Version July 2025
Infantile hemangioma, second-line treatment: Note: Use if oral propranolol is contraindicated, poorly tolerated, or produces inadequate response (Ref).
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).
Dosage guidance:
Dosing: Individualize dosing and use the lowest possible dose to control the condition; when dose reduction is possible, reduce dose gradually. Consider alternate day therapy for long-term therapy. All pediatric dosing is based on IR products; patients switching from IR product to delayed-release product (eg, Rayos) should be dosed based on relative potency.
Asthma :
National Asthma Education and Prevention Program guidelines (Ref):
Acute exacerbation/short course "burst":
Infants and Children <12 years: Oral: 1 to 2 mg/kg/day in divided doses 1 to 2 times daily; maximum daily dose: 60 mg/day. Usual duration: 3 to 10 days.
Children ≥12 years and Adolescents: Oral: 40 to 60 mg in divided doses 1 to 2 times daily. Usual duration: 3 to 10 days.
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: 40 to 50 mg/day for 5 to 7 days.
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 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: 0.35 to 1 mg/kg/day beginning after initial methylprednisolone; maximum daily dose 80 mg/day; use as part of an appropriate combination regimen. Taper over ~6 months to a dose ≤5 mg/day based on clinical response. Use lowest dose necessary after initial flare and consider discontinuation once patient has had complete clinical renal response for ≥12 months (Ref).
Nephrotic syndrome:
Initial episode: Children and Adolescents: Oral: 2 mg/kg/dose or 60 mg/m2/dose once daily (maximum dose: 60 mg/dose) for 4 to 6 weeks; then decrease to 1.5 mg/kg/dose or 40 mg/m2/dose every other day (maximum dose: 50 mg/dose) for 4 to 6 weeks (Ref).
Relapse: Children and Adolescents: Oral: 2 mg/kg/dose or 60 mg/m2/dose once daily (maximum dose: 60 mg/dose) until complete remission for at least 3 days; then decrease to 1.5 mg/kg/dose or 40 mg/m2/dose every other day (maximum dose: 50 mg/dose) for at least 4 weeks, then taper. Duration of alternate-day dosing is variable; some patients require maintenance dosing to prevent relapse; use lowest effective dose (preferably <0.5 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.
(For additional information see "Prednisone: Drug information")
Dosage guidance:
Dosing: Individualize glucocorticoid dosing and use the minimum effective dose/duration. Evidence to support an optimal dose and duration is lacking for most indications; recommendations provided are general guidelines only.
Clinical considerations: In patients receiving chronic glucocorticoids (eg, ≥3 to 4 weeks) at supraphysiologic doses (>5 mg/day prednisone) for indications other than adrenal insufficiency, risk of hypothalamic-pituitary-adrenal axis suppression is increased. If glucocorticoid discontinuation is indicated, reduce dose gradually and monitor for signs of adrenal insufficiency. Higher doses may be needed during acute illness or surgery (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 dose taper example is from the commercially available tapered-dosage product:
Day 1: Administer 30 mg on day 1 as 10 mg at breakfast, 5 mg at lunch, 5 mg at dinner, and 10 mg at bedtime.
Day 2: Administer 25 mg on day 2 as 5 mg at breakfast, 5 mg at lunch, 5 mg at dinner, and 10 mg at bedtime.
Day 3: Administer 20 mg on day 3 as 5 mg at breakfast, 5 mg at lunch, 5 mg at dinner, and 5 mg at bedtime.
Day 4: Administer 15 mg on day 4 as 5 mg at breakfast, 5 mg at lunch, and 5 mg at bedtime.
Day 5: Administer 10 mg on day 5 as 5 mg at breakfast and 5 mg at bedtime.
Day 6: Administer 5 mg on day 6 as 5 mg at breakfast.
Adrenal insufficiency, chronic (alternative agent):
Note: For use in patients with severe symptoms of cortisol deficiency while using a short-acting glucocorticoid (eg, hydrocortisone) or who have difficulty adhering to multiple daily dosing regimens. Use in combination with fludrocortisone in patients with mineralocorticoid deficiency (eg, primary adrenal insufficiency) (Ref).
