Version July 2023
Note: Dosing: Evidence to support an optimal dose and duration is lacking for most indications; recommendations provided are general guidelines only and primarily based on expert opinion. In general, glucocorticoid dosing should be individualized and the minimum effective dose/duration should be used. Hypothalamic-pituitary-adrenal (HPA) suppression: Although some patients may become HPA suppressed with lower doses or briefer exposure, some experts consider HPA-axis suppression 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 (Ref); do not abruptly discontinue treatment in these patients; dose tapering may be necessary (Ref).
Usual dosage range:
Oral: 10 to 60 mg/day given in a single daily dose or in 2 to 4 divided doses; Low dose: 2.5 to 10 mg/day; High dose: 1 to 1.5 mg/kg/day (usually not to exceed 80 to 100 mg/day).
The following dosing is from the commercially available tapered-dosage product (eg, dose pack containing 21 x 5 mg tablets):
Day 1: Administer 30 mg on day 1 as 10 mg (2 tablets) at breakfast, 5 mg (1 tablet) at lunch, 5 mg (1 tablet) at dinner, and 10 mg (2 tablets) at bedtime.
Day 2: Administer 25 mg on day 2 as 5 mg (1 tablet) at breakfast, 5 mg (1 tablet) at lunch, 5 mg (1 tablet) at dinner, and 10 mg (2 tablets) at bedtime.
Day 3: Administer 20 mg on day 3 as 5 mg (1 tablet) at breakfast, 5 mg (1 tablet) at lunch, 5 mg (1 tablet) at dinner, and 5 mg (1 tablet) at bedtime.
Day 4: Administer 15 mg on day 4 as 5 mg (1 tablet) at breakfast, 5 mg (1 tablet) at lunch, and 5 mg (1 tablet) at bedtime.
Day 5: Administer 10 mg on day 5 as 5 mg (1 tablet) at breakfast and 5 mg (1 tablet) at bedtime.
Day 6: Administer 5 mg on day 6 as 5 mg (1 tablet) at breakfast.
Indication-specific dosing:
Adrenal insufficiency, primary chronic (alternative agent):
Note: In general, hydrocortisone is preferred. Use in conjunction with fludrocortisone. Dose is based on prednisolone equivalency.
Chronic maintenance dosing:
Oral: Usual dosage range: 2.5 to 7.5 mg once daily (Ref).
Stress dosing:
Note: Patients who are unable to tolerate oral medication (eg, due to vomiting or diarrhea), are in active labor, or are under moderate to major surgical stress may require parenteral corticosteroid therapy (preferably with hydrocortisone) to prevent adrenal crisis (Ref).
Patients with febrile illness: Double the chronic maintenance dose until recovery for fever 38°C (100.4°F) to 39°C (102.2°F) or triple the chronic maintenance dose until recovery for fever >39°C (102.2°F), then return to baseline dose within 1 to 3 days (Ref).
Minor surgical stress (eg, hernia repair, procedures with local anesthetic): Continue chronic maintenance dose (no additional supplementation needed) (Ref); may give an additional 5 mg (equivalent to ~20 mg hydrocortisone) postoperatively if signs or symptoms of adrenal insufficiency are present (Ref).
Alcoholic hepatitis, severe (Maddrey Discriminant Function [MDF] score ≥32) (off-label use): Oral: 40 mg daily for 28 days (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).
Oral: The optimal dosing strategy has not been defined; an example regimen is 20 to 60 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: 40 to 60 mg daily for 5 to 7 days; administer in 1 or 2 divided doses. If symptoms do not resolve and peak expiratory flow is not at least 70% of personal best, then longer treatment may be required (Ref).
Bell palsy, new onset (off-label use): Oral: 60 to 80 mg daily for 5 to 7 days; administer in 1 or 2 divided doses; may be followed by a 5-day taper. Treatment should begin within 72 hours of onset of symptoms; a concomitant antiviral agent may be indicated in select patients (Ref).
Chronic obstructive pulmonary disease, acute exacerbation (off-label use):
Note: In patients with severe but not life-threatening exacerbations, oral regimens are recommended. In patients who cannot tolerate oral therapy (eg, shock, mechanically ventilated), use IV methylprednisolone (Ref).
Oral: 40 to 60 mg once daily for 5 to 14 days (Ref). Note: The 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: Prednisone 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 prednisone. Dosing is extrapolated from a study that used dexamethasone; the equivalent dose of prednisone (or other glucocorticoid) may be substituted if necessary (Ref).
Oral: 40 mg once daily or 20 mg twice daily for up to 10 days (or until discharge, if sooner) as part of an appropriate combination regimen (Ref).
Duchenne muscular dystrophy (off-label use): Oral: 0.75 mg/kg/day (Ref). Some experts use a maximum dose of 40 mg/day due to potential for greater adverse effects and decreased benefit at higher doses (Ref).
Note: In patients who experience intolerable adverse effects, may decrease the dose by 25% to 33% (Ref). If adverse effects persist, continue to gradually taper to as low as 0.3 mg/kg/day, which may provide benefit (Ref). Doses as high as 1.5 mg/kg/day have been studied, but there is no evidence that doses >0.75 mg/kg/day provide greater efficacy (Ref).
Focal segmental glomerulosclerosis, primary (off-label use):
Note: Initial therapy for patients with nephrotic syndrome (eg, proteinuria >3.5 g/day and serum albumin <3.5 g/dL) (Ref).
Oral: 1 mg/kg (maximum dose: 60 to 80 mg/day) once daily or 2 mg/kg (maximum dose: 120 mg) every other day; duration of therapy depends on clinical response and tapering schedule can vary (Ref).
Giant cell arteritis, treatment (off-label use):
Note: To reduce the risk of visual loss, start treatment immediately once diagnosis is highly suspected (Ref). In patients presenting with threatened vision loss, pulse IV methylprednisolone is suggested as initial therapy prior to an oral glucocorticoid (eg, prednisone) (Ref).
Oral: 40 to 60 mg once daily for 2 to 4 weeks; if reversible symptoms persist or worsen, may increase dose up to a maximum dose of 80 mg once daily until symptomatic control is achieved (Ref). Alternatively, may initiate at 1 mg/kg once daily (maximum: 80 mg/day), particularly in patients with signs of ischemic organ damage (eg, vision loss) (Ref). Once signs/symptoms have declined and laboratory values have returned to normal or near normal, begin to taper until discontinuation over the next 6 to 12 months (Ref).
Gout, treatment (acute flares):
Note: Avoid use in patients with known or suspected septic arthritis. Some experts reserve use for patients who are not candidates for intra-articular glucocorticoids or when intra-articular glucocorticoid administration is not feasible (Ref).
Oral: 30 to 40 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).
Graft-versus-host disease, acute, treatment (off-label use):
Note: For grade II or higher 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).
Oral: Initial: 2 to 2.5 mg/kg/day in divided doses; dose may vary based on organ involvement and severity. Continue for several weeks then taper over several months (Ref).
