 10 days); transition to an equivalent dose of an oral glucocorticoid (eg, prednisone) as soon as possible to complete taper (Ref).
Graft-vs-host disease, acute, treatment (off-label use): Note: For grade ≥2 acute graft-versus-host disease. An optimal regimen has not been identified; refer to institutional protocols as variations exist. Treatment is dependent on the severity and the rate of progression (Ref).
IV (succinate): Initial: 2 mg/kg/day in 2 divided doses; dose may vary based on organ involvement and severity. Continue for several weeks, then taper over several months (Ref).
IgA nephropathy, primary, nonvariant (adjunctive agent) (off-label use):
Note: May consider for use in selected patients at high risk of chronic kidney disease progression (eg, proteinuria ≥0.75 to 1 g/day) despite 3 to 6 months of optimized doses of nonimmunosuppressive therapies (eg, renin-angiotensin system inhibitors) (Ref). The optimal dose of methylprednisolone has not been established and may vary based on institutional protocols and patient-specific factors; an example regimen is provided below.
Oral: 0.4 mg/kg once daily for 2 months (maximum dose: 32 mg/day). Taper daily dose every month over an additional 4 to 7 months. Note: Antimicrobial prophylaxis for Pneumocystis pneumonia was also prescribed for the first 12 weeks of therapy (Ref).
Immune-mediated adverse reactions associated with checkpoint inhibitor therapy:
Note: Consider withholding checkpoint inhibitor therapy for most grade 2 toxicities, withholding the checkpoint inhibitor for grade 3 toxicity, and permanently discontinuing for most grade 4 toxicities (Ref). Refer to each checkpoint inhibitor monograph for specific dosage modification and management details.
Cardiovascular toxicity: Myocarditis, pericarditis, arrhythmias, impaired ventricular function with heart failure, or vasculitis; for patients without an immediate response to high-dose corticosteroids (eg, prednisone): IV: 1 g once daily in combination with other immunosuppressive therapy; once clinically stable, taper methylprednisolone over a minimum of 4 weeks (Ref).
Dermatologic toxicity:
Bullous dermatoses, grade 3 or 4: IV: 1 to 2 mg/kg/day; convert to oral corticosteroids when appropriate; taper over at least 4 weeks (Ref).
Rash or inflammatory dermatitis, grade 4: IV: 1 to 2 mg/kg/day with slow tapering once toxicity resolves (Ref).
Severe cutaneous adverse reaction, grade 3: IV: 0.5 to 1 mg/kg/day; convert to oral corticosteroids on response; taper over 4 at least weeks (Ref).
Severe cutaneous adverse reaction, grade 4: IV: 1 to 2 mg/kg/day with tapering when toxicity resolves to normal (Ref).
GI toxicity: Colitis, grade 4 (may also consider for grade 3, particularly with concurrent upper GI inflammation): IV: 1 to 2 mg/kg/day until symptoms improve to grade 1 and then taper over 4 to 6 weeks (Ref).
Hematologic conditions: Acquired thrombotic thrombocytopenic purpura, grade 3 or 4: IV: 1 g once daily for 3 days; begin the first dose immediately after plasma exchange. If no exacerbation within 3 to 5 days after stopping plasma exchange, taper corticosteroids over 2 to 3 weeks (Ref).
Hepatotoxicity:
Hepatitis, grade 3: IV: 1 to 2 mg/kg/day; attempt taper around 4 to 6 weeks when symptoms improve to ≤ grade 1; re-escalate if needed. If steroid refractory, consider liver biopsy (Ref).
Hepatitis, grade 4: IV: 2 mg/kg/day; attempt taper around 4 to 6 weeks when symptoms improve to ≤ grade 1; re-escalate if needed. If steroid refractory, consider liver biopsy (Ref).
Note: Based on data from a retrospective cohort study in patients with grade 3 or 4 immune-mediated hepatitis, initial treatment with methylprednisolone 1 mg/kg/day demonstrated similar time to ALT normalization (compared with higher methylprednisolone doses), while reducing the potential for corticosteroid-related complications (Ref).
Musculoskeletal toxicities: Myositis, grade 3 or 4 with severe compromise: IV: 1 to 2 mg/kg/day or higher dose bolus (Ref).
Nervous system toxicities:
Aseptic meningitis, moderate to severe symptoms: IV: 1 mg/kg/day, taper after 2 to 4 weeks (Ref).
Autonomic neuropathy, grade 3 or 4: IV: 1 g once daily for 3 days, followed by oral corticosteroid taper (Ref).
Demyelinating diseases, grade 3 or 4: IV: 1 g once daily (Ref).
Encephalitis:
Any grade: IV: 1 to 2 mg/kg/day; taper over at least 4 to 6 weeks (Ref).
Severe or progressing symptoms or the presence of oligoclonal bands: IV: 1 g once daily for 3 to 5 days (in combination with IVIG or plasmapheresis); taper over at least 4 to 6 weeks (Ref).
Guillain-Barré syndrome: Note: Corticosteroids are usually not recommended for idiopathic Guillain-Barré syndrome (GBS); however, a trial of methylprednisolone may be reasonable with checkpoint inhibitor immune-mediated GBS (refer to guideline for details). IV: 2 to 4 mg/kg/day followed by a slow taper; for grade 3 or 4 GBS, may consider pulse dosing of 1 g once daily for 5 days (with taper over 4 to 6 weeks) (Ref).
Peripheral neuropathy, grade 3 or 4: Initial dose: IV: 2 to 4 mg/kg/day followed by a slow taper; refer to guideline for further details (Ref).
Ocular toxicity: Uveitis or iritis, grade 4: IV: 0.8 to 1.6 mg/kg/day in combination with intravitreal or periocular or topical ophthalmic corticosteroids (Ref).
Pulmonary toxicity: Pneumonitis grade 3 or 4: IV: 1 to 2 mg/kg/day with taper over 4 to 6 weeks (or longer for chronic pneumonitis); if not improved within 48 hours, may add additional immunosuppressant agent (Ref).
Corticosteroid conversion and tapering (general recommendations): When converting from IV corticosteroids to oral, the initial conversion from methylprednisolone ≥1 mg/kg IV is to oral prednisone 1 mg/kg/day at minimum (refer to Prednisone monograph for prednisone tapering). Steroid tapering should occur slowly, generally over 4 weeks or longer, with the length of the taper correlating with the severity of the immune-mediated adverse event, the initial corticosteroid dose, and individual patient response. For immune-mediated hepatitis, steroid taper may be attempted at ~4 to 6 weeks (when ≤ grade 1); re-escalate, if needed. Monitor closely for rebound or recurrence (Ref).
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 (Ref).
Patients with severe bleeding (in combination with other treatments): IV (succinate): 1 g once daily for 3 doses and then stop (no taper) (Ref). Note: Due to the short-term response, maintenance therapy with an oral glucocorticoid (eg, prednisone) may be required (Ref).
Inflammatory bowel disease:
Crohn disease, acute (eg, severe/fulminant disease and/or unable to take oral) (adjunctive agent): Note: Not for long-term use (Ref). In patients with localized peritonitis, some experts recommend against initiating corticosteroids due to the potential of masking further clinical deterioration; however, if already receiving corticosteroids, continued use may be appropriate (Ref).
IV (succinate): 40 to 60 mg/day (Ref).
Note: For patients who have been receiving chronic treatment with a corticosteroid, a small increase in their daily dose may be required during an acute exacerbation (Ref). Steroid-sparing agents (eg, biologic agents, immunomodulators) should be introduced with a goal of discontinuing corticosteroid therapy as soon as possible (Ref).
Ulcerative colitis, acute (severe or fulminant): Note: Not for long-term use.
IV (succinate): 40 to 60 mg/day in 1 to 3 divided doses. If response to treatment is inadequate after 5 days (severe) or 3 days (fulminant), second-line therapy is initiated (Ref).
Iodinated contrast media allergic-like reaction, prevention: Note: Generally reserved 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 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. Efficacy of premedication regimens starting <4 to 5 hours before the use of contrast has not been demonstrated (Ref).
Nonurgent regimen:
Oral: 32 mg administered 12 hours and 2 hours before contrast medium administration in combination with oral or IV diphenhydramine (Ref).
Urgent (accelerated) regimen:
IV (succinate): 40 mg every 4 hours until contrast medium administration in combination with IV diphenhydramine (Ref). Some experts administer methylprednisolone 40 mg at 5 hours and 1 hour before contrast medium administration in combination with diphenhydramine (Ref).
Multiple sclerosis, acute exacerbation: Note: For patients with an acute exacerbation resulting in neurologic symptoms and increased disability or impairments in vision, strength, or cerebellar function (Ref).
Initial pulse therapy: IV (succinate): 500 mg to 1 g daily for 3 to 7 days (5 days typically), either alone or followed by an oral taper with prednisone (Ref).
Myopathies (dermatomyositis/polymyositis), treatment:
Initial pulse therapy in patients presenting with severe systemic involvement or profound weakness: IV (succinate): 1 g daily for 3 to 5 days, followed by oral prednisone (Ref).
Nausea and vomiting of pregnancy, severe/refractory (off-label use): Note: Reserve use as an add-on therapy when all other pharmacologic regimens have failed.
IV (succinate): 16 mg every 8 hours for 3 days. If no response within 3 days, discontinue treatment. If symptoms improve, complete 3-day course of treatment, then taper dose over 2 weeks (Ref).
Pneumocystis pneumonia, adjunctive therapy for moderate to severe disease (off-label use):
Note: Recommended for patients with PaO2 <70 mm Hg on room air or PAO2-PaO2 ≥35 mm Hg on room air (Ref); some experts additionally recommend for patients with oxygen saturation <92% on room air (Ref). Dosing is based on an equivalent dose of prednisone.