Maintenance dosing: Oral: Initial: 5 mg once daily. May adjust daily dose if needed based on signs and symptoms of under- or over-replacement; use the lowest effective dose. Usual dosage range: 2.5 to 7.5 mg/day (Ref).
Stress dosing: Note: For use in patients with chronic adrenal insufficiency (AI) and acute physiologic stressors (eg, illness, surgery) to prevent development of adrenal crisis. Patients without known chronic AI with recent or current chronic glucocorticoid use at supraphysiologic doses (eg, >5 mg/day prednisone) may have hypothalamic-pituitary-adrenal axis suppression and may require stress dosing; individualize treatment decisions in these patients (Ref). If a parenteral glucocorticoid is required (eg, unable to take oral medications, critical illness, labor/delivery, moderate/severe surgical stress), switch to hydrocortisone (Ref). Dosing provided is calculated based on hydrocortisone equivalency.
Acute physiologic stress/illness:
Febrile illness: Double the chronic maintenance dose for fever 38°C (100.4°F) to 39°C (102.2°F) or triple the chronic maintenance oral dose for fever >39°C (>102.2°F) or persistent nausea. Continue higher dose for 3 days, then return to baseline dose if fever has resolved. If fever has not resolved by day 4, further evaluation (with continued use of higher steroid doses if needed) is required (Ref).
Illness requiring hospitalization (eg, community acquired pneumonia): Oral: 12.5 to 20 mg once daily. For patients requiring a parenteral glucocorticoid, switch to hydrocortisone. Taper and return to baseline dose within 2 to 3 days following improvement of underlying condition (Ref).
Surgical stress:
Minor surgical stress (eg, hernia repair, procedures with local anesthetic): Oral: Give an additional 5 mg supplemental dose on the day of surgery (Ref).
Adrenal insufficiency due to classic congenital adrenal hyperplasia:
Note: For use as an alternative agent when preferred glucocorticoids (eg, hydrocortisone) are unavailable or cannot be taken. In patients with mineralocorticoid deficiency, use in combination with fludrocortisone (Ref).
Oral: 5 to 7.5 mg/day in 2 divided doses (Ref).
Stress dosing: Patients undergoing physiologic stress (eg, febrile illness, surgery, labor/delivery) require increased glucocorticoid doses to prevent adrenal crisis. Individualize treatment decisions; refer to "Dosing: Adrenal Insufficiency, Chronic” for stress dosing instructions (Ref).
Alcoholic hepatitis, severe (Maddrey Discriminant Function [MDF] score ≥32) (off-label use): Oral: 40 mg daily for 28 days (Ref).
Anaphylaxis-associated residual symptoms (eg, persistent asthma, significant angioedema):
Note: Patient should be initially treated with epinephrine for the anaphylaxis event and stabilized. Do not use prednisone for initial or sole treatment of anaphylaxis because corticosteroids do not result in the prompt relief of upper or lower airway obstruction or shock and do not prevent biphasic anaphylaxis (Ref).
Oral: 1 mg/kg daily for 3 to 5 days; maximum daily dose: 60 mg/day (Ref).
Angioedema (acute allergic) and/or new-onset urticaria:
Note: For moderate to severe symptoms without signs of anaphylaxis. Use epinephrine if anaphylaxis symptoms (eg, risk of airway or cardiovascular compromise) are present (Ref). In patients with new-onset urticaria, reserve use for those with significant angioedema or with symptoms that are unresponsive to antihistamines (Ref).
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/day in 1 or 2 divided doses; continue for at least 5 to 7 days or until symptoms are resolved (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).
Bullous pemphigoid (off-label use): Oral: Initial: 0.5 mg/kg/day. May begin gradual taper over 4 to 6 months when disease is controlled (eg, no new lesions or pruritic symptoms for ≥2 weeks and most established lesions have healed). May discontinue therapy if complete remission maintained for at least 3 to 6 months on doses ≤0.1 mg/kg/day (usual total duration: 9 to 12 months) (Ref).