Hepatitis, autoimmune (off-label use):
Note: Approach to treatment should be patient specific and guided by response to treatment. Monotherapy induction regimen included below; other induction regimens (eg, combination therapy with a glucocorticoid-sparing agent) may be used in select patients (Ref).
Induction: Initial: Oral: 40 to 60 mg once daily for 1 week or until biochemical remission achieved, followed by a taper (eg, reduce daily dose by 5 to 10 mg at weekly intervals) based on symptoms and laboratory values to 20 mg once daily or a dose sufficient for maintenance of remission (Ref). Some experts initiate therapy at 20 to 30 mg once daily depending on severity of disease and tolerance to glucocorticoids (Ref).
Maintenance: Further taper dose to one that maintains remission (eg, taper the dose by 2.5 to 5 mg every 2 to 4 weeks to reach 5 to 10 mg/day). Specific maintenance approach will depend on patient response to initial treatment and tapering (Ref).
Immune thrombocytopenia:
Note: Goal of therapy is to provide a safe platelet count to prevent clinically important bleeding rather than normalization of the platelet count. For patients with severe bleeding, a pulse of dexamethasone or methylprednisolone is recommended; due to the short-term response associated with methylprednisolone, a prednisone taper may be required following pulse doses of methylprednisolone. For minor bleeding, prednisone is an appropriate initial therapy (Ref).
I nitial therapy: Oral: 1 mg/kg/day (range: 0.5 to 2 mg/kg/day; maximum: 80 mg/day) for 1 to 3 weeks, followed by a gradual taper (Ref). Total duration of therapy should not exceed 6 weeks; if there is no response within 2 weeks, taper over 1 week and discontinue (Ref).
Pregnancy associated: Oral: Initial: 10 to 20 mg once daily (Ref). Adjust to the minimum effective dose to achieve response; generally, continue for at least 21 days, then taper to the minimum effective dose required to maintain platelet count to prevent major bleeding (Ref) or 1 mg/kg/day for 2 weeks, followed by a gradual taper (Ref).
Fetal alloimmune thrombocytopenia (maternal administration): Oral: 0.5 to 1 mg/kg/day. Dose is dependent upon gestational age and risk of fetal/neonatal intracranial hemorrhage and is administered in addition to immune globulin IV (Ref).
Immune-mediated adverse reactions associated with checkpoint inhibitor therapy:
Note: Consider withholding checkpoint inhibitor therapy for most grade 2 toxicities, withhold the checkpoint inhibitor for grade 3 toxicity and permanently discontinue for most grade 4 toxicities (Ref). Refer to each checkpoint inhibitor monograph for specific dosage modification and management details.
General prednisone dosing recommendations:
Grade 2 toxicity (if checkpoint inhibitor is withheld): Oral: Consider 0.5 to 1 mg/kg/day until improvement to ≤ grade 1, then taper prednisone over at least 4 weeks (Ref).
Immune-mediated hepatitis, grade 2: Withhold immune checkpoint inhibitor (ICI). If no improvement within 3 to 5 days after ICI is withheld, consider initiation of corticosteroids (prednisone 0.5 to 1 mg/kg/day or equivalent) (Ref).
Grade 3 or higher toxicity: Oral: 1 to 2 mg/kg/day until improvement to ≤ grade 1, then taper prednisone over 4 to 6 weeks; consider other systemic immunosuppressants if symptoms do not improve with 48 to 72 hours of corticosteroid therapy (Ref).
Immune-mediated hepatitis, grade 3 or 4: Based on data from a retrospective cohort study in patients with grade 3 or 4 immune-mediated hepatitis, initial treatment with lower corticosteroid doses (eg, methylprednisolone 1 mg/kg/day or equivalent) demonstrated similar time to ALT normalization (compared with higher corticosteroid doses), while reducing the potential for corticosteroid-related complications (Ref).
Prednisone tapering (general recommendations): Oral: Reduce prednisone dose by 10 mg every 3 to 7 days (as immune-mediated adverse reaction allows) until the dose is 10 mg/day, then reduce dose by 5 mg every 3 to 7 days. Consider more prolonged tapering for patients who received several weeks of corticosteroids; longer tapering may be required for complete resolution or to avoid adverse reaction rebound. For grade 3 or 4 immune-mediated hepatitis, steroid taper may be attempted at ~4 to 6 weeks (after improvement to ≤ grade 1) (Ref).
Inflammatory bowel disease:
Crohn disease (moderate to severe or select patients with mild disease), induction:
Note: Not for long-term use (Ref).
Oral: 40 to 60 mg once daily for 7 to 14 days, followed by a taper of up to 3 months (eg, reduce dose by 5 mg/day at weekly intervals until 20 mg/day is reached, then further reduce by 2.5 to 5 mg/day at weekly intervals) (Ref). Tapering regimens vary; some experts recommend a more rapid taper with a goal of discontinuing therapy within 1 to 2 months; if symptoms return, may resume therapy and taper more slowly (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 (moderate to severe), induction:
Note: Not for long-term use (Ref).
Oral: 40 to 60 mg/day in 1 to 2 divided doses. Clinical improvement is expected within 7 days; pace of tapering (usually over 1 to 3 months) should be guided by symptoms, cumulative steroid exposure, and onset of action of additional therapies (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 (eg, methylprednisolone) 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: 50 mg administered 13 hours, 7 hours, and 1 hour before contrast medium administration in combination with diphenhydramine (Ref).
Minimal change disease, treatment (off-label use): Initial therapy: Oral: 1 mg/kg/day (maximum: 80 mg/day) once daily or 2 mg/kg every other day (maximum: 120 mg every other day) for 4 to 16 weeks (if no response by 16 weeks, patient is most likely glucocorticoid resistant); ~2 weeks after achieving complete remission, gradually taper (eg, decrease by 5 to 10 mg/week for a total period of glucocorticoid exposure of up to 6 months); the duration of initial pulse therapy and tapering schedule can vary (Ref).
Multiple myeloma, previously untreated, transplant ineligible (off-label use):
≥65 years of age or <65 years of age and transplant ineligible: Oral: 60 mg/m2/day for 4 days (days 1 to 4) every 6 weeks for 9 cycles (dexamethasone at a dose of 20 mg was substituted for prednisone on day 1 of each cycle) in combination with daratumumab, bortezomib, and melphalan; after cycle 9, daratumumab is continued as a single agent (Ref) or 60 mg/m2/day for 4 days (days 1 to 4) every 6 weeks (in combination with bortezomib and melphalan) for 9 cycles (Ref) or 2 mg/kg/day for 4 days (days 1 to 4) every 6 weeks (in combination with melphalan and thalidomide) for 12 cycles (Ref).
≥65 years of age: Oral: 2 mg/kg/day for 4 days (days 1 to 4) every 6 weeks (in combination with melphalan) for 12 cycles (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 using an oral glucocorticoid (alternative agent to IV methylprednisolone pulse therapy): Oral: 625 mg to 1.25 g daily for 3 to 7 days (5 days typically), either alone or followed by a taper (Ref).