IV (succinate): 30 mg twice daily on days 1 to 5 beginning as early as possible, followed by 30 mg once daily on days 6 to 10, then 15 mg once daily on days 11 to 21 (Ref).
Prostate cancer, metastatic, castration-resistant (off-label use): Oral: 4 mg twice daily (in combination with micronized abiraterone acetate) (Ref).
Sarcoidosis, severe, acute (off-label use):
Note: For use in patients with life-threatening extrapulmonary disease manifestations (eg, ventricular arrhythmias, transverse myelitis) or rapidly progressive disease (eg, severe optic neuritis) (Ref).
Fixed dose: IV (succinate): 500 mg/day to 1 g per day for 3 to 5 days, followed by an oral glucocorticoid (eg, prednisone) (Ref).
Weight-based dosing : IV (succinate): 10 to 20 mg/kg/day for 3 days, followed by an oral glucocorticoid (eg, prednisone) (Ref).
Systemic rheumatic disorders (eg, antineutrophil cytoplasmic antibody-associated vasculitis, mixed cryoglobulinemia syndrome, polyarteritis nodosa, rheumatoid arthritis, systemic lupus erythematosus), organ-threatening or life-threatening: Note: The following dosage ranges are for guidance only; dosing should be highly individualized, taking into account disease severity, the specific disorder, and disease manifestations.
Initial pulse therapy (optional): IV (succinate): 7 to 15 mg/kg/day (maximum dose: 500 mg to 1 g/day) typically for up to 3 days, followed by an oral glucocorticoid (eg, prednisone); may be given as part of an appropriate combination regimen. Lower doses (eg, 250 mg/day) may be appropriate in some patients (eg, less severe manifestations) (Ref).
Thyroid eye disease (off-label use):
Note: In patients with sight-threatening disease (eg, compressive optic neuropathy), urgent administration of IV glucocorticoids is required (Ref).
Sight-threatening disease: IV (succinate): 500 mg to 1 g daily or every other day for 3 doses during the first week with daily monitoring of response. In patients without disease response after ~7 days, orbital decompression surgery is required. In patients with disease response, may repeat this dosing cycle during the second week, followed by lower doses of IV or oral glucocorticoids thereafter (Ref).
Moderate to severe disease: IV (succinate): 500 mg once weekly for 6 weeks, followed by 250 mg once weekly for an additional 6 weeks (Ref). Note: If response is inadequate after 6 to 8 weeks or if disease progresses, consider alternative treatment options or administering an additional course of methylprednisolone (limit cumulative dose to ≤8 g) (Ref).
Warm autoimmune hemolytic anemia:
IV (succinate): 250 mg to 1 g daily for 1 to 3 days, followed by an oral glucocorticoid (eg, prednisone) (Ref); a clinician experienced with the treatment of hemolytic anemia should be involved with therapy.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Note: The pharmacokinetics and pharmacodynamics of methylprednisolone in kidney impairment are not well understood (Ref). Methylprednisolone clearance appears unaltered in patients with uremia (Ref) and it is slightly dialyzable (Ref).
Altered kidney function: No dosage adjustment necessary for any degree of kidney impairment (Ref).
Hemodialysis, intermittent (thrice weekly): No supplemental dose or dosage adjustment necessary (Ref).
Peritoneal dialysis: No dosage adjustment necessary (Ref).
CRRT: No dosage adjustment necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).
There are no dosage adjustments provided in the manufacturer’s labeling; use with caution.
The recommendations for dosing in patients with obesity are based upon the best available evidence and clinical expertise. Senior Editorial Team: Jeffrey F. Barletta, PharmD, FCCM; Manjunath P. Pai, PharmD, FCP; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC.
Class 1, 2, and 3 obesity (BMI ≥30 kg/m2):
IV, Oral:
Non-weight–based dosing: No dosage adjustment necessary (Ref). Refer to adult dosing for indication-specific doses.
Weight-based dosing: Use ideal body weight to avoid overdosing and subsequent toxicity (Ref). Refer to adult dosing for indication-specific doses.
Rationale for recommendations: Corticosteroids are lipophilic compounds; however, the reported pharmacokinetic variability due to obesity is limited and inconsistent. One study reported similar Vd values with reduced clearance with IV methylprednisolone in males with obesity compared to males without obesity, resulting in a longer half-life (Ref). Dosing based on actual body weight could lead to supratherapeutic levels (Ref).
Refer to adult dosing.
(For additional information see "Methylprednisolone: Pediatric drug information")
Dosage guidance:
Safety: Only the methylprednisolone succinate formulation (Solu-Medrol) may be given IV. Methylprednisolone acetate suspension (Depo-Medrol) is intended for IM or intra-articular administration only; do not administer the acetate preparation IV (Ref).
Dosing: Adjust dose depending upon condition being treated and response of patient. Individualize dosing and use the lowest possible dose to control the condition; when dose reduction is possible, reduce dose gradually.
General dosing; anti-inflammatory or immunosuppressive (Ref):
Methylprednisolone sodium succinate (immediate acting): Infants, Children, and Adolescents: Oral, IV, IM: 0.11 to 1.6 mg/kg/day in 3 to 4 divided doses.
Methylprednisolone acetate (long acting): Infants, Children, and Adolescents:
IM: 0.11 to 1.6 mg/kg/dose; frequency depends upon condition being treated, usually administered as a one-time dose or every 1 to 2 weeks.
Intra-articular: Dosing varies based on affected joint; general range: 4 to 80 mg every 1 to 5 weeks.
Anaphylaxis, adjunctive therapy: Limited data available:
Note: Administer epinephrine first when treating anaphylaxis. Corticosteroids are considered second- or third-line therapy and do not result in prompt resolution of airway obstruction or shock. Use of corticosteroids for anaphylaxis is controversial; they have little to no benefit on initial symptoms; typically administered to prevent biphasic or prolonged episodes of anaphylaxis (Ref).
Infants, Children, and Adolescents: IV, IM (succinate): 1 to 2 mg/kg/dose as a single dose; maximum dose: 125 mg/dose (Ref).
Asthma:
Acute exacerbation:
Outpatient management (short-course "burst") (Ref):
Oral: Note: Burst should be continued until symptoms resolve or patient achieves peak expiratory flow 80% of personal best; usually requires 3 to 10 days of treatment (~5 days on average); longer treatment may be required.
Infants and Children <12 years: Oral: 1 to 2 mg/kg/day in 1 or 2 divided doses for 3 to 10 days; maximum daily dose: 60 mg/day.
Children ≥12 years and Adolescents: Oral: 40 to 60 mg/day in 1 or 2 divided doses for 3 to 10 days.
IM (acetate): Note: This may be given in place of short-course "burst" of oral steroids in patients who are vomiting or if compliance is a problem.
Children ≤4 years: IM: 7.5 mg/kg as a one-time dose; maximum dose: 240 mg.
Children ≥5 years and Adolescents: IM: 240 mg as a one-time dose.
Emergency/acute care management:
Infants and Children <12 years: Oral, IV (succinate): 1 to 2 mg/kg/day in 2 divided doses; maximum daily dose: 60 mg/day; continue until peak expiratory flow is 70% of predicted or personal best (Ref). Some experts suggest infants and children ≤5 years may receive IV doses of 1 mg/kg/dose every 6 hours on day 1, followed by transition to oral corticosteroids to complete a 3 to 5 days course (Ref).
Children ≥12 years and Adolescents: Oral, IV (succinate): 40 to 80 mg/day in 1 or 2 divided doses until peak expiratory flow is 70% of predicted or personal best (Ref).
Status asthmaticus: Children and Adolescents: IV (succinate): Loading dose: 2 mg/kg/dose, then 0.5 to 1 mg/kg/dose every 6 hours (Ref).
Long-term treatment (non-acute), severe, persistent asthma (Ref):
Infants and Children <12 years: Oral: 0.25 to 2 mg/kg/day once daily in the morning or every other day as needed for asthma control; maximum daily dose: 60 mg/day.
Children ≥12 years and Adolescents: Oral: 7.5 to 60 mg once daily in the morning or every other day as needed for asthma control.
Graft-versus-host disease, acute (GVHD): Limited data available: Infants, Children, and Adolescents: IV (succinate): 1 to 2 mg/kg/dose once daily; if using low dose (1 mg/kg) and no improvement after 3 days, increase dose to 2 mg/kg. Continue therapy for 5 to 7 days; if improvement observed, may taper by 10% of starting dose every 4 days; if no improvement, then considered steroid-refractory GVHD and additional agents should be considered (Ref).
Immune thrombocytopenia, moderate to severe bleeding or at risk for severe bleeding: Limited data available:
Infants, Children, and Adolescents: IV (succinate): Initial: Pulse: 30 mg/kg/dose once daily for 1 to 3 doses; number of doses is determined by patient clinical status, initial and postdose platelet counts, and if used in conjunction with other therapies; maximum dose: 1,000 mg/dose; follow with oral corticosteroid therapy as clinically indicated (Ref).
Juvenile idiopathic arthritis, systemic: Note: Therapy should be individualized based on disease severity and activity (Ref). Limited data available:
Children and Adolescents: IV (succinate): Pulse therapy: 30 mg/kg/day once daily for 3 days; maximum dose: 1,000 mg/dose. Follow pulse therapy with oral corticosteroids; evaluate initial response at 1 to 2 weeks and then at 1 month of therapy; if condition worsens or unchanged at either time interval, may repeat methylprednisolone 30 mg/kg/dose at weekly intervals as clinically indicated (Ref).
Kawasaki disease: Limited data available; optimal regimen not established; efficacy variable:
Primary adjunctive treatment, patients at high risk for intravenous immune globulin (IVIG) resistance or coronary artery aneurysms: Note: Use in combination with IVIG and aspirin:
Infants and Children: IV (succinate): 1.6 mg/kg/day in divided doses every 8 hours for 5 days or until afebrile, then transition to oral prednisolone; maximum daily dose: 48 mg/day; some centers use less frequent dosing intervals (eg, every 12 hours) to minimize adverse effects (Ref). Note: Dosing based on use of IV prednisolone product (2 mg/kg/day), which is not available in the United States; dosing converted to equivalent methylprednisolone dosing; however, clinical necessity of conversion is unknown.