Inadequate initial control: In patients who do not achieve disease control within 1 to 3 weeks of initial therapy, may increase to 0.75 mg/kg/day; may also consider addition of other agents (eg, topical corticosteroids, immunosuppressants) (Ref).
Disease recurrence: Return to the preceding lowest effective treatment dose; if not effective, return to initial effective dose (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 mg once daily for 5 days (Ref). Note: Higher dosing, extended durations, and/or longer tapers may be used based on exacerbation severity and individual patient response to prior courses (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 (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).
Hodgkin lymphoma: BEACOPP and escalated BEACOPP regimen: Oral: 40 mg/m2 on days 1 to 14 of a 21-day cycle (in combination with bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, and procarbazine) for 8 cycles (Ref).
IgA nephropathy, primary, nonvariant (adjunctive agent) (off-label use):
Note: May consider for use in selected patients at high risk of chronic kidney disease progression (eg, proteinuria ≥0.75 to 1 g/day) despite 3 to 6 months of optimized doses of nonimmunosuppressive therapies (eg, renin-angiotensin system inhibitors) (Ref). The optimal dose has not been established and may vary based on institutional protocols and patient-specific factors; an example regimen (based on an equivalent dose of methylprednisolone) is provided below.
Oral: 0.5 mg/kg once daily for 2 months (maximum dose: 40 mg/day). Taper daily dose every month over an additional 4 to 7 months. Note: Antimicrobial prophylaxis for Pneumocystis pneumonia was also prescribed for the first 12 weeks of therapy (Ref).
Immune 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 immune checkpoint inhibitor therapy:
Note: Consider withholding immune checkpoint inhibitor (ICI) therapy for most grade 2 toxicities, withhold the ICI for grade 3 toxicity and permanently discontinue for most grade 4 toxicities (Ref). Refer to each ICI monograph for specific dosage modification and management details.
General prednisone dosing recommendations:
Grade 2 toxicity (if ICI 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 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).
ICI-induced hypophysitis: In patients without adrenal insufficiency, high doses of corticosteroids (short-term courses [as above]) may only be necessary in cases of pituitary enlargement that could lead to chiasma compression or with severe compressive symptoms (eg, headache, double vision) (Ref). Higher corticosteroid doses may be associated with worse clinical outcomes in patients with ICI-induced hypophysitis and are otherwise not recommended (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: 0.5 to 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).
Non-Hodgkin lymphomas:
CHOP or R-CHOP regimen: Oral: 40 mg/m2 once daily on days 1 to 5 of a 21-day cycle (in combination with cyclophosphamide, doxorubicin, and vincristine ± rituximab) for 8 cycles (Ref) or 100 mg once daily on days 1 to 5 of a 21-day cycle (in combination with cyclophosphamide, doxorubicin, vincristine, and rituximab) for 6 cycles (Ref) or 100 mg once daily on days 1 to 5 of a 21-day cycle (in combination with cyclophosphamide, doxorubicin, vincristine, and rituximab) for 4 cycles (Ref).
Mini-CHOP or Mini-R-CHOP regimen: Oral: 40 mg/m2 once daily on days 1 to 5 of a 21-day cycle (in combination with cyclophosphamide, doxorubicin, vincristine, and rituximab) for 6 cycles (Ref).
Dose-adjusted EPOCH or REPOCH regimen: Oral: 60 mg/m2 once daily on days 1 to 5 of a 21-day cycle (in combination with doxorubicin, etoposide, vincristine, and cyclophosphamide ± rituximab) for 6 to 8 cycles (Ref) or 60 mg/m2 twice daily on days 1 to 5 of a 21-day cycle (in combination with doxorubicin, etoposide, vincristine, and cyclophosphamide ± rituximab) for 6 to 8 cycles (Ref).