Taper following IV methylprednisolone or prednisone pulse therapy: Oral: 1 mg/kg/day (maximum: 80 mg/day), followed by a taper; total duration of oral therapy is usually 11 to 14 days (Ref). Tapering schedules vary and some experts prefer to omit taper following initial pulse glucocorticoid therapy (Ref).
Myasthenia gravis (off-label use):
Acute exacerbation (adjunctive therapy):
Note: For severe exacerbations, use in conjunction with or several days following initiation of immune globulin IV or plasma exchange, as high-dose glucocorticoids may transiently worsen myasthenic weakness (Ref).
Oral: 1 mg/kg once daily (usual dose range: 60 to 80 mg daily), followed by an individualized taper as tolerated (Ref).
Chronic immunosuppression: Oral: 10 to 20 mg once daily; may increase in 5 mg/day increments every 3 to 7 days to a target dose of 60 to 80 mg daily, followed by an individualized gradual taper as tolerated (Ref).
Myopathies (dermatomyositis/polymyositis), treatment:
Initial therapy (or following initial therapy with pulse IV methylprednisolone in select patients): Oral: 1 mg/kg/day (maximum: 80 mg/day) as a single daily dose until improvement (usually for 4 to 6 weeks); then gradually tapered (total duration usually 9 to 12 months) (Ref). Note: Continuing high dose (1 mg/kg/day) for more than 6 weeks may increase risk of developing glucocorticoid-associated myopathy (Ref).
Pericarditis, acute or recurrent (alternative agent) (off-label use):
Note: May be used for patients with contraindications or incomplete response to nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine. Glucocorticoid therapy early in the course of pericarditis is more likely to be associated with recurrent episodes (Ref). Glucocorticoid therapy should be avoided in patients with pericarditis secondary to acute myocardial infarction given lack of benefit and potential harm (Ref).
Oral: Initial: 0.2 to 0.5 mg/kg/day until resolution of symptoms for at least 24 hours and normalization of inflammatory biomarkers (eg, C-reactive protein) if monitored; the initial dose is typically continued for 2 to 4 weeks then gradually tapered over 2 to 3 months if patient remains asymptomatic and inflammatory biomarkers remain normal (if monitored). Use in combination with colchicine (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 (Ref); some experts additionally recommend for patients with oxygen saturation <92% on room air (Ref).
Oral: 40 mg twice daily on days 1 to 5 beginning as early as possible, followed by 40 mg once daily on days 6 to 10, then 20 mg once daily on days 11 to 21 (Ref).
Poison ivy dermatitis, severe (adjunctive agent):
Note: For use as an adjunct to topical therapies in patients with severe or extensive dermatitis (eg, covering >50% of body surface, involvement of genitals and/or face) (Ref).
Oral: The optimal dosing strategy has not been defined; an example regimen is 1 mg/kg/day (maximum: 60 mg/day) as a single daily dose initially, followed by a taper over 2 to 3 weeks (Ref).
Polymyalgia rheumatica:
Note: Goal of therapy is to alleviate symptoms; therapy has not been shown to improve prognosis or prevent progression to giant cell arteritis (Ref).
Oral: Initial: Usual dose: 15 mg/day in a single daily dose or in divided doses; some experts consider lower initial doses of 7.5 to 10 mg/day for smaller patients with mild symptoms or at high risk for side effects (eg, labile diabetes) and higher initial doses of 20 mg/day (or 25 mg/daily [rarely]) for patients with more severe symptoms. Divided doses may help with pain and stiffness in evenings and following morning. Once symptoms are controlled, maintain dose for 2 to 4 weeks and gradually taper (generally over a 1- to 2-year period); some patients may require longer treatment (Ref).
Prostate cancer, metastatic, castration resistant (off-label use ): Oral: 5 mg twice daily (in combination with abiraterone) until disease progression or unacceptable toxicity (Ref) or 10 mg once daily (in combination with cabazitaxel) for up to 10 cycles (Ref) or 5 mg twice daily (in combination with docetaxel) for up to 10 cycles (Ref).
Systemic rheumatic disorders (eg, antineutrophil cytoplasmic antibody-associated vasculitis, mixed cryoglobulinemia syndrome, polyarteritis nodosa, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus):
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:
Mild to moderate disease: Oral: Initial: 5 to 30 mg/day in a single daily dose or in divided doses, then taper to the minimum effective dose, depending on response (Ref).
Severe disease: Initial therapy (or following initial therapy with pulse IV methylprednisolone in select patients):
Oral: Usual dose: Initial: 1 mg/kg/day (maximum: 60 to 80 mg/day) in a single daily dose or in divided doses; typically given for several weeks, then tapered gradually; may be given as part of an appropriate combination regimen; for severe systemic lupus erythematosus, up to 2 mg/kg/day may be given initially (Ref).
Takayasu arteritis (off-label use): Oral: Initial: 40 to 60 mg daily in combination with appropriate steroid-sparing agent; gradually taper to lowest effective dose (Ref); some experts initiate treatment with 1 mg/kg/day (maximum: 60 to 80 mg/day) (Ref). Note: Long-term therapy may be required to prevent progression (Ref).
Thyroiditis, subacute (off-label use):
Note: For use in patients whose pain does not respond to full dose of NSAIDs over several days or patients who present initially with moderate to severe pain (Ref).
Oral: Initial: 40 mg/day for 1 to 2 weeks; gradually taper (eg, by 5 to 10 mg/day every 5 to 7 days) based on clinical response. If pain recurs, increase to the lowest dose that controlled the pain; maintain that dose for ~2 weeks and attempt to taper again (Ref).
Tuberculosis, pulmonary (prevention of immune reconstitution inflammatory syndrome in HIV-infected patients) (off-label use):
Note: For use in antiretroviral-naive patients with CD4 count ≤100 cells/mm3 who start antiretroviral therapy within 30 days of antituberculosis therapy initiation (Ref).
Oral: 40 mg once daily for 14 days, followed by 20 mg once daily for 14 days, during the first 4 weeks after initiation of antiretroviral therapy (Ref).
Urticaria, chronic spontaneous, acute exacerbation (off-label use):
Note: For the temporary control of severe exacerbations (Ref).
Oral: 35 to 40 mg once daily until symptoms are controlled (usually occurs after 2 to 3 days of therapy) (Ref); then taper by 5 to 10 mg/day over a period of 2 to 3 weeks followed by discontinuation (Ref).
Warm autoimmune hemolytic anemia: Oral: 1 to 2 mg/kg/day until a hemoglobin response has occurred (typically within 1 to 3 weeks). After hemoglobin stabilization, begin tapering to the lowest dose to maintain remission followed by gradual tapering with an eventual goal of discontinuation (total duration of therapy: 3 to 12 months); a clinician experienced with the treatment of hemolytic anemia should be involved with therapy (Ref).
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 prednisone in kidney impairment are not well understood (Ref). Prednisolone (active metabolite) clearance is reduced ~40% in patients with uremia (Ref) and is minimally dialyzable (≤17.5%) (Ref); however, the clinical implications of these findings are unclear.