Treatment, refractory/resistant disease: Note: Reserve use for patients who remain febrile after initial IVIG dose:
Pulse dosing: Infants and Children: IV (succinate): 30 mg/kg/dose once daily for 1 or 3 days; may be given in combination with additional IVIG dose (Ref).
Taper dosing: Infants and Children: IV (succinate): 1.6 mg/kg/day in divided doses every 8 hours for 5 days or until afebrile, then transition to oral prednisolone; maximum daily dose: 48 mg/day; give in combination with aspirin and an additional dose of IVIG (Ref). Note: Dosing based on use of IV prednisolone product (2 mg/kg/day) which is not available in the United States; dosing converted to equivalent methylprednisolone dosing; however, clinical necessity of conversion is unknown.
Lupus nephritis, proliferative (induction): Limited data available: Children and Adolescents: IV (succinate): Initial pulse therapy: 30 mg/kg/dose once daily for 3 doses; maximum dose: 1,000 mg/dose (Ref). Reported dosage range: 10 to 30 mg/kg/dose or 500 to 1,000 mg/m2/dose once daily for 3 days. Following pulse therapy transition to oral corticosteroids and taper as clinically indicated. May be given as part of an appropriate combination dosage regimen (Ref).
Multisystem inflammatory syndrome in children (MIS-C) associated with SARS-CoV-2: Limited data available:
Infants, Children, and Adolescents:
Initial therapy: IV (succinate): 1 to 2 mg/kg/day divided twice daily in combination with IVIG; duration is dependent on clinical course; may then transition to oral steroids, with taper over at least 2 to 3 weeks (Ref). Note: High-dose corticosteroid therapy at doses of 10 to 30 mg/kg/day (maximum dose: 1,000 mg/dose) for 1 to 3 days has also been reported as initial therapy of MIS-C in patients with more severe disease (eg, shock symptoms) (Ref).
Intensification therapy (in patients who do not improve within 24 hours of initial MIS-C therapy with low- to moderate-dose corticosteroid therapy and IVIG): IV (succinate): 10 to 30 mg/kg/day (maximum dose: 1,000 mg/dose) for 1 to 3 days (Ref).
Nephrotic syndrome, steroid resistant: Limited data available, variable regimens reported: Children and Adolescents: Pulse therapy: IV (succinate): 15 to 30 mg/kg/dose or 500 mg/m2/dose once daily for 3 days; maximum dose: 1,000 mg/dose. Transition to oral corticosteroid and taper as clinically indicated (Ref). Additional pulse doses may be required; some regimens include multiple pulses over a few months until remission (Ref).
Pneumocystis pneumonia (PCP), adjunctive therapy for moderate or severe infection: Limited data available: Note: Recommended when on room air PaO2 <70 mm Hg or PAO2-PaO2 ≥35 mm Hg. Begin as soon as possible after diagnosis and within 72 hours of PCP therapy.
Infants and Children: IV (succinate): 1 mg/kg/dose every 6 hours on days 1 to 7, then 1 mg/kg/dose twice daily on days 8 to 9, then 0.5 mg/kg/dose twice daily on days 10 and 11, and 1 mg/kg/dose once daily on days 12 to 16 (Ref).
Adolescents: IV (succinate): 30 mg twice daily on days 1 to 5, then 30 mg once daily on days 6 to 10, then 15 mg once daily on days 11 to 21 (Ref).
Radiocontrast media reaction, prevention of rebound reaction: Limited data available: Note: If patient is experiencing anaphylaxis, administer epinephrine first. Corticosteroids may be utilized to prevent rebound reactions.
Infants, Children, and Adolescents: IV (succinate): 1 mg/kg/dose; maximum dose: 40 mg/dose (Ref).
Ulcerative colitis, acute, severe: Limited data available: Children and Adolescents: IV (succinate): 1 to 1.5 mg/kg/day once daily or in divided doses 2 times daily; maximum daily dose: 60 mg/day. Higher doses should be reserved for patients with severe disease and/or who have failed oral steroids. Transition to oral therapy when clinically appropriate. If inadequate response after 3 to 5 days of IV therapy, initiate second-line therapy (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling. The pharmacokinetic and pharmacodynamic properties of methylprednisolone in kidney impairment are not well understood (Ref). Methylprednisolone clearance appears unaltered in patients with uremia (Ref) and it is slightly dialyzable (Ref).
There are no dosage adjustments provided in the manufacturer's labeling.
Adrenal suppression (tertiary adrenal insufficiency) may occur with glucocorticoids, including methylprednisolone, and results from inadequate stimulation of the adrenal glands (Ref). Glucocorticoid-induced adrenal insufficiency usually resolves with discontinuation of methylprednisolone, but symptoms may persist for 6 to 12 months (Ref). Adrenal insufficiency may lead to adrenal crisis, a life-threatening emergency that may present like a hypotensive shock state (Ref). High-dose methylprednisolone therapy for conditions such as Crohn disease in females who are pregnant may cause adrenal suppression in the newborn (Ref).
Mechanism: Dose- and time-related; occurs due to lack of or diminished cortisol production by the adrenal gland (Ref). Exogenous glucocorticoids produce a similar negative feedback mechanism as endogenous cortisol, causing a subsequent decrease in adrenocorticotrophic hormone (ACTH) secretion; thus, cortisol production is suppressed, resulting in adrenal atrophy and subsequent insufficiency (ie, hypothalamic-pituitary-adrenal-axis [HPA-axis] suppression) (Ref). In times of stress (eg, critical illness, trauma, surgery), the body requires stress doses in patients taking glucocorticoids chronically (Ref).
Onset: Varied; acute (minutes after administration) and/or chronic (2 to 20 hours to days) (Ref). Chronic glucocorticoid use does not allow for the HPA axis to recover quickly (Ref).
Risk factors:
• High doses for prolonged periods: Although some patients may become HPA suppressed with lower doses or briefer exposure, some experts consider HPA-axis suppression likely in any adult receiving a dose comparable to prednisone >20 mg/day (daytime dosing) or a dose comparable to prednisone ≥5 mg per 24 hours (evening or night dosing) for >3 weeks or with cushingoid appearance (Ref)
• Nighttime administration may inhibit early morning ACTH surge (Ref)
• Potency of glucocorticoids (Ref)
• Abrupt withdrawal (Ref)
• Concurrent interacting medications (eg, carbamazepine, St John's wort, mitotane, rifampicin, itraconazole, diltiazem, thyroid replacement therapy) (Ref)
• History of previous adrenal crisis (Ref)
• Use of glucocorticoid therapy delivered by various routes of administration (oral and inhaled greater risk than topical or intra-articular) (Ref)
Glucocorticoids may inhibit bone growth (linear growth) in pediatric patients (Ref).
Mechanism: Dose-related; glucocorticoids decrease bone formation and increase bone resorption by a combination of factors, including decreasing calcium absorption and increasing calcium secretion; suppressing the somatotropic axis, resulting in suppressed growth hormone secretion; and increasing catabolism of the bone protein matrix and decreasing sex hormone production (Ref).
Risk factors:
• Drug exposure (Ref)
Glucocorticoids, including methylprednisolone, may cause a myriad of CNS and psychiatric/behavioral adverse reactions (Ref). Patients may develop apathy or depression. More commonly, patients develop excitatory psychiatric disturbances (including agitation, anxiety, distractibility, fear, hypomania, insomnia, irritability, lethargy, labile mood, mania, pressured speech, restlessness, and tearfulness) (Ref). Exact incidences are unclear but range from 1.8% to 57% (Ref). Severe psychiatric effects have been reported in 6% of adults receiving high-dose regimens, while depression or mania have been reported in 36% (Ref). Larger doses of methylprednisolone (500 to 1,000 mg) may be associated with more hypomania or mania (Ref). Discontinuation or dose reductions generally resolve symptoms over days to weeks (Ref).
Mechanism: Dose-related; not clearly established. Methylprednisolone and other glucocorticoids may alter feedback on the hypothalamic-pituitary-adrenal axis, which may lead to mood changes (Ref). Glucocorticoids may induce glutamate release, which may be responsible for neuronal toxicity (Ref). Exogenous glucocorticoids may also inhibit synthesis of cortical GABAergic steroids (Ref).
Onset: Varied; most cases occur early in treatment (within the first 5 days), average of 11.5 days. The majority develop within 6 weeks of initiation (Ref).
Risk factors:
• Higher doses (comparable to prednisone ≥80 mg) (Ref)
Possible additional risk factors:
• Age >30 years (Ref)
• Females (Ref)
• History of neuropsychiatric disorders (Ref)
Glucocorticoids may cause a cushingoid appearance (truncal obesity, facial adipose tissue, dorsocervical adipose tissue) which are adverse reactions related to patient's physical features (Ref). Reactions are more metabolic than weight gain, which is related to fluid retention (edema) (Ref). Iatrogenic Cushing syndrome resulting from glucocorticoid therapy increases morbidity and mortality and decreases quality of life (Ref).
Mechanism: Dose- and time-related; excess cortisol from exogenous source (methylprednisolone) results in suppression of adrenocorticotrophic hormone, commonly called iatrogenic Cushing syndrome (Ref).
Onset: Delayed; may develop within the first 2 months of glucocorticoid therapy, with the risk dependent on the dose and duration of treatment (Ref).