Pola-R-CHP regimen: Oral: 100 mg once daily on days 1 through 5 of a 21-day cycle (in combination with polatuzumab vedotin, cyclophosphamide, doxorubicin, and rituximab) for 6 cycles, followed by rituximab monotherapy in cycles 7 and 8 (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:
Note: For use in patients with severe or extensive dermatitis (eg, covering ≥10% of body surface, severe blistering, or involvement of face, hands, or genitals) (Ref). The optimal dosing strategy has not been defined; an example regimen is provided.
Oral: 1 mg/kg once daily initially (maximum: 60 mg/day), 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 : Oral: 5 mg twice daily in combination with abiraterone) until disease progression or unacceptable toxicity (Ref) or 5 mg twice daily (in combination with docetaxel) for up to 10 cycles (Ref) or 10 mg once daily (in combination with cabazitaxel) for up to 10 cycles (Ref) or 5 mg twice daily (in combination with abiraterone and olaparib) until disease progression or unacceptable toxicity (Ref) or 5 mg twice daily (in combination with niraparib and abiraterone) until disease progression or unacceptable toxicity (Ref) or 5 mg twice daily (in combination with mitoxantrone) for up to ten 21-day cycles (Ref).
Prostate cancer, metastatic, castration sensitive: Oral: 5 mg once daily (in combination with abiraterone); continue until disease progression or unacceptable toxicity (Ref) or 5 mg twice daily (in combination with abiraterone and docetaxel); continue until disease progression or unacceptable toxicity (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).
Thyroid eye disease, moderate to severe (off-label use):
Note: For use as an alternative to IV glucocorticoids (eg, methylprednisolone); in patients with sight-threatening disease (eg, compressive optic neuropathy), urgent administration of IV glucocorticoids is required (Ref).
Oral: 60 to 100 mg once daily for 7 days, then gradually taper dose by 5 to 10 mg/week over 4 to 6 months based on clinical response and then discontinue (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), then taper by 5 to 10 mg/day over a period of 1 to 3 weeks followed by discontinuation (Ref).
Waldenström macroglobulinemia (alternative regimen): Note: While other treatments are preferred, R-CHOP is an option for the treatment of Waldenström macroglobulinemia (Ref).
R- CHOP regimen: Oral: 100 mg/m2 on days 1 to 5 every 3 weeks (in combination with rituximab, cyclophosphamide, doxorubicin, and vincristine) for 4 to 8 cycles (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.
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:
• Higher doses (eg, prednisone ≥4 mg daily) for prolonged periods (eg, ≥3 weeks) (Ref)
• Glucocorticoid potency (prednisone: moderate risk) (Ref)
• Route of glucocorticoid administration (eg, systemic: high risk) (Ref)
• Concurrent use of other glucocorticoids delivered by various routes of administration (eg, inhaled, topical, intraarticular injections) (Ref)
• History of previous adrenal crisis (Ref)
• Higher BMI (Ref)
• Older adults (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 excitatory psychiatric disturbances (including agitation, anxiety, distractibility, fear, hypomania, insomnia, irritability, lethargy, labile mood, mania, pressured speech, restlessness, and tearfulness) (Ref). Patients may also develop apathy or depression. Severe psychiatric effects, depression, and mania have been reported in adults receiving high-dose glucocorticoid regimens (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 reactions occur early in therapy (ie, within 1 to 2 weeks after initiation). May also occur later or after therapy discontinuation (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 (Ref), hypertension (Ref), venous thrombosis (Ref)
Endocrine & metabolic: Adrenal suppression (tertiary) (Ref), Cushing syndrome (iatrogenic) (Ref), cushingoid appearance (Ref), dyslipidemia (Ref), exacerbation of diabetes mellitus (Ref), hyperglycemia (Ref), impaired glucose tolerance (Ref), moon face (Ref), redistribution of body fat (Ref)
Gastrointestinal: Abdominal distention (Ref), peptic ulcer (with possible perforation and hemorrhage) (Ref), ulcerative esophagitis (Ref)
Hematologic & oncologic: Kaposi sarcoma (Ref)
Hypersensitivity: Anaphylaxis (Ref)
Infection: Infection (Ref)
Nervous system: Apathy (Ref), depression (Ref), psychiatric disturbance (dose-dependent; including agitation, anxiety, distractibility, euphoria, fear, hypomania, insomnia, irritability, labile mood, lethargy, pressured speech, restlessness, tearfulness) (Ref)
Neuromuscular & skeletal: Bone fracture (Ref), myopathy (Ref), osteonecrosis (femoral and humeral heads) (Ref), osteoporosis (Ref), steroid myopathy (Ref), vertebral compression fracture (Ref)
Ophthalmic: Glaucoma (Ref), increased intraocular pressure (Ref), retinopathy (Ref) subcapsular posterior cataract (Ref)
Hypersensitivity to prednisone or any component of the formulation; administration of live or live attenuated vaccines with immunosuppressive doses of prednisone; systemic fungal infections.
Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
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.
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children.
• Kaposi sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi sarcoma; clinical improvement may occur with prednisone discontinuation.
Disease-related concerns:
• Bariatric surgery: Presurgical assessment of the indication for use, symptoms, and goals of therapy should be documented to enable postsurgical assessment. Monitor for continued efficacy after bariatric surgery and consider switching to an alternate medication if treatment failure or ulceration occurs.
• 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 patients with hyperthyroidism and decreases in patients with hypothyroidism.
Special populations:
• Older adult: Use with caution in older adults with the smallest possible effective dose for the shortest duration.
• Pediatric: May affect growth velocity; growth 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).
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
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): $0.09 - $0.91
20 mg (per each): $0.15 - $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.
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.
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.
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: Prednisone is available as a delayed-release formulation and the release characteristics may be significantly altered in an unknown manner in patients who have undergone bariatric surgery; providers should determine if the condition being treated can be safety monitored or if a switch to an alternative formulation is necessary (Ref). Prednisone is also available in an IR formulation. Consider minimizing dose and duration to mitigate the risk of GI irritation or ulceration. Proton pump inhibitor therapy is recommended if therapy is to continue chronically (Ref).
Oral solution, concentrate: Administer only with provided calibrated dropper.
Store at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F). Protect from light and moisture.
Oral solution, concentrate: Discard opened bottle after 90 days.
Note: Approved indications and ages vary by product; see product-specific labeling for details.
Anti-inflammatory or immunosuppressant agent in the treatment of a variety of diseases, including those of allergic, hematologic (eg, immune thrombocytopenia, autoimmune hemolytic anemia), dermatologic, gastrointestinal (eg, Crohn disease, ulcerative colitis), inflammatory, ophthalmic, neoplastic, rheumatic (eg, acute gouty arthritis, dermatomyositis/polymyositis, rheumatoid arthritis [including juvenile idiopathic arthritis], systemic lupus erythematosus), autoimmune, nervous system (eg, acute exacerbations of multiple sclerosis), renal (eg, nephrotic syndrome), respiratory (eg, asthma), and endocrine (eg, primary or secondary adrenocorticoid deficiency) origin (Immediate release: FDA approved in pediatric patients [age not specified] and adults; delayed release [Rayos]: FDA approved in pediatric patients [age not specified] and adults); solid organ rejection (acute/chronic) (delayed release [Rayos]: FDA approved in pediatric patients [age not specified] and adults); has also been used for treatment of Bell palsy, autoimmune hepatitis, Duchenne muscular dystrophy (DMD), infantile hemangioma, Kawasaki disease, and Pneumocystis jirovecii pneumonia (PCP).
PredniSONE may be confused with methylPREDNISolone, Pramosone, prazosin, prednisoLONE, PriLOSEC, primidone, promethazine
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drugs (pediatric liquid medications requiring measurement) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Community/Ambulatory Care Settings).
Prednisone is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age) as osteoarthritis treatment (unless as periodic intra-articular use) or long-term monotherapy (>3 months) for rheumatoid arthritis. In addition, some disease states of concern include heart failure, peptic ulcer disease, erosive esophagitis, and chronic obstructive pulmonary disease (inhaled therapies preferred) (O’Mahony 2023).