Altered kidney function: Mild to severe impairment: No dosage adjustment necessary (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.
(For additional information see "Prednisone: Pediatric drug information")
Note: All pediatric dosing based on immediate-release products; patients switching from immediate-release product to delayed-release product (eg, Rayos) should receive an equivalent dose based on relative potency. Adjust dose depending upon condition being treated and response of patient. The lowest possible dose should be used to control the condition; when dose reduction is possible, the dose should be reduced gradually. Consider alternate day therapy for long-term therapy.
Asthma :
National Asthma Education and Prevention Program guidelines (Ref):
Acute exacerbation (emergency care or hospital doses):
Infants and Children <12 years: Oral: 1 to 2 mg/kg/day in 2 divided doses, continue until peak expiratory flow is 70% of predicted or personal best; maximum daily dose: 60 mg/day.
Children ≥12 years and Adolescents: Oral: 40 to 80 mg in divided doses 1 to 2 times daily until peak expiratory flow is 70% of predicted or personal best.
Short-course "burst" (outpatient acute asthma):
Infants and Children <12 years: Oral: 1 to 2 mg/kg/day in divided doses 1 to 2 times daily for 3 to 10 days; maximum daily dose: 60 mg/day; 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.
Children ≥12 years and Adolescents: Oral: 40 to 60 mg in divided doses 1 to 2 times daily for 3 to 10 days; 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.
Long-term treatment for severe, persistent asthma (nonacute):
Infants and Children <12 years: Oral: 0.25 to 2 mg/kg/day given as a single dose 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 daily given as a single dose in the morning or every other day as needed for asthma control.
Global Initiative for Asthma guidelines (Ref): Management in primary care or acute care facility:
Infants and Children <12 years: Oral: 1 to 2 mg/kg/day for 3 to 5 days.
Maximum daily dose age-dependent:
Infants and Children ≤2 years: 20 mg/day.
Children 3 to 5 years: 30 mg/day.
Children 6 to 11 years: 40 mg/day.
Children ≥12 years and Adolescents: Oral: 1 mg/kg/day for 5 to 7 days; maximum daily dose: 50 mg/day.
Bell palsy: Limited data available:
Infants, Children, and Adolescents <16 years: Optimal regimen not defined: Oral: 1 to 2 mg/kg/day for 5 to 7 days, followed by a 7-day taper. Begin treatment within 72 hours of onset of symptoms (Ref). Adult maximum daily dose: 60 mg/day. Pediatric patients with Bell palsy may experience spontaneous recovery, even without treatment; potential benefit of treatment is unclear (Ref).
Adolescents ≥16 years: Oral: 60 mg daily for 5 days, followed by a 5-day taper. Treatment should begin within 72 hours of onset of symptoms (Ref).
Congenital adrenal hyperplasia: Note: Individualize dose by monitoring growth, hormone levels, and bone age; mineralocorticoid (eg, fludrocortisone) and sodium supplement may be required in salt losers (Ref):
Adolescents (fully grown): Oral: 5 to 7.5 mg daily in divided doses 2 times daily (Ref). Note: For younger patients who are still growing, hydrocortisone or fludrocortisone are preferred.
Crohn disease: Note: Use for induction in patients with active luminal disease if exclusive enteral nutrition is poorly tolerated or ineffective (Ref). Limited data available:
Weight-directed dosing: Children and Adolescents: Oral: 1 to 2 mg/kg/day; maximum daily dose: 60 mg/day; continue for 2 to 4 weeks until remission, then gradually taper over 4 to 8 weeks (Ref).
Fixed dose (Ref): Children and Adolescents:
10 to 20 kg: Oral: 20 mg once daily until clinical remission or a maximum of 4 weeks (whichever occurs first) followed by tapering in 2.5 to 5 mg increments every 5 to 7 days. Goal to discontinue by ≤10 weeks.
>20 to 30 kg: Oral: 30 mg once daily until clinical remission or a maximum of 4 weeks (whichever occurs first) followed by tapering in 5 mg increments every 5 to 7 days. Goal is to discontinue by ≤10 weeks.
>30 kg: Oral: 40 mg once daily until clinical remission or a maximum of 4 weeks (whichever occurs first) followed by tapering in 5 mg increments every 5 to 7 days. Goal is to discontinue by ≤10 weeks.
Dermatomyositis, juvenile: Limited data available: Children and Adolescents: Oral: 1 to 2 mg/kg/day; usual recommended maximum daily dose: 60 mg/day; higher doses of 80 mg/day have also been reported; continue for 4 weeks then if adequate patient response, begin taper; taper dose by 0.5 mg/kg increments every 2 weeks based on response until dose is 0.5 mg/kg/day, then taper every 4 weeks as tolerated; optimal duration is unknown; use in combination with other immunosuppressants (eg, methotrexate) (Ref).
Duchenne muscular dystrophy (DMD): Children ≥4 years and Adolescents: Oral: Usual recommended dose: 0.75 mg/kg/day; maximum dose: 40 mg/dose (Ref). If adverse effects persist, continue to gradually taper to as low as 0.3 mg/kg/day, which may provide benefit (Ref). Doses as high as 1.5 mg/kg/day have been studied, but there is no evidence that doses >0.75 mg/kg/day provide greater efficacy and they are associated with more adverse effects (Ref).
Hepatitis, autoimmune (monotherapy or in combination with azathioprine): Limited data available: Infants, Children, and Adolescents: Oral: Initial: 1 to 2 mg/kg/day until biochemical remission is achieved; maximum daily dose: 60 mg/day; lower maximum daily dose (eg, 40 mg/day) recommended when administering in combination with azathioprine; taper upon response over ~4 to 8 weeks to a dose of 0.1 to 0.3 mg/kg/day or 2.5 to 5 mg daily; an alternate day schedule to decrease risk of adverse effect has been used; however, a higher incidence of relapse has been observed in some cases and use is not suggested (Ref).
Immune thrombocytopenia (ITP), newly diagnosed (non-life threatening bleeding): Variable regimens reported: Infants, Children, and Adolescents: Oral: Initial: 2 to 4 mg/kg/day in 3 to 4 divided doses for 5 to 7 days; maximum daily dose: 120 mg/day; higher maximum doses of 200 mg/day have also been reported (Ref); alternatively, 1 to 2 mg/kg/day up to 80 mg/day for 1 to 2 weeks followed by a taper with goal of discontinuing therapy by 3 weeks (Ref).
Infantile hemangioma, second-line treatment: Note: Use if oral propranolol is contraindicated, poorly tolerated, or produces inadequate response (Ref).
Infants: Oral: 2 to 3 mg/kg/day up to 5 mg/kg/day; may be administered once daily or in divided doses up to 4 times daily; duration depends on response rate, patient age, and phase of hemangioma growth, but usually ranges from 4 to 12 weeks followed by a gradual taper and completion of therapy by 9 to 12 months of age (Ref).
Juvenile idiopathic arthritis (JIA): Note: Therapy should be individualized based on type of JIA as well as disease severity and activity (Ref).