Risk factors:
• Higher doses (Ref)
• Longer duration of use (Ref)
• Drug interactions prolonging the half-life of glucocorticoids via cytochrome P450 (Ref)
• BMI (high) (Ref)
• Daily caloric intake (>30 kcal/kg/day) (Ref)
Glucocorticoids, including methylprednisolone, may cause GI effects, including peptic ulcer (with possible perforation and hemorrhage), dyspepsia, gastritis, abdominal distention, and ulcerative esophagitis (Ref). Meta-analyses suggest that glucocorticoid monotherapy carries little to no risk of peptic ulcer disease in the general population (Ref).
Mechanism: Dose-related; glucocorticoids inhibit gastroprotective prostaglandin synthesis and reduce gastric mucus and bicarbonate secretion (Ref). Glucocorticoid immunosuppressive effects may prevent wound healing as well as mask GI signs and symptoms (Ref).
Risk factors:
• Higher methylprednisolone doses (≥4 mg/day) (Ref)
• Concurrent aspirin or nonsteroidal anti-inflammatory drugs (Ref)
• Hospitalized (but not ambulatory) patients (Ref)
• Recent methylprednisolone users (7 to 28 days) versus remote or nonusers (Ref)
Glucocorticoids, including methylprednisolone, may provoke new-onset hyperglycemia in patients without a history of diabetes and may cause an exacerbation of diabetes mellitus (Ref). Glucose levels have been noted to increase 68% above baseline (Ref). Certain patient populations (eg, transplant, cancer, chronic rheumatologic conditions) are at particular risk due to medication combinations (Ref). Resolution may occur within 12 to 16 hours after methylprednisolone discontinuation (Ref).
Mechanism: Dose- and time-related; increased insulin resistance (Ref). May also interfere with insulin signaling by direct effects on the insulin receptor and the glucose transporter and may promote gluconeogenesis via liver stimulation (Ref).
Onset: Rapid; 6 hours, with a peak of 8 hours (Ref). Rapid onset of steroid-induced hyperglycemia occurred within 2 days after initiation of glucocorticoids with a peak in the late afternoon following daily dosing in the morning (Ref).
Risk factors:
• Dose and type of glucocorticoid (Ref)
• Duration of use (Ref)
• Divided dosing versus once-daily dosing (Ref)
• IV and oral routes of administration (Ref)
• Older age (Ref)
• Males (Ref)
• BMI >25 kg/m2 (Ref)
• African American or Hispanic (Ref)
• eGFR <40 mL/minute/1.73 m2 (Ref)
• HbA1c ≥6% (Ref)
• History of gestational diabetes (Ref)
• Family history of diabetes mellitus (Ref)
• Concurrent use of mycophenolate mofetil and calcineurin inhibitors (Ref)
• Previous history of impaired fasting glucose or impaired glucose tolerance (Ref)
Glucocorticoids, including methylprednisolone, have immunosuppressive and anti-inflammatory effects that are reversible with discontinuation. Infection may occur after prolonged use, including Pneumocystis jirovecii pneumonia (PJP), herpes zoster, tuberculosis, and other more common bacterial infections (Ref).
Mechanism: Dose- and time-related; related to pharmacologic action (ie, multiple activities on cell macrophage production and differentiation, inhibition of T-cell activation, effects on dendritic cells (Ref).
Onset: Varied; in one study, the median duration of glucocorticoid use prior to PJP diagnosis was 12 weeks but also occurred earlier or later in some cases (Ref).
Risk factors:
• Higher dose and longer duration of glucocorticoid (Ref); however, may also increase risk at lower doses (eg, prednisone ≤5 mg/day or equivalent) (Ref)
• Comorbidities (Ref)
• Immunocompromised state (Ref)
• Concurrent medications (immunosuppressive) (Ref)
• Rheumatoid arthritis (Ref)
• Interstitial lung disease (Ref)
• Older adults (Ref)
• Males (Ref)
• Low performance status (Ref)
Glucocorticoid (including methylprednisolone)-induced neuromuscular and skeletal effects can take the form of various pathologies in patients ranging from osteoporosis and vertebral compression fracture to myopathy to osteonecrosis in adult and pediatric patients (Ref). Glucocorticoid use is the most common cause of secondary osteoporosis; may be underrecognized and undertreated due to underestimation of risk in this patient population (Ref). Vertebral fractures are the most common glucocorticoid-related fracture (Ref). Myopathies can also occur secondary to direct skeletal muscle catabolism (Ref). Acute steroid myopathy is rare (Ref).
Mechanism: Dose- and time-related; glucocorticoids have direct/indirect effects on bone remodeling with osteoblast recruitment decreasing and apoptosis increasing (Ref). Myopathies or myasthenia result from reductions in protein synthesis and protein catabolism, which can manifest as proximal muscle weakness and atrophy in the upper and lower extremities (Ref)
Onset: Delayed; vertebral fracture risk is increased within 3 months of initiation and peaks at 12 months (Ref).
Risk factors:
Drug-related risks:
• Cumulative dose of glucocorticoids prednisone >5 g or equivalent (Ref)
• Children receiving ≥4 courses of glucocorticoids (Ref)
• Prednisone ≥2.5 to 7.5 mg daily or equivalent for ≥3 months (Ref)
• Myopathy may occur at prednisone doses ≥10 mg/day or equivalent, with higher doses potentiating more of a rapid onset (Ref)
• Fluorinated glucocorticoid preparations (eg, dexamethasone, betamethasone, triamcinolone) have a higher risk of myopathies than methylprednisolone (Ref)
General fracture risks:
• Age >55 years (Ref)
• BMI <18.5 kg/m2 (Ref)
• Bone mineral T score below -1.5 (Ref)
• Endocrine disorders (eg, hypogonadism, hyper- or hypoparathyroidism) (Ref)
• Excess alcohol use (>2 units/day) (Ref)
• Females (Ref)
• History of falls (Ref)
• Malabsorption (Ref)
• Menopause and duration of menopause (Ref)
• White race (Ref)
• Patients with cancer (Ref)
• Previous fracture (Ref)
• Smoking (Ref)
• Underlying inflammatory condition in all ages (eg, inflammatory bowel disease, rheumatoid arthritis) (Ref)
Glucocorticoid (including methylprednisolone)-induced ocular effects may include increased intraocular pressure (IOP), glaucoma (open-angle), and subcapsular posterior cataract in adult and pediatric patients (Ref). Cataracts may persist after discontinuation of glucocorticoid therapy (Ref).
Mechanism: Dose- and time-related; glucocorticoids can induce cataracts by covalently bonding to lens proteins, causing destabilization of the protein structure, and oxidative changes leading to cataracts formation (Ref). There are various proposed mechanisms of IOP contributing to glaucoma, including accumulation of polymerized glycosaminoglycans in the trabecular meshwork, producing edema and increasing outflow resistance (Ref). Another mechanism may include inhibition of phagocytic endothelial cells, leading to accumulation of aqueous debris (Ref). Glucocorticoids can also alter the trabecular meshwork causing an increase in nuclear size and DNA content (Ref). In addition, they can decrease the synthesis of prostaglandins which regulate the aqueous outflow (Ref).
Onset: Delayed; cataracts may occur at least 1 year after initiation of chronic glucocorticoid therapy (Ref). IOP may occur at 4 years or more after initiation (Ref).
Risk factors:
• Dose (Ref)
• Topical > Systemic (Ref)
• Duration of use in all ages (Ref)
• Family history of open-angle glaucoma (Ref)
• Type I diabetes mellitus (Ref)
• High myopia (Ref)
• Pseudophakia (Ref)
• Prior vitrectomies (Ref)
• Connective tissue disease and sex (eg, rheumatoid arthritis in males) (Ref)
• Older patients or age <6 years (Ref)
• Genetics (Ref)
• Angle recessive glaucoma (Ref)
The following adverse drug reactions are derived from product labeling unless otherwise specified. Reactions listed may include other corticosteroids and may not be specifically reported for methylprednisolone.
Postmarketing:
Cardiovascular: Bradycardia (including sinus bradycardia) (Beyler 2023, Tripathy 2023), cardiac arrhythmia, cardiomegaly, circulatory shock, edema, embolism (fat), heart failure (in susceptible patients), hypertension, hypertrophic cardiomyopathy (premature infants), myocardial rupture (after recent myocardial infarction), syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis, venous thrombosis (Johannesdottir 2013)
Dermatologic: Acne vulgaris, allergic dermatitis, atrophic striae, burning sensation of skin, desquamation, diaphoresis, ecchymoses, epidermal thinning, erythema of skin, facial erythema, hyperpigmentation, hypertrichosis, hypopigmentation, inadvertent suppression of skin test reaction, skin atrophy, skin rash, thinning hair (scalp), urticaria, xeroderma
Endocrine & metabolic: Adrenal suppression (Dineen 2019), calcinosis (intraarticular or intralesional), Cushing syndrome (iatrogenic) (Pivonello 2016), cushingoid appearance (fat accumulation in cheeks and temporal fossae) (Liu 2013), decreased serum potassium, exacerbation of diabetes mellitus (Tamez-Pérez 2015), fluid retention, growth suppression (children), hirsutism, hyperglycemia (Tamez-Pérez 2015), hypokalemic alkalosis, impaired glucose tolerance (Tamez-Pérez 2015), menstrual disease, negative nitrogen balance (due to protein catabolism), prediabetes, sodium retention, weight gain
Gastrointestinal: Abdominal distention (Liu 2013), hiccups, impaired intestinal carbohydrate absorption, increased appetite, intestinal perforation, nausea, pancreatitis, peptic ulcer (with possible perforation and hemorrhage) (Liu 2013), ulcerative esophagitis (Liu 2013)
Genitourinary: Glycosuria, spermatozoa disorder (including asthenospermia and oligospermia)
Hematologic & oncologic: Increased INR (Gutkowski 2011), Kaposi sarcoma (Goedert 2002), leukocytosis, petechia
Hepatic: Hepatic necrosis (Rotondo 2018), hepatitis (Ferraro 2015), hepatomegaly, increased gamma-glutamyl transferase (Gutkowski 2011), increased serum alanine aminotransferase (Ferraro 2015), increased serum alkaline phosphatase (Gutkowski 2011), increased serum aspartate aminotransferase (Ferraro 2015), increased serum bilirubin (including increased direct serum bilirubin) (Gutkowski 2011), liver steatosis (Candelli 2003)
Hypersensitivity: Anaphylaxis (Kim 2014), angioedema, hypersensitivity reaction (Szempruch 2022), nonimmune anaphylaxis (van den Berg 1997)
Infection: Infection (Youssef 2016), sterile abscess
Local: Postinjection flare (intraarticular)
Nervous system: Apathy (Ciriaco 2013; Warrington 2006), depression (Ciriaco 2013; Warrington 2006), emotional lability, euphoria, headache, increased intracranial pressure (with papilledema), insomnia, malaise, myasthenia, neuritis, neuropathy, paresthesia, personality changes, psychiatric disturbance (including agitation, anxiety, distractibility, euphoria, fear, hypomania, insomnia, irritability, labile mood, lethargy, pressured speech, restlessness, tearfulness) (Ciriaco 2013; Warrington 2006), seizure, tingling of skin, vertigo
Neuromuscular & skeletal: Amyotrophy, bone fracture (Buckley 2018), Charcot arthropathy, lipotrophy, myopathy (Liu 2013), osteonecrosis (femoral and humoral heads) (Liu 2013), osteoporosis (Buckley 2018, Leonard 2007), rupture of Achilles tendon, steroid myopathy (Haran 2018), vertebral compression fracture (Buckley 2018)
Ophthalmic: Blindness, glaucoma (Phulke 2017), increased intraocular pressure (Phulke 2017), subcapsular posterior cataract (Phulke 2017)
Respiratory: Acute respiratory distress syndrome (Ashtari 2021), pulmonary edema
Miscellaneous: Wound healing impairment
Hypersensitivity to methylprednisolone or any component of the formulation; systemic fungal infection (except intra-articular injection for localized joint conditions); intrathecal administration; live or attenuated virus vaccines (with immunosuppressive doses of corticosteroids); use in premature infants (formulations containing benzyl alcohol preservative only); immune thrombocytopenia (formerly known as idiopathic thrombocytopenic purpura) (IM administration only).
Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Additional contraindication: Methylprednisolone sodium succinate 40 mg vial only: Hypersensitivity to cow's milk or its components or other dairy products which may contain trace amounts of milk ingredients (known or suspected).
Canadian labeling: Additional contraindications (not in US labeling):
Methylprednisolone tablets: Herpes simplex of the eye, vaccinia and varicella (except for short-term or emergency therapy)
Methylprednisolone acetate injection: Epidural or intravascular administration; intra-articular injections in unstable joints; herpes simplex of the eye, vaccinia and varicella (except for short-term or emergency therapy)
Methylprednisolone sodium succinate: Epidural administration; herpes simplex keratitis, vaccinia and varicella, arrested tuberculosis, acute psychoses, Cushing syndrome, peptic ulcer, markedly elevated serum creatinine (except for short-term or emergency therapy)
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children.
• Hepatic effects: High doses of methylprednisolone IV (usually doses of 1 g/day in adults) may induce a toxic form of acute hepatitis (rare); serious hepatic injury may occur, resulting in acute liver failure and death. Time to onset can be several weeks or longer; resolution has been observed after discontinuation of therapy. Discontinue methylprednisolone if toxic hepatitis occurs. Avoid use of high doses in patients with a history of methylprednisolone-induced toxic hepatitis.
• Septic arthritis: May occur as a complication to parenteral therapy; institute appropriate antimicrobial therapy as required.
Disease-related concerns:
• Cardiovascular disease: Use with caution in patients with heart failure (HF) and/or hypertension; use has been associated with fluid retention, electrolyte disturbances, and hypertension. Use with caution following acute myocardial infarction (MI); corticosteroids have been associated with myocardial rupture.
• 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.
• Hepatic impairment: Use with caution in patients with hepatic impairment, including cirrhosis; long-term use has been associated with fluid retention.
• Myasthenia gravis: Use may cause transient worsening of myasthenia gravis (MG) (eg, within first 2 weeks of treatment); monitor for worsening MG (AAN [Narayanaswami 2021]).
• Ocular disease: Not recommended for the treatment of optic neuritis; may increase frequency of new episodes. Use with caution in patients with a history of ocular herpes simplex; corneal perforation has occurred; do not use in active ocular herpes simplex.
• 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.
• Septic shock or sepsis syndrome: Corticosteroids should not be administered for the treatment of sepsis in the absence of shock (SCCM/ESICM [Annane 2017]). A study has failed to demonstrate efficacy in septic shock or sepsis syndrome treatment; use may increase mortality in some populations (eg, patients with elevated serum creatinine, patients who develop secondary infections after use).
• 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.
Special populations:
• Older adult: Use with caution in older adults 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: Methylprednisolone acetate IM injection (multiple-dose vial) and the diluent for methylprednisolone sodium succinate injection may contain 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 with caution in neonates. Additionally, benzyl alcohol may also be toxic to neural tissue when administered locally (eg, intra-articular, intralesional). See manufacturer's labeling.
• Polysorbate 80: Some dosage forms may contain polysorbate 80 (also known as Tweens). Hypersensitivity reactions, usually a delayed reaction, have been reported following exposure to pharmaceutical products containing polysorbate 80 in certain individuals (Isaksson 2002; Lucente 2000; Shelley 1995). Thrombocytopenia, ascites, pulmonary deterioration, and renal and hepatic failure have been reported in premature neonates after receiving parenteral products containing polysorbate 80 (Alade 1986; CDC 1984). See manufacturer's labeling.
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.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Kit, Injection, as acetate:
P-Care D40: 40 mg/mL [DSC] [contains polyethylene glycol (macrogol)]
P-Care D80: 40 mg/mL [DSC] [contains polyethylene glycol (macrogol)]
Solution Reconstituted, Injection, as sodium succinate [strength expressed as base]:
SOLU-Medrol: 500 mg (1 ea)
Generic: 40 mg (1 ea); 125 mg (1 ea); 500 mg (1 ea); 1000 mg (1 ea)
Solution Reconstituted, Injection, as sodium succinate [strength expressed as base, preservative free]:
SOLU-Medrol: 40 mg (1 ea) [contains lactose]
SOLU-Medrol: 125 mg (1 ea); 500 mg (1 ea); 1000 mg (1 ea); 2 g (1 ea)
Suspension, Injection, as acetate:
DEPO-Medrol: 20 mg/mL (5 mL); 40 mg/mL (5 mL, 10 mL) [contains benzyl alcohol, polyethylene glycol (macrogol), polysorbate 80]
DEPO-Medrol: 40 mg/mL (1 mL) [contains polyethylene glycol (macrogol)]
DEPO-Medrol: 80 mg/mL (5 mL) [contains benzyl alcohol, polyethylene glycol (macrogol), polysorbate 80]
DEPO-Medrol: 80 mg/mL (1 mL) [contains polyethylene glycol (macrogol)]
Generic: 40 mg/mL (1 mL [DSC], 5 mL, 10 mL); 80 mg/mL (1 mL, 5 mL)
Suspension, Injection, as acetate [preservative free]:
DEPO-Medrol: 40 mg/mL (1 mL) [contains polyethylene glycol (macrogol)]
Generic: 40 mg/mL (1 mL); 80 mg/mL (1 mL)
Tablet, Oral:
Medrol: 2 mg, 8 mg, 16 mg, 32 mg [DSC], 4 mg [scored]
Generic: 8 mg, 16 mg, 32 mg, 4 mg
Tablet Therapy Pack, Oral:
Medrol: 4 mg (21 ea) [scored]
Generic: 4 mg (21 ea)
Yes
Solution (reconstituted) (methylPREDNISolone Sodium Succ Injection)
40 mg (per each): $4.90 - $7.30
125 mg (per each): $7.75 - $13.98
500 mg (per each): $26.40 - $27.74
1000 mg (per each): $39.00 - $50.27
Solution (reconstituted) (SOLU-Medrol (PF) Injection)
40 mg (per each): $7.76
125 mg (per each): $12.50
500 mg (per each): $56.86
1000 mg (per each): $82.70
Solution (reconstituted) (SOLU-Medrol Injection)
2 g (per each): $124.42
500 mg (per each): $29.14
1000 mg (per each): $52.78
Suspension (DEPO-Medrol Injection)
20 mg/mL (per mL): $8.53
40 mg/mL (per mL): $13.63
80 mg/mL (per mL): $23.67
Suspension (methylPREDNISolone Acetate Injection)
40 mg/mL (per mL): $11.56 - $11.57
80 mg/mL (per mL): $19.58
Tablet Therapy Pack (Medrol Oral)
4 mg (per each): $0.37
Tablet Therapy Pack (methylPREDNISolone Oral)
4 mg (per each): $1.43 - $1.65
Tablets (Medrol Oral)
2 mg (per each): $1.97
4 mg (per each): $0.37
8 mg (per each): $2.14
16 mg (per each): $3.45
Tablets (methylPREDNISolone Oral)
4 mg (per each): $1.43 - $2.23
8 mg (per each): $2.01
16 mg (per each): $3.11 - $3.54
32 mg (per each): $4.62 - $5.18
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution Reconstituted, Injection:
SOLU-Medrol (PF): 40 mg (1 ea) [contains lactose]
SOLU-Medrol (PF): 125 mg (1 ea); 500 mg (1 ea); 1000 mg (1 ea)
Solution Reconstituted, Injection, as sodium succinate [strength expressed as base]:
Solu-MEDROL: 500 mg (1 ea); 1000 mg (1 ea)
Generic: 40 mg (1 ea); 500 mg (1 ea); 1000 mg (1 ea)
Suspension, Injection, as acetate:
Depo-Medrol: 20 mg/mL (5 mL) [contains benzyl alcohol]
Depo-Medrol: 40 mg/mL (1 mL)
Depo-Medrol: 40 mg/mL (2 mL, 5 mL) [contains benzyl alcohol]
Depo-Medrol: 80 mg/mL (1 mL)
Depo-Medrol: 80 mg/mL (5 mL) [contains benzyl alcohol]
Generic: 40 mg/mL ([DSC]); 80 mg/mL ([DSC])
Tablet, Oral:
Medrol: 16 mg, 4 mg
Oral: Administer tablets after meals or with food or milk to decrease GI upset. If prescribed once daily, administer in the morning.