Polyarticular JIA: Note: In patients with polyarticular JIA with high or moderate disease activity, bridging therapy with a limited course (<3 months) of oral glucocorticoids during initiation or escalation of therapy is recommended; chronic low dose glucocorticoids is not recommended (Ref).
Children and Adolescents (Ref): Variable regimens reported:
Low dose: Oral: 0.25 mg/kg/day; maximum daily dose: 20 mg/day; after 1 week begin tapering dose by decreasing dose to 0.125 mg/kg/day, then in 3 to 4 days, decrease to 0.05 mg/kg/day and discontinue after a total of 2 weeks.
Medium dose: Oral: 0.5 mg/kg/day; maximum daily dose: 30 mg/day; after 1 week begin taper by decreasing dose to 0.4 mg/kg/day for 7 days, then decrease to 0.25 mg/kg/day for 7 days and then 0.1 mg/kg/day for 7 days; discontinue after a total of 4 weeks.
High dose: Oral: 1 mg/kg/day; maximum daily dose: 60 mg/day; begin tapering dose after 1 to 2 weeks; decrease dose in 0.25 mg/kg/day increments every 1 to 4 weeks; tapering duration varies with some tapering doses over 4 weeks and others use a slower taper and taper off over 3 months.
Systemic JIA: Infants ≥6 months, Children, and Adolescents: Oral: Initial: 1 mg/kg/day administered once daily (initial maximum daily dose: 60 mg/day); may be used in combination with methylprednisolone pulse therapy; evaluate initial response at 1 to 2 weeks and then at 1 month of therapy; if patient improves then taper prednisone, if unchanged then continue current prednisone therapy and if worsened then increase dose to 2 mg/kg/day (maximum daily dose: 100 mg/day). After 1 month, if improvement, begin taper; if condition worsens or unchanged then increase or continue prednisone dose at 2 mg/kg/day (maximum daily dose: 100 mg/day) and/or may add or repeat methylprednisolone pulse therapy. After 3 months of glucocorticoid therapy, if improvement (prednisone dose <50% starting dose), continue taper and reassess monthly; if patient remains unchanged (prednisone dose >50% of starting dose) or worsened, additional therapy should be considered (Ref).
Kawasaki disease (KD), primary adjunctive treatment for patients at high risk for intravenous immune globulin (IVIG) resistance or coronary artery aneurysms: Limited data available: Note: Use to transition patients receiving IV corticosteroids for treatment of KD (in combination with IVIG and aspirin):
Infants and Children: Oral: 2 mg/kg/day in divided doses every 8 hours until C-reactive protein (CRP) normalizes; maximum daily dose: 60 mg/day (Ref). Some centers use less frequent dosing (eg, every 12 hours) to minimize adverse reactions (eg, effect on sleep) and for convenience (eg, ease of dosing at home). Once CRP normalized, taper over 15 days according to institutional practice (tapers may vary); a longer course, tapering over 2 to 3 weeks, may be considered (Ref).
Lupus nephritis: Children and Adolescents: Oral: Initial therapy:
With concurrent methylprednisolone pulse therapy: Prednisone: 0.5 to 1.5 mg/kg/day; maximum daily dose: 60 mg/day, taper usually over 6 months to a dose ≤10 mg/day according to clinical response; use in combination with cyclophosphamide or mycophenolate (Ref).
Without concurrent methylprednisolone pulse therapy: Prednisone: 2 mg/kg/day for 6 weeks, maximum daily dose variable: For weeks 1 to 4: Maximum daily dose: 80 mg/day; for weeks 5 and 6: Maximum daily dose: 60 mg/day; taper over 6 months; use in combination with cyclophosphamide or mycophenolate (Ref).
Nephrotic syndrome; steroid-sensitive (SSNS): Children and Adolescents: Note: Obese patients should be dosed based on ideal body weight: Oral:
Initial episode: 2 mg/kg/day or 60 mg/m2/day once daily, maximum daily dose: 60 mg/day for 4 to 6 weeks; then adjust to an alternate-day schedule of 1.5 mg/kg/dose or 40 mg/m2/dose on alternate days as a single dose, maximum dose: 40 mg/dose (Ref); prolonged durations have not been shown to reduce risk of relapse; treatment duration should be limited to 2 to 3 months for the first episode of SSNS (Ref).
Relapse: 2 mg/kg/day or 60 mg/m2/day once daily, maximum daily dose: 60 mg/day continue until complete remission for at least 3 days; then adjust to an alternate-day schedule of 1.5 mg/kg/dose or 40 mg/m2/dose on alternate days as a single dose, maximum dose: 40 mg/dose, recommended duration of alternate day dosing is variable: may continue for at least 4 weeks then taper. Longer duration of treatment may be necessary in patients who relapse frequently, some patients may require up to 3 months of treatment (Ref).
Maintenance therapy for frequently relapsing SSNS: Taper previous dose down to lowest effective dose which maintains remission using an alternate day schedule; usual effective range: 0.1 to 0.5 mg/kg/dose on alternating days; other patients may require doses up to 0.7 mg/kg/dose every other day (Ref).
Pneumocystis jirovecii pneumonia (PCP), adjunctive treatment; HIV-exposed/-infected: Note: Begin as soon as possible after diagnosis and within 72 hours of PCP therapy initiation.
Infants and Children: Oral: 1 mg/kg/dose twice daily on days 1 to 5, then 0.5 to 1 mg/kg/dose twice daily on days 6 to 10, then 0.5 mg/kg/dose once daily for days 11 to 21 (Ref).
Adolescents: Oral: 40 mg twice daily on days 1 to 5, followed by 40 mg once daily on days 6 to 10, and then 20 mg once daily on days 11 to 21 or until antimicrobial regimen is completed (Ref).
Ulcerative colitis, moderate to severe: Note: Not for long-term maintenance; use for induction only.
Children and Adolescents: Oral: 1 to 2 mg/kg/day administered in the morning for 2 to 3 weeks; maximum daily dose: 60 mg/day; if no response after 7 to 14 days optimal dosing and compliance should be assessed; after the initial 2 to 3 weeks, the dose is gradually decreased over 8 to 10 weeks (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; use with caution.
There are no dosage adjustments provided in the manufacturer's labeling. Prednisone is inactive and must be metabolized by the liver to prednisolone. This conversion may be impaired in patients with liver disease; however, prednisolone levels are observed to be higher in patients with severe liver failure than in normal patients. Therefore, compensation for the inadequate conversion of prednisone to prednisolone occurs.
Refer to adult dosing; use the lowest effective dose.