IM (acetate, succinate): Avoid injection into the deltoid muscle due to a high incidence of subcutaneous atrophy. Avoid injection or leakage into the dermis. Do not inject into areas that have evidence of acute local infection.
IV (succinate):
IV push: May administer as a slow IV injection. Recommended rates range from over several minutes (dose not specified (Ref)) to over at least 5 minutes for doses ≤250 mg (Ref). Also refer to institution-specific policies and procedures.
Intermittent IV infusion: Rate dependent upon dose and severity of condition; typically administered as an intermittent infusion over 15 to 60 minutes. Administer doses >250 mg over at least 30 to 60 minutes; severe adverse effects, including hypotension, cardiac arrhythmia, and sudden death, have been reported in patients receiving methylprednisolone doses ≥250 mg administered over <30 minutes (Ref). Also refer to institution-specific policies and procedures. Note: In some spinal cord injury trials, bolus doses (30 mg/kg) have been administered over 15 minutes. Do not administer acetate form IV.
Intra-articular or soft tissue (acetate): See manufacturer's labeling for details.
Intralesional: Inject directly into the lesion. For large lesions, administer multiple small injections (20 to 40 mg) into the area of the lesion. Avoid injection of sufficient material to cause blanching because this may be followed by a small slough.
Oral: Administer after meals or with food or milk to decrease GI upset. If prescribed once daily, administer dose in the early morning to mimic the normal diurnal variation of endogenous cortisol.
Parenteral:
IM: Acetate, succinate: Avoid injection into the deltoid muscle due to a high incidence of subcutaneous atrophy. Avoid injection or leakage into the dermis. Do not inject into areas that have evidence of acute local infection. Discard contents of single-dose vial after use.
IV: Succinate:
IV push: May administer as a slow IV injection. Recommended rates range from over several minutes (dose not specified (Ref)) to over at least 5 minutes for doses ≤250 mg (Ref). Also refer to institution-specific policies and procedures.
Intermittent IV infusion: Rate dependent upon dose and severity of condition; typically administered as an intermittent infusion over 15 to 60 minutes. Administer doses >250 mg over at least 30 to 60 minutes; severe adverse effects, including hypotension, cardiac arrhythmia, and sudden death, have been reported in patients receiving methylprednisolone doses ≥250 mg administered over <30 minutes (Ref). Pulse doses of 15 to 30 mg/kg used in rheumatic or kidney diseases in pediatric patients have been infused over 1 to 4 hours (Ref). Also refer to institution-specific policies and procedures. Do not administer acetate form IV.
Oral, IM (acetate or succinate), and IV (succinate only) administration: Anti-inflammatory or immunosuppressant agent in the treatment of a variety of diseases, including those of hematologic (eg, immune thrombocytopenia, warm autoimmune hemolytic anemia), allergic (eg, asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity, perennial or seasonal allergic rhinitis [oral only], serum sickness, transfusion reactions, new-onset urticaria), GI (eg, Crohn disease, ulcerative colitis), inflammatory, neoplastic, neurologic (eg, multiple sclerosis), rheumatic (eg, antineutrophil cytoplasmic antibody-associated vasculitis, dermatomyositis/polymyositis, giant-cell arteritis, gout [acute flare], mixed cryoglobulinemia syndrome, polyarteritis nodosa, rheumatoid arthritis, systemic lupus erythematosus), and/or autoimmune origin.
Intra-articular or soft tissue administration (acetate only): Gout (acute flare), acute and subacute bursitis, acute nonspecific tenosynovitis, epicondylitis, rheumatoid arthritis, and/or synovitis of osteoarthritis.
Intralesional administration (acetate only): Alopecia areata; discoid lupus erythematosus; keloids; localized hypertrophic, infiltrated, inflammatory lesions of granuloma annulare, lichen planus, lichen simplex chronicus (neurodermatitis), and psoriatic plaques; and necrobiosis lipoidica diabeticorum. May be useful in cystic tumor of an aponeurosis or tendon (ganglia).
Acute respiratory distress syndrome, moderate to severe; Cardiac transplant: Acute cellular rejection (treatment); Cardiac transplant: Antibody-mediated rejection (treatment); Chronic obstructive pulmonary disease (acute exacerbation); COVID-19, hospitalized patients; Deceased organ donor management (hormonal resuscitation for the deceased organ donor); Graft-vs-host disease, acute; IgA nephropathy, primary, nonvariant; Nausea and vomiting of pregnancy, severe/refractory; Pneumocystis pneumonia, adjunctive therapy for moderate to severe disease; Prostate cancer, metastatic, castration-resistant; Sarcoidosis, severe, acute; Thyroid eye disease
MethylPREDNISolone may be confused with medroxyPROGESTERone, methotrexate, methylTESTOSTERone, predniSONE
DEPO-Medrol may be confused with Depo-Provera, SOLU-Medrol
Medrol may be confused with Mebaral
SOLU-Medrol may be confused with salmeterol, Solu-CORTEF
Methylprednisolone is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age) as long-term monotherapy (>3 months) for rheumatoid arthritis. In addition, some disease states of concern include heart failure, peptic ulcer disease, erosive esophagitis, osteoarthritis (unless as periodic intra-articular use), and moderate to severe chronic obstructive pulmonary disease (inhaled therapies preferred) (O’Mahony 2023).
Medrol [US, Canada, and multiple international markets] may be confused with Medral brand name for omeprazole [Mexico]
Substrate of CYP3A4 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Abrocitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Abrocitinib. Management: The use of abrocitinib in combination with other immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor therapy
Aldesleukin: Corticosteroids (Systemic) may diminish the therapeutic effect of Aldesleukin. Risk X: Avoid combination
Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Risk C: Monitor therapy
Androgens: Corticosteroids (Systemic) may enhance the fluid-retaining effect of Androgens. Risk C: 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. Risk D: Consider therapy modification
Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Antithymocyte Globulin (Equine): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Antithymocyte Globulin (Equine). Specifically, these effects may be unmasked if the dose of systemic corticosteroid is reduced. Corticosteroids (Systemic) may enhance the immunosuppressive effect of Antithymocyte Globulin (Equine). Specifically, infections may occur with greater severity and/or atypical presentations. Risk C: Monitor therapy
Aprepitant: May increase the serum concentration of MethylPREDNISolone. Management: Decrease oral methylprednisolone dose by 50%, and decrease intravenous methylprednisolone dose by 25%, with aprepitant. No dose adjustment is required when used with only a single 40 mg oral dose or 32 mg injectable dose of aprepitant. Risk D: Consider therapy modification
Baricitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Baricitinib. Management: The use of baricitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
BCG Products: Corticosteroids (Systemic) may enhance the adverse/toxic effect of BCG Products. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of BCG Products. Risk X: Avoid combination
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Brincidofovir: Corticosteroids (Systemic) may diminish the therapeutic effect of Brincidofovir. Risk C: Monitor therapy
Brivudine: May enhance the adverse/toxic effect of Corticosteroids (Systemic). Risk X: Avoid combination
Calcitriol (Systemic): Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol (Systemic). Risk C: Monitor therapy
CAR-T Cell Immunotherapy: Corticosteroids (Systemic) may enhance the adverse/toxic effect of CAR-T Cell Immunotherapy. Specifically, the severity and duration of neurologic toxicities may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of CAR-T Cell Immunotherapy. Management: Avoid use of corticosteroids as premedication before treatment with CAR-T cell immunotherapy agents. Corticosteroids are indicated and may be required for treatment of toxicities such as cytokine release syndrome or neurologic toxicity. Risk D: Consider therapy modification
Chikungunya Vaccine (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Chikungunya Vaccine (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Chikungunya Vaccine (Live). Risk X: Avoid combination
Cladribine: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Cladribine. Risk X: Avoid combination
Clofazimine: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy
Coccidioides immitis Skin Test: Corticosteroids (Systemic) may diminish the diagnostic effect of Coccidioides immitis Skin Test. Management: Consider discontinuing systemic corticosteroids (dosed at 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks) several weeks prior to coccidioides immitis skin antigen testing. Risk D: Consider therapy modification
Corticorelin: Corticosteroids (Systemic) may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Risk C: Monitor therapy
Cosyntropin: Corticosteroids (Systemic) may diminish the diagnostic effect of Cosyntropin. Risk C: Monitor therapy
COVID-19 Vaccine (Adenovirus Vector): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Adenovirus Vector). Management: Administer a 2nd dose using an mRNA COVID-19 vaccine (at least 4 weeks after the primary vaccine dose) and a bivalent booster dose (at least 2 months after the additional mRNA dose or any other boosters) Risk D: Consider therapy modification
COVID-19 Vaccine (Inactivated Virus): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Inactivated Virus). Risk C: Monitor therapy
COVID-19 Vaccine (mRNA): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (mRNA). Management: Give a 3-dose primary series for all patients aged 6 months and older taking immunosuppressive medications or therapies. Booster doses are recommended for certain age groups. See CDC guidance for details. Risk D: Consider therapy modification
COVID-19 Vaccine (Subunit): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Subunit). Risk C: Monitor therapy
COVID-19 Vaccine (Virus-like Particles): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Virus-like Particles). Risk C: Monitor therapy
CycloSPORINE (Systemic): May enhance the neuroexcitatory and/or seizure-potentiating effect of MethylPREDNISolone. MethylPREDNISolone may decrease the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy
CYP3A4 Inducers (Moderate): May decrease the serum concentration of MethylPREDNISolone. Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May decrease the serum concentration of MethylPREDNISolone. Management: Consider methylprednisolone dose increases in patients receiving strong CYP3A4 inducers and monitor closely for reduced steroid efficacy. Risk D: Consider therapy modification
CYP3A4 Inhibitors (Moderate): May increase the serum concentration of MethylPREDNISolone. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May increase the serum concentration of MethylPREDNISolone. Risk C: 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. Risk C: Monitor therapy
Dengue Tetravalent Vaccine (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Dengue Tetravalent Vaccine (Live). Specifically, the risk of vaccine associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Dengue Tetravalent Vaccine (Live). Risk X: Avoid combination
Denosumab: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Management: Consider the risk of serious infections versus the potential benefits of coadministration of denosumab and systemic corticosteroids. If combined, monitor patients for signs/symptoms of serious infections. Risk D: Consider therapy modification
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. Risk D: Consider therapy modification
Desmopressin: Corticosteroids (Systemic) may enhance the hyponatremic effect of Desmopressin. Risk X: Avoid combination
Deucravacitinib: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Management: The use of deucravacitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Dinutuximab Beta: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Dinutuximab Beta. Management: Corticosteroids are not recommended for 2 weeks prior to dinutuximab beta, during therapy and for 1 week after treatment. Doses equivalent to over 2 mg/kg or 20 mg/day of prednisone (persons over 10 kg) for 2 or more weeks are considered immunosuppressive Risk D: Consider therapy modification