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):
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, especially with longer durations of therapy (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 small study in patients with asthma reported higher prevalence of abnormal prednisone absorption and fast prednisolone clearance when BMI exceeded 25 kg/m2 (Ref). A second small study in males with obesity described increases in both volume of distribution and clearance following IV prednisolone administration compared to males without obesity (Ref). The clinical significance of these pharmacokinetic changes requires further study, especially in patients with BMI ≥40 kg/m2, where there are minimal data. Glucocorticoid pharmacodynamics may be enhanced in obesity; weight-based dosing using actual body weight could lead to supratherapeutic levels (Ref).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Concentrate, Oral:
predniSONE Intensol: 5 mg/mL (30 mL) [contains alcohol, usp; unflavored flavor]
Solution, Oral:
Generic: 5 mg/5 mL (120 mL, 500 mL)
Tablet, Oral:
Generic: 1 mg, 2.5 mg, 5 mg, 10 mg, 20 mg, 50 mg
Tablet Delayed Release, Oral:
Rayos: 1 mg, 2 mg, 5 mg
Tablet Therapy Pack, Oral:
Generic: 10 mg (21 ea, 48 ea); 5 mg (21 ea, 48 ea)
May be product dependent
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Winpred: 1 mg
Generic: 5 mg, 50 mg
Oral:
Administer after meals or with food or milk to decrease GI upset. May administer antacids between meals to help prevent peptic ulcers.
Delayed-release tablets: Swallow whole; do not break, divide, crush, or chew.
Bariatric surgery: Some institutions may have specific protocols that conflict with these recommendations; refer to institutional protocols as appropriate. IR tablet and oral solution formulations are available. If safety and efficacy can be effectively monitored, no change in formulation or administration is required after bariatric surgery; however, minimum necessary dose and duration of prednisone therapy is recommended to minimize risk of GI irritation or ulceration. Proton pump inhibitor therapy is recommended if therapy is to continue chronically.
Oral solution, concentrate: Administer only with provided calibrated dropper.
Oral: Administer after meals or with food or milk to decrease GI upset.
Delayed-release tablet (Rayos): Swallow whole; do not crush, divide, or chew.
Oral solution: Administer with an accurate measuring device; do not use a household teaspoon (under or overdosage may occur).
Oral concentrate (Intensol): Administer with the provided calibrated dropper.
Anti-inflammatory or immunosuppressant agent in the treatment of a variety of diseases, including allergic (eg, angioedema, contact dermatitis, new-onset urticaria), hematologic (eg, immune thrombocytopenia, warm autoimmune hemolytic anemia), dermatologic, GI, inflammatory, ophthalmic, neoplastic, rheumatic (eg, acute gout flare, vasculitis, dermatomyositis, mixed cryoglobulinemia syndrome, polyarteritis nodosa, polymyositis, polymyalgia rheumatica, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus), autoimmune, nervous system (eg, acute exacerbations of multiple sclerosis), renal, respiratory (eg, asthma), and endocrine (eg, primary or secondary adrenocorticoid deficiency); solid organ rejection (acute/chronic).
Alcoholic hepatitis (severe); Bell palsy, new onset; Chronic obstructive pulmonary disease, acute exacerbation; COVID-19, hospitalized patients; Duchenne muscular dystrophy; Focal segmental glomerulosclerosis, primary; Giant cell arteritis, treatment; Graft-versus-host disease, acute, treatment; Hepatitis, autoimmune; Minimal change disease, treatment; Multiple myeloma (previously untreated; transplant-ineligible); Myasthenia gravis, acute exacerbation or chronic immunosuppressive therapy; Pericarditis, acute or recurrent; Pneumocystis pneumonia, adjunctive therapy for moderate to severe disease; Prostate cancer, metastatic; Takayasu arteritis; Thyroiditis, subacute; Tuberculosis, pulmonary; Urticaria, chronic spontaneous, acute exacerbation
PredniSONE may be confused with methylPREDNISolone, Pramosone, prazosin, prednisoLONE, PriLOSEC, primidone, promethazine
Adrenal suppression (tertiary adrenal insufficiency) may occur with glucocorticoids, including prednisone, and results from inadequate stimulation of the adrenal glands (Ref). Glucocorticoid-induced adrenal insufficiency usually resolves with discontinuation of prednisone, 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).
Mechanism: Dose- and time-related; occurs due to lack of or diminished cortisol production which is decreased 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 prednisone chronically (Ref).
Onset: Varied; acute (minutes after administration) and/or chronic (2 to 20 hours to days) (Ref). Chronic prednisone 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 >20 mg/day (daytime dosing) or ≥5 mg per 24 hours (evening or night dosing) for >3 weeks or with cushingoid appearance (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)
Prednisone has potent cardiovascular effects which include hypertension, dyslipidemia, fluid retention, electrolyte disturbances (decreased serum potassium, sodium retention), and arrhythmias (from rare cases of bradycardia to more common reports of atrial fibrillation). Fluid retention can worsen cardiac failure in some patients because of its mineralocorticoid properties (Ref). Prednisone can increase blood pressure in a dose-dependent manner. Dyslipidemia occurring with long-term prednisone use manifests as increased total cholesterol, low density lipoprotein, and triglycerides (Ref). Chronic glucocorticoid use has been associated with an increased risk of developing cardiovascular disease/events (Ref).
Mechanism: Dose- and time-related; prednisone increases systemic vascular resistance (hypertension), increases extracellular volume (fluid retention), and increases cardiac contractility (potentiating atrial fibrillation/flutter). It is the combination of these cardiac effects (hypertension and edema) in patients with hyperglycemia and obesity that can lead to metabolic syndrome (Ref).
Onset: Varied. Prednisone-induced hypertension: One type occurs in patients without risk factors early in therapy and a second (more classic) type occurs with weight gain and adipose tissue redistribution later in therapy (Ref).
Risk factors:
• Higher doses (Ref)
• Family history of essential hypertension (Ref)
• Longer duration of use (Ref)
• Pulse therapy (Ref)
• Older adults (Ref)
Glucocorticoids, including prednisone, 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). Discontinuation or dose reductions generally resolve symptoms over days to weeks (Ref).
Mechanism: Dose-related; not clearly established. Prednisone and other corticosteroids 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 (≥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 (prednisone) results in suppression of adrenocorticotrophic hormone (ACTH), commonly called iatrogenic Cushing syndrome (Ref).
Onset: Delayed; may develop within the first 2 months of prednisone 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 prednisone, 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).
Risk factors:
• Higher doses (equivalent to methylprednisolone ≥4 mg/day) (Ref)
• Concurrent aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) (Ref)
• Hospitalized (but not ambulatory) patients (Ref)
• Recent glucocorticoid users (7 to 28 days) versus remote or nonusers (Ref)
Glucocorticoids, including prednisone, 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 prednisone 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; 4 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 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 prednisone, 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, and 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)
• Immunocompromised state (Ref)
• Concurrent medications (immunosuppressive) (Ref)
• Rheumatoid arthritis (Ref)
• Interstitial lung disease (Ref)
• Older adults (Ref)
• Male (Ref)
• Low performance status (Ref)
Glucocorticoid (including prednisone)-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 daily, with higher doses potentiating more of a rapid onset (Ref)
• Fluorinated glucocorticoid preparations (eg, dexamethasone, betamethasone, triamcinolone) have a higher risk of myopathies than prednisone (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 prednisone)-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 and incidences are derived from product labeling unless otherwise specified.
Frequency not defined:
Cardiovascular: Bradycardia, cardiomegaly, circulatory shock, edema, heart failure (in susceptible patients), hypertrophic cardiomyopathy (premature infants), myocardial rupture (after recent myocardial infarction), syncope, tachycardia, thrombophlebitis, vasculitis
Dermatologic: Acne vulgaris, allergic dermatitis, atrophic striae, diaphoresis, facial erythema, hyperpigmentation, hypopigmentation, skin atrophy, skin rash, thinning hair (scalp), urticaria
Endocrine & metabolic: Decreased serum potassium, fluid retention, growth retardation (children), hirsutism, hypokalemic alkalosis, menstrual disease, negative nitrogen balance (due to protein catabolism), sodium retention, weight gain
Gastrointestinal: Hiccups, increased appetite, nausea
Genitourinary: Asthenospermia, oligospermia
Hematologic & oncologic: Bruise, petechia
Hepatic: Hepatomegaly, increased serum transaminases
Hypersensitivity: Angioedema
Infection: Sterile abscess
Nervous system: Abnormal sensory symptoms, arachnoiditis, headache, increased intracranial pressure (with papilledema), malaise, meningitis, myasthenia, neuritis, neuropathy, paraplegia, paresthesia, seizure, vertigo
Neuromuscular & skeletal: Charcot arthropathy
Respiratory: Pulmonary edema
Miscellaneous: Wound healing impairment
Postmarketing:
Cardiovascular: Atrial fibrillation (van der Hooft 2006), hypertension (Mebrahtu 2020), venous thrombosis (Johannesdottir 2013)
Endocrine & metabolic: Adrenal suppression (tertiary) (Broersen 2015), Cushing syndrome (iatrogenic) (Hopkins 2005), cushingoid appearance (Hopkins 2005), dyslipidemia (Vodnala 2012), exacerbation of diabetes mellitus (Tamez-Pérez 2015), hyperglycemia (Tamez-Pérez 2015), impaired glucose tolerance (Tamez-Pérez 2015), moon face (Hopkins 2005), redistribution of body fat (Hopkins 2005)
Gastrointestinal: Abdominal distention (Liu 2013), peptic ulcer (with possible perforation and hemorrhage) (Liu 2013), ulcerative esophagitis (Liu 2013)
Hematologic & oncologic: Kaposi sarcoma (Trattner 1993)
Hypersensitivity: Anaphylaxis (Polosa 1998)
Infection: Infection (Youssef 2016)
Nervous system: Apathy (Ciriaco 2013; Warrington 2006), depression (Ciriaco 2013; Warrington 2006), psychiatric disturbance (dose-dependent; including agitation, anxiety, distractibility, euphoria, fear, hypomania, insomnia, irritability, labile mood, lethargy, pressured speech, restlessness, tearfulness) (Ciriaco 2013; Warrington 2006)
Neuromuscular & skeletal: Bone fracture (Buckley 2018), myopathy (Liu 2013), osteonecrosis (femoral and humeral heads) (Liu 2013), osteoporosis (Buckley 2018), steroid myopathy (Haran 2018), vertebral compression fracture (Buckley 2018)
Ophthalmic: Glaucoma (Razeghinejed 2012), increased intraocular pressure (Phulke 2017), retinopathy (Tarabishy 2011) subcapsular posterior cataract (Urban 1986)
Hypersensitivity to prednisone or any component of the formulation; administration of live or live attenuated vaccines with immunosuppressive doses of prednisone; systemic fungal infections
Canadian labeling: Additional contraindications (not in US labeling): Herpes simplex of the eye, measles, or chickenpox (except when being used for short-term or emergency therapy); peptic ulcer; nonspecific ulcerative colitis; diverticulitis; viral or bacterial infection not controlled by anti-infectives
Documentation of allergenic cross-reactivity for corticosteroids is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children.
Disease-related concerns:
• Gastrointestinal disease: Use with caution in patients with GI diseases (diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, ulcerative colitis [nonspecific]) 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; effects may be enhanced.
• 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: 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.
• Systemic sclerosis: Use with caution in patients with systemic sclerosis; an increase in scleroderma renal crisis incidence has been observed with corticosteroid use. Monitor BP and renal function in patients with systemic sclerosis treated with corticosteroids (EULAR [Kowal-Bielecka 2017]).
• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid patients.
Special populations:
• Older adult: Use with caution in elderly patients with the smallest possible effective dose for the shortest duration.
• Pediatric: May affect growth velocity; growth and development should be routinely monitored in pediatric patients.
Dosage form specific issues:
• Benzyl alcohol and derivatives: Some dosage forms may contain sodium benzoate/benzoic acid; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol derivative with caution in neonates. See manufacturer's labeling.
• Propylene glycol: Some dosage forms may contain propylene glycol; large amounts are potentially toxic and have been associated hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP ["Inactive" 1997]; Zar 2007).
Other warnings/precautions:
• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.
Some dosage forms may contain propylene glycol; in neonates, large amounts of propylene glycol delivered orally, intravenously (eg, >3,000 mg/day), or topically have been associated with potentially fatal toxicities which can include metabolic acidosis, seizures, renal failure, and CNS depression; toxicities have also been reported in children and adults including hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP 1997; Shehab 2009).
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 Lexicomp 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 may diminish the antineoplastic 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
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 [INT]: 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
Cladribine: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Cladribine. Risk X: Avoid combination
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 PredniSONE. CycloSPORINE (Systemic) may increase serum concentrations of the active metabolite(s) of PredniSONE. PredniSONE may decrease the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy
CYP3A4 Inducers (Moderate): May decrease the serum concentration of PredniSONE. Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May decrease the serum concentration of PredniSONE. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May increase the serum concentration of PredniSONE. 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
Disulfiram: May enhance the adverse/toxic effect of Products Containing Ethanol. Management: Do not use disulfiram with dosage forms that contain ethanol. Risk X: Avoid combination
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
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
Gallium Ga 68 Dotatate: Corticosteroids (Systemic) may diminish the diagnostic effect of Gallium Ga 68 Dotatate. Risk C: Monitor therapy
Growth Hormone Analogs: PredniSONE may diminish the therapeutic effect of Growth Hormone Analogs. Growth Hormone Analogs may decrease serum concentrations of the active metabolite(s) of PredniSONE. 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: Corticosteroids (Systemic) may diminish the therapeutic effect of Immune Checkpoint Inhibitors. 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
Methotrimeprazine: Products Containing Ethanol may enhance the adverse/toxic effect of Methotrimeprazine. Specifically, CNS depressant effects may be increased. Management: Avoid products containing alcohol in patients treated with methotrimeprazine. 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
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
Ornidazole: May enhance the adverse/toxic effect of Products Containing Ethanol. Specifically, a disulfiram-like reaction may occur. Risk X: Avoid combination
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
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
Secnidazole: Products Containing Ethanol may enhance the adverse/toxic effect of Secnidazole. Risk X: Avoid combination
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
Tesamorelin: May decrease serum concentrations of the active metabolite(s) of PredniSONE. Risk C: Monitor therapy
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 (Inactivated/Non-Replicating): Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (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
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 prior to therapy whenever possible. 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
Prednisone is acceptable for use in patients with rheumatic and musculoskeletal diseases who are planning to become pregnant. Doses should be tapered to <20 mg/day with the addition of pregnancy compatible immunosuppressants. Conception should be planned during a period of quiescent/low disease activity. Empiric/prophylactic dose increases of prednisone are not recommended for patients with systemic lupus erythematosus requiring assisted reproductive technology; patients should be monitored and treated if flares occur (ACR [Sammaritano 2020]).