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Etrasimod: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Etrasimod. Risk C: Monitor therapy
Fexinidazole: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination
Filgotinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Filgotinib. Management: Coadministration of filgotinib with systemic corticosteroids at doses equivalent to greater than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks is not recommended. Risk D: Consider therapy modification
Fosaprepitant: May increase the serum concentration of MethylPREDNISolone. Management: Decrease the oral methylprednisolone dose by 50%, and decrease the intravenous methylprednisolone dose by 25%, when combined with fosaprepitant. Risk D: Consider therapy modification
Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Management: Consider avoiding this combination if possible. If required, monitor patients closely for increased adverse effects of the CYP3A4 substrate. Risk D: Consider therapy modification
Gallium Ga 68 Dotatate: Corticosteroids (Systemic) may diminish the diagnostic effect of Gallium Ga 68 Dotatate. Risk C: Monitor therapy
Grapefruit Juice: May increase the serum concentration of MethylPREDNISolone. Risk C: Monitor therapy
Growth Hormone Analogs: Corticosteroids (Systemic) may diminish the therapeutic effect of Growth Hormone Analogs. Growth Hormone Analogs may decrease serum concentrations of the active metabolite(s) of Corticosteroids (Systemic). Risk C: Monitor therapy
Hyaluronidase: Corticosteroids (Systemic) 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. Risk D: Consider therapy modification
Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies): Corticosteroids (Systemic) may diminish the therapeutic effect of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Management: Carefully consider the need for corticosteroids, at doses of a prednisone-equivalent of 10 mg or more per day, during the initiation of immune checkpoint inhibitor therapy. Use of corticosteroids to treat immune related adverse events is still recommended Risk D: Consider therapy modification
Indium 111 Capromab Pendetide: Corticosteroids (Systemic) may diminish the diagnostic effect of Indium 111 Capromab Pendetide. Risk X: Avoid combination
Inebilizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Inebilizumab. Risk C: Monitor therapy
Influenza Virus Vaccines: Corticosteroids (Systemic) may diminish the therapeutic effect of Influenza Virus Vaccines. Management: Administer influenza vaccines at least 2 weeks prior to initiation of systemic corticosteroids at immunosuppressive doses. Influenza vaccines administered less than 14 days prior to or during such therapy should be repeated 3 months after therapy. Risk D: Consider therapy modification
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Risk C: Monitor therapy
Leflunomide: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Leflunomide. Management: Increase the frequency of chronic monitoring of platelet, white blood cell count, and hemoglobin or hematocrit to monthly, instead of every 6 to 8 weeks, if leflunomide is coadministered with immunosuppressive agents, such as systemic corticosteroids. Risk D: Consider therapy modification
Licorice: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Lutetium Lu 177 Dotatate: Corticosteroids (Systemic) may diminish the therapeutic effect of Lutetium Lu 177 Dotatate. Management: Avoid repeated use of high-doses of corticosteroids during treatment with lutetium Lu 177 dotatate. Use of corticosteroids is still permitted for the treatment of neuroendocrine hormonal crisis. The effects of lower corticosteroid doses is unknown. Risk D: Consider therapy modification
Macimorelin: Corticosteroids (Systemic) may diminish the diagnostic effect of Macimorelin. Risk X: Avoid combination
MetyraPONE: Corticosteroids (Systemic) may diminish the diagnostic effect of MetyraPONE. Management: Consider alternatives to the use of the metyrapone test in patients taking systemic corticosteroids. Risk D: Consider therapy modification
Mifamurtide: Corticosteroids (Systemic) may diminish the therapeutic effect of Mifamurtide. Risk X: 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 (eg, for immunosuppression following transplantation). Corticosteroid effects may be reduced by mifepristone treatment. Risk X: Avoid combination
Mumps- Rubella- or Varicella-Containing Live Vaccines: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Mumps- Rubella- or Varicella-Containing Live Vaccines. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Mumps- Rubella- or Varicella-Containing Live Vaccines. Risk X: Avoid combination
Nadofaragene Firadenovec: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nadofaragene Firadenovec. Specifically, the risk of disseminated adenovirus infection may be increased. Risk X: Avoid combination
Natalizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Natalizumab. Risk X: Avoid combination
Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse neuromuscular effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Management: If concomitant therapy is required, use the lowest dose for the shortest duration to limit the risk of myopathy or neuropathy. Monitor for new onset or worsening muscle weakness, reduction or loss of deep tendon reflexes, and peripheral sensory decriments Risk D: Consider therapy modification
Nicorandil: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nicorandil. Gastrointestinal perforation has been reported in association with this combination. Risk C: Monitor therapy
Nirmatrelvir and Ritonavir: May increase the serum concentration of MethylPREDNISolone. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May enhance the adverse/toxic effect of Corticosteroids (Systemic). Specifically, the risk of gastrointestinal bleeding, ulceration, and perforation may be increased. Risk C: Monitor therapy
Ocrelizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ocrelizumab. Risk C: Monitor therapy
Ofatumumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ofatumumab. Risk C: Monitor therapy
Ozanimod: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ozanimod. Risk C: Monitor therapy
Pidotimod: Corticosteroids (Systemic) may diminish the therapeutic effect of Pidotimod. Risk C: Monitor therapy
Pimecrolimus: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Risk X: Avoid combination
Pneumococcal Vaccines: Corticosteroids (Systemic) may diminish the therapeutic effect of Pneumococcal Vaccines. Risk C: Monitor therapy
Poliovirus Vaccine (Live/Trivalent/Oral): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Poliovirus Vaccine (Live/Trivalent/Oral). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Poliovirus Vaccine (Live/Trivalent/Oral). Risk X: Avoid combination
Polymethylmethacrylate: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Polymethylmethacrylate. Specifically, the risk for hypersensitivity or implant clearance may be increased. Management: Use caution when considering use of bovine collagen-containing implants such as the polymethylmethacrylate-based Bellafill brand implant in patients who are receiving immunosuppressants. Consider use of additional skin tests prior to administration. Risk D: Consider therapy modification
Quinolones: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolones. Specifically, the risk of tendonitis and tendon rupture may be increased. Risk C: Monitor therapy
Rabies Vaccine: Corticosteroids (Systemic) may diminish the therapeutic effect of Rabies Vaccine. Management: Complete rabies vaccination at least 2 weeks before initiation of immunosuppressant therapy if possible. If combined, check for rabies antibody titers, and if vaccination is for post exposure prophylaxis, administer a 5th dose of the vaccine. Risk D: Consider therapy modification
Ritlecitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ritlecitinib. Risk X: Avoid combination
Ritodrine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Ritodrine. Risk C: Monitor therapy
Ruxolitinib (Topical): Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ruxolitinib (Topical). Risk X: Avoid combination
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. Risk C: Monitor therapy
Sargramostim: Corticosteroids (Systemic) may enhance the therapeutic effect of Sargramostim. Specifically, corticosteroids may enhance the myeloproliferative effects of sargramostim. Risk C: Monitor therapy
Sipuleucel-T: Corticosteroids (Systemic) may diminish the therapeutic effect of Sipuleucel-T. Management: Consider reducing the dose or discontinuing immunosuppressants, such as systemic corticosteroids, prior to initiating sipuleucel-T therapy. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone given for 2 or more weeks are immunosuppressive. Risk D: Consider therapy modification
Sodium Benzoate: Corticosteroids (Systemic) may diminish the therapeutic effect of Sodium Benzoate. Risk C: Monitor therapy
Sphingosine 1-Phosphate (S1P) Receptor Modulator: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Risk C: Monitor therapy
Succinylcholine: Corticosteroids (Systemic) may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
Tacrolimus (Systemic): Corticosteroids (Systemic) may decrease the serum concentration of Tacrolimus (Systemic). Conversely, when discontinuing corticosteroid therapy, tacrolimus concentrations may increase. Risk C: Monitor therapy
Tacrolimus (Topical): Corticosteroids (Systemic) may enhance the immunosuppressive effect of Tacrolimus (Topical). Risk X: Avoid combination
Talimogene Laherparepvec: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Talimogene Laherparepvec. Specifically, the risk of infection from the live, attenuated herpes simplex virus contained in talimogene laherparepvec may be increased. Risk X: Avoid combination
Tertomotide: Corticosteroids (Systemic) may diminish the therapeutic effect of Tertomotide. Risk X: Avoid combination
Thiazide and Thiazide-Like Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor therapy
Tofacitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Tofacitinib. Management: Coadministration of tofacitinib with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Typhoid Vaccine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Typhoid Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Typhoid Vaccine. Risk X: Avoid combination
Ublituximab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ublituximab. Risk C: Monitor therapy
Upadacitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Upadacitinib. Management: Coadministration of upadacitinib with systemic corticosteroids at doses equivalent to greater than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks is not recommended. Risk D: Consider therapy modification
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. Risk C: Monitor therapy
Vaccines (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Vaccines (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Live). Management: Avoid live vaccines during and for 1 month after therapy with immunosuppressive doses of corticosteroids (equivalent to prednisone > 2 mg/kg or 20 mg/day in persons over 10 kg for at least 2 weeks). Give live vaccines 4 weeks prior to therapy if possible. Risk D: Consider therapy modification
Vaccines (Non-Live/Inactivated/Non-Replicating): Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Non-Live/Inactivated/Non-Replicating). Management: Administer vaccines at least 2 weeks prior to immunosuppressive corticosteroids if possible. If patients are vaccinated less than 14 days prior to or during such therapy, repeat vaccination at least 3 months after therapy if immunocompetence restored. Risk D: Consider therapy modification
Vitamin K Antagonists (eg, warfarin): Corticosteroids (Systemic) may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Yellow Fever Vaccine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Yellow Fever Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Yellow Fever Vaccine. Risk X: Avoid combination
Corticosteroids do not decrease fertility in patients with inflammatory bowel disease (IBD) who wish to become pregnant; however, active IBD may decrease fertility; pregnancy should be planned after a 3- to 6-month remission (Mahadevan 2019).
Methylprednisolone crosses the placenta (Anderson 1981). Some products contain benzyl alcohol, which may also cross the placenta.
Some studies have shown an association between first trimester systemic corticosteroid use and oral clefts; however, information is conflicting and may be influenced by maternal dose, duration/frequency of exposure, and indication for use. Additional data are needed to evaluate any potential risk of systemic corticosteroids and other adverse pregnancy outcomes (eg, gestational diabetes mellitus, low birth weight, preeclampsia, preterm birth) (ACOG 776 2019; Bandoli 2017; Skuladottir 2014). Hypoadrenalism may occur in newborns following maternal use of corticosteroids; monitor infants exposed to prolonged or high doses of methylprednisolone in utero (Homar 2008; Kurtoğlu 2011).
Methylprednisolone is a preferred oral corticosteroid for the treatment of maternal conditions during pregnancy because placental enzymes limit passage to the embryo (ACOG 776 2019).
When systemic corticosteroids are needed in pregnancy for rheumatic disorders, nonfluorinated corticosteroids such as methylprednisolone are preferred. Chronic high doses should be avoided (ACR [Sammaritano 2020]). Methylprednisolone may also be used to treat acute exacerbations of multiple sclerosis during pregnancy (Canibaño 2020; Dobson 2019).
Corticosteroids may be used as needed for disease flares in pregnant patients with inflammatory bowel disease; however, maintenance therapy should be avoided (Mahadevan 2019).
Uncontrolled asthma is associated with adverse events on pregnancy (increased risk of perinatal mortality, preeclampsia, preterm birth, low birth weight infants, cesarean delivery, and the development of gestational diabetes). Poorly controlled asthma or asthma exacerbations may have a greater fetal/maternal risk than what is associated with appropriately used asthma medications. Maternal treatment improves pregnancy outcomes by reducing the risk of some adverse events (eg, preterm birth, gestational diabetes). Maternal asthma symptoms should be monitored monthly during pregnancy. Inhaled corticosteroids are recommended for the treatment of asthma during pregnancy; however, systemic corticosteroids should be used to control acute exacerbations or treat severe persistent asthma (ERS/TSANZ [Middleton 2020]; GINA 2023).
Methylprednisolone may be considered for adjunctive treatment of severe nausea and vomiting in pregnant patients. Due to risks of adverse fetal events associated with first trimester exposure, use is reserved for refractory cases in women with dehydration (ACOG 189 2018).
High dose methylprednisolone may be used in the management of immune thrombocytopenia in pregnant patients refractory to oral corticosteroids; use in combination with other therapies is suggested (Provan 2019).
Systemic corticosteroids are used off label in the management of COVID-19 (NIH 2023). Methylprednisolone was not the corticosteroid evaluated in the initial study and large numbers of pregnant patients were not included (Horby 2021). In general, the treatment of COVID-19 during pregnancy is the same as in nonpregnant patients. However, because data for most therapeutic agents in pregnant patients are limited, treatment options should be evaluated as part of a shared decision-making process (NIH 2023). Patients who do not require corticosteroids for other indications, or in those who have already completed a course of corticosteroids to enhance fetal lung development, equivalent doses of methylprednisolone may be preferred for use in pregnant patients with severe or critical COVID-19 due to limited placental transfer and less fetal risk. Suggested treatment algorithms are available for pregnant patients with severe or critical COVID-19 requiring corticosteroids (Saad 2020; Teelucksingh 2022). The risk of severe illness from COVID-19 infection is increased in symptomatic pregnant patients compared to nonpregnant patients (ACOG 2023). Information related to the treatment of COVID-19 during pregnancy continues to emerge; refer to current guidelines for the treatment of pregnant patients.
The Transplant Pregnancy Registry International (TPR) is a registry that follows pregnancies that occur in maternal transplant recipients or those fathered by male transplant recipients. The TPR encourages reporting of pregnancies following solid organ transplant by contacting them at 1-877-955-6877 or https://www.transplantpregnancyregistry.org.
Methylprednisolone is present in breast milk (Boz 2018; Cooper 2015; Strijbos 2015; Zengin Karahan 2020).
Data related to the presence of methylprednisolone in breast milk are available from a study following maternal administration of methylprednisolone 1,000 mg IV infused over 2 hours. Using the highest milk concentration (5.55 mcg/mL), the estimated daily infant dose via breast milk was 0.8325 mg/kg/day, providing a relative infant dose (RID) of methylprednisolone of 2.8% to 5.6% compared to a weight-adjusted infant dose of 15 to 30 mg/kg/day. The maximum milk concentration occurred 1 hour after the maternal dose and methylprednisolone was below the limits of quantification 12 hours after the dose (Cooper 2015). In general, breastfeeding is considered acceptable when the RID is <10% (Anderson 2016; Ito 2000).
The manufacturer notes that when used systemically, maternal use of corticosteroids have the potential to cause adverse events in a breastfeeding infant (eg, growth suppression, interfere with endogenous corticosteroid production) and therefore recommends a decision be made whether to discontinue breastfeeding or to discontinue the drug, taking into account the importance of treatment to the mother.
Corticosteroids are generally considered acceptable in patients who are breastfeeding when used in usual doses; however, monitoring of the breastfeeding infant is recommended (WHO 2002). Methylprednisolone is classified as a nonfluorinated corticosteroid; when systemic corticosteroids are needed in a lactating patient for rheumatic disorders, low doses of nonfluorinated corticosteroids are preferred (ACR [Sammaritano 2020]).
If there is concern about exposure to the infant, waiting 2 to 4 hours after administration of methylprednisolone IV decreases exposure via breast milk (recommendation based on methylprednisolone pulse dosing for multiple sclerosis) (Cooper 2015; Zengin Karahan 2020). In addition, some guidelines recommend waiting 4 hours after the maternal dose of an oral systemic corticosteroid before breastfeeding (based on a study using prednisolone) (ACR [Sammaritano 2020]; Ost 1985).
Take tablets with meals to decrease GI upset; need diet rich in pyridoxine, vitamin C, vitamin D, folate, calcium, phosphorus, and protein.
Blood pressure, blood glucose, electrolytes; weight; intraocular pressure (use >6 weeks); consider routine eye exams with chronic use; creatine kinase; bone mineral density; growth and development in children; HPA axis suppression.
In a tissue-specific manner, corticosteroids regulate gene expression subsequent to binding specific intracellular receptors and translocation into the nucleus. Corticosteroids exert a wide array of physiologic effects including modulation of carbohydrate, protein, and lipid metabolism and maintenance of fluid and electrolyte homeostasis. Moreover cardiovascular, immunologic, musculoskeletal, endocrine, and neurologic physiology are influenced by corticosteroids. Decreases inflammation by suppression of migration of polymorphonuclear leukocytes and reversal of increased capillary permeability.
Onset of action: IV (succinate): Within 1 hour; Intra-articular (acetate): 1 week
Duration: Intra-articular (acetate): 1 to 5 weeks
Absorption: Oral: Well absorbed (Czock 2005)
Bioavailability: Oral: 88% ± 23% (Czock 2005)
Distribution: Vd: IV (succinate): 24 L ± 6 L (Czock 2005)
Metabolism: Hepatic to metabolites (Czock 2005)
Half-life elimination:
Adolescents: IV: 1.9 ± 0.7 hours (age range: 12 to 20 years; Rouster-Stevens 2008)
Adults: Oral: 2.5 ± 1.2 hours (Czock 2005); IV (succinate): 0.25 ± 0.1 hour (Czock 2005)
Time to peak, plasma:
Oral: 2.1 ± 0.7 hours (Czock 2005)
IV (succinate): 0.8 hours (Czock 2005)
Excretion: Urine (1.3% [oral], 9.2% [IV succinate] as unchanged drug) (Czock 2005)
Older adult: Decreased clearance and increased half-life (Czock 2005).
Obesity: Decreased clearance and increased half-life (Czock 2005; Dunn 1991).
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