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).
Prednisone and its metabolite, prednisolone, cross the placenta.
In the mother, prednisone is converted to the active metabolite prednisolone by the liver. Prior to reaching the fetus, prednisolone is converted by placental enzymes back to prednisone. As a result, the level of prednisone remaining in the maternal serum and reaching the fetus are similar; however, the amount of prednisolone reaching the fetus is ~8 to 10 times lower than the maternal serum concentration (healthy women at term) (Beitins 1972).
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 potential risks of systemic corticosteroids and other adverse pregnancy outcomes (eg, gestational diabetes mellitus, low birth weight, preeclampsia, preterm birth) (ACOG 2019b; Bandoli 2017; Skuladottir 2014). Hypoadrenalism may occur in newborns following maternal use of corticosteroids in pregnancy; monitor infants exposed to prolonged or high doses of prednisone in utero (Saulnier 2010).
Due to pregnancy-induced physiologic changes, clearance of prednisone may be increased (may be dose dependent) (Ryu 2018).
Prednisone is a preferred oral corticosteroid for the treatment of maternal conditions during pregnancy because placental enzymes limit passage to the embryo (ACOG 2019b).
Prednisone ≤10 mg/day is acceptable for use in pregnant patients with rheumatic and musculoskeletal diseases. Higher doses should be tapered to <20 mg/day with the addition of pregnancy compatible immunosuppressants. Stress dosing is not recommended during vaginal delivery (ACR [Sammaritano 2020]).
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 in 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. Inhaled corticosteroids are recommended for the treatment of asthma during pregnancy; however, systemic corticosteroids, including prednisone, should be used to control acute exacerbations or treat severe persistent asthma. Maternal asthma symptoms should be monitored monthly during pregnancy (ERS/TSANZ [Middleton 2020]; GINA 2022).
Prednisone is recommended for use in fetal-neonatal alloimmune thrombocytopenia and pregnancy-associated immune thrombocytopenia (ACOG 2019a; Provan 2019). Prednisone is the preferred immunosuppressant for the treatment of myasthenia gravis in pregnancy (Sanders 2016).
Prednisone and its metabolite, prednisolone, are present in breast milk.
According to the manufacturer, prednisolone breast milk concentrations are 5% to 25% of the maternal serum levels, providing a total infant dose <1% of the maternal dose. Actual concentrations are dependent upon maternal dose (Berlin 1979; Katz 1975; Ryu 2018; Sagraves 1981). Peak concentrations of prednisone and prednisolone in breast milk occur ~2 to 3 hours after an oral maternal dose (Berlin 1979; Ryu 2018; Sagraves 1981); the half-life in breast milk is 1.9 hours (prednisone) and 4.2 hours (prednisolone) (Sagraves 1981).
In a study which included six mother-infant pairs, adverse events were not observed in breastfeeding infants (maternal prednisone dose not provided) (Ito 1993).
The manufacturer notes that maternal use of high doses of systemic corticosteroids have the potential to cause adverse events in a breastfeeding infant (eg, growth suppression, interfere with endogenous corticosteroid production); therefore, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother. The lowest effective dose should be used to minimize potential infant exposure via breast milk.
Corticosteroids are generally considered acceptable in breastfeeding women when used in usual doses; however, monitoring of the breastfeeding infant is recommended (WHO 2002). Prednisone is one of the oral corticosteroids preferred for use in breastfeeding women (Butler 2014). Breastfeeding is acceptable for patients with rheumatic and musculoskeletal diseases taking prednisone <20 mg/day (ACR [Sammaritano 2020]). If there is concern about exposure to the infant, some guidelines recommend waiting up to 4 hours after the maternal dose of an oral systemic corticosteroid before breastfeeding in order to decrease potential exposure to the breastfeeding infant (based on a study using prednisolone) (Butler 2014; ERS/TSANZ [Middleton 2020]; Mahadevan 2019; Ost 1985).
May require increased dietary intake of pyridoxine, vitamin C, vitamin D, folate, calcium, and phosphorus; may require decreased dietary intake of sodium and potassium supplementation
Blood pressure; weight; serum glucose; electrolytes; creatine kinase; growth in pediatric patients; presence of infection, bone mineral density; assess HPA axis suppression (eg, ACTH stimulation test, morning plasma cortisol test, urinary free cortisol test); Hgb, occult blood loss; chest x-ray (at regular intervals during prolonged therapy); IOP with therapy >6 weeks, eye examination (periodically during therapy [AASLD (Mack 2020)]).
Decreases inflammation by suppression of migration of polymorphonuclear leukocytes and reversal of increased capillary permeability; suppresses the immune system by reducing activity and volume of the lymphatic system; suppresses adrenal function at high doses. Antitumor effects may be related to inhibition of glucose transport, phosphorylation, or induction of cell death in immature lymphocytes. Antiemetic effects are thought to occur due to blockade of cerebral innervation of the emetic center via inhibition of prostaglandin synthesis.
Absorption: 50% to 90% (may be altered in hepatic failure, chronic renal failure, inflammatory bowel disease, hyperthyroidism, and in the elderly) (Frey 1990)
Protein binding (concentration dependent): <50% (Frey 1990)
Metabolism: Hepatic to metabolite prednisolone (active)
Half-life elimination: 2 to 3 hours
Time to peak: Oral: Immediate-release tablet: 2 hours; Delayed-release tablet: 6 to 6.5 hours
Excretion: Urine (as conjugates)
Hepatic function impairment: Prednisone is inactive and must be metabolized by the liver to prednisolone. This conversion may be impaired in patients with liver disease; however, prednisolone levels are observed to be higher in patients with severe liver failure than in normal patients.
Concentrate (predniSONE Intensol Oral)
5 mg/mL (per mL): $5.20
Solution (predniSONE Oral)
5 mg/5 mL (per mL): $0.80
Tablet Therapy Pack (predniSONE Oral)
5MG (21) (per each): $0.80
5MG (48) (per each): $0.58
10MG (21) (per each): $1.39
10MG (48) (per each): $0.86
Tablet, EC (Rayos Oral)
1 mg (per each): $110.48
2 mg (per each): $110.48
5 mg (per each): $110.48
Tablets (predniSONE Oral)
1 mg (per each): $0.18 - $0.63
2.5 mg (per each): $0.16 - $0.20
5 mg (per each): $0.20 - $0.73
10 mg (per each): $0.19 - $0.91
20 mg (per each): $0.20 - $1.50
50 mg (per each): $0.41 - $0.65
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.
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