Substrate of CYP3A4 (Major with inducers), CYP3A4 (Minor with inhibitors); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program
Abrocitinib: Corticosteroids (Systemic) may increase immunosuppressive effects 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 increase adverse/toxic effects of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor
Aldesleukin: Corticosteroids (Systemic) may decrease therapeutic effects of Aldesleukin. Risk X: Avoid
Amphotericin B: Corticosteroids (Systemic) may increase hypokalemic effects of Amphotericin B. Risk C: Monitor
Androgens: Corticosteroids (Systemic) may increase fluid-retaining effects of Androgens. Risk C: Monitor
Antacids: May decrease 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 decrease therapeutic effects of Antidiabetic Agents. Risk C: Monitor
Antithymocyte Globulin (Equine): Corticosteroids (Systemic) may increase adverse/toxic effects of Antithymocyte Globulin (Equine). Specifically, these effects may be unmasked if the dose of systemic corticosteroid is reduced. Corticosteroids (Systemic) may increase immunosuppressive effects of Antithymocyte Globulin (Equine). Specifically, infections may occur with greater severity and/or atypical presentations. Risk C: Monitor
Baricitinib: Corticosteroids (Systemic) may increase immunosuppressive effects 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 decrease therapeutic effects of BCG Products. Corticosteroids (Systemic) may increase adverse/toxic effects of BCG Products. Specifically, the risk of vaccine-associated infection may be increased. Risk X: Avoid
Bile Acid Sequestrants: May decrease absorption of Corticosteroids (Oral). Risk C: Monitor
Brincidofovir: Corticosteroids (Systemic) may decrease therapeutic effects of Brincidofovir. Risk C: Monitor
Brivudine: May increase adverse/toxic effects of Corticosteroids (Systemic). Risk X: Avoid
Calcitriol (Systemic): Corticosteroids (Systemic) may decrease therapeutic effects of Calcitriol (Systemic). Risk C: Monitor
CAR-T Cell Immunotherapy: Corticosteroids (Systemic) may decrease therapeutic effects of CAR-T Cell Immunotherapy. Corticosteroids (Systemic) may increase adverse/toxic effects of CAR-T Cell Immunotherapy. Specifically, the severity and duration of neurologic toxicities may be increased. 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
Cardiac Glycosides: Corticosteroids (Systemic) may increase adverse/toxic effects of Cardiac Glycosides. Risk C: Monitor
Chikungunya Vaccine (Live): Corticosteroids (Systemic) may increase adverse/toxic effects of Chikungunya Vaccine (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may decrease therapeutic effects of Chikungunya Vaccine (Live). Risk X: Avoid
Cladribine: Corticosteroids (Systemic) may increase immunosuppressive effects of Cladribine. Risk X: Avoid
Coccidioides immitis Skin Test: Coadministration of Corticosteroids (Systemic) and Coccidioides immitis Skin Test may alter diagnostic results. 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 decrease therapeutic effects of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Risk C: Monitor
Cosyntropin: Coadministration of Corticosteroids (Systemic) and Cosyntropin may alter diagnostic results. Risk C: Monitor
COVID-19 Vaccine (Inactivated Virus): Corticosteroids (Systemic) may decrease therapeutic effects of COVID-19 Vaccine (Inactivated Virus). Risk C: Monitor
COVID-19 Vaccine (mRNA): Corticosteroids (Systemic) may decrease therapeutic effects 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 decrease therapeutic effects of COVID-19 Vaccine (Subunit). Risk C: Monitor
CycloSPORINE (Systemic): May increase neuroexcitatory and/or seizure-potentiating effects of PredniSONE. PredniSONE may decrease serum concentration of CycloSPORINE (Systemic). CycloSPORINE (Systemic) may increase active metabolite exposure of PredniSONE. Risk C: Monitor
CYP3A4 Inducers (Moderate): May decrease serum concentration of PredniSONE. Risk C: Monitor
CYP3A4 Inducers (Strong): May decrease serum concentration of PredniSONE. Risk C: Monitor
CYP3A4 Inhibitors (Strong): May increase serum concentration of PredniSONE. Risk C: Monitor
Deferasirox: Corticosteroids (Systemic) may increase adverse/toxic effects of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor
Dengue Tetravalent Vaccine (Live): Corticosteroids (Systemic) may decrease therapeutic effects of Dengue Tetravalent Vaccine (Live). Corticosteroids (Systemic) may increase adverse/toxic effects of Dengue Tetravalent Vaccine (Live). Specifically, the risk of vaccine associated infection may be increased. Risk X: Avoid
Denosumab: May increase immunosuppressive effects 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 increase anticoagulant effects 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 increase hyponatremic effects of Desmopressin. Risk X: Avoid
Deucravacitinib: May increase immunosuppressive effects of Corticosteroids (Systemic). Management: The use of deucravacitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider Therapy Modification
Dinutuximab Beta: Corticosteroids (Systemic) may increase immunosuppressive effects of Dinutuximab Beta. Management: Corticosteroids are not recommended for 2 weeks prior to dinutuximab beta, during therapy and for 1 week after treatment. Doses equivalent to over 2 mg/kg or 20 mg/day of prednisone (persons over 10 kg) for 2 or more weeks are considered immunosuppressive Risk D: Consider Therapy Modification
Disulfiram: May increase adverse/toxic effects of Products Containing Ethanol. Management: Do not use disulfiram with dosage forms that contain ethanol. Risk X: Avoid
Estrogen Derivatives: May increase serum concentration of Corticosteroids (Systemic). Risk C: Monitor
Etrasimod: Corticosteroids (Systemic) may increase immunosuppressive effects of Etrasimod. Risk C: Monitor
Filgotinib: Corticosteroids (Systemic) may increase immunosuppressive effects 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: Coadministration of Corticosteroids (Systemic) and Gallium Ga 68 Dotatate may alter diagnostic results. Risk C: Monitor
Growth Hormone Analogs: PredniSONE may decrease therapeutic effects of Growth Hormone Analogs. Growth Hormone Analogs may decrease active metabolite exposure of PredniSONE. Risk C: Monitor
Hyaluronidase: Corticosteroids (Systemic) may decrease therapeutic effects of Hyaluronidase. Management: Patients receiving corticosteroids (particularly at larger doses) may not experience the desired clinical response to standard doses of hyaluronidase. Larger doses of hyaluronidase may be required. Risk D: Consider Therapy Modification
Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies): Corticosteroids (Systemic) may decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Management: Carefully consider the need for corticosteroids, at doses of a prednisone-equivalent of 10 mg or more per day, during the initiation of immune checkpoint inhibitor therapy. Use of corticosteroids to treat immune related adverse events is still recommended Risk D: Consider Therapy Modification
Indium 111 Capromab Pendetide: Coadministration of Corticosteroids (Systemic) and Indium 111 Capromab Pendetide may alter diagnostic results. Risk X: Avoid
Inebilizumab: Corticosteroids (Systemic) may increase immunosuppressive effects of Inebilizumab. Risk C: Monitor
Influenza Virus Vaccines: Corticosteroids (Systemic) may decrease therapeutic effects 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 serum concentration of Isoniazid. Risk C: Monitor
Leflunomide: Corticosteroids (Systemic) may increase immunosuppressive effects 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 serum concentration of Corticosteroids (Systemic). Risk C: Monitor
Loop Diuretics: Corticosteroids (Systemic) may increase hypokalemic effects of Loop Diuretics. Risk C: Monitor
Lutetium Lu 177 Dotatate: Corticosteroids (Systemic) may decrease therapeutic effects 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: Coadministration of Corticosteroids (Systemic) and Macimorelin may alter diagnostic results. Risk X: Avoid
Methotrimeprazine: May increase CNS depressant effects of Products Containing Ethanol. Management: Avoid products containing alcohol in patients treated with methotrimeprazine. Risk X: Avoid
MetroNIDAZOLE (Systemic): May increase adverse/toxic effects of Products Containing Ethanol. A disulfiram-like reaction may occur. Risk X: Avoid
MetroNIDAZOLE (Topical): May increase adverse/toxic effects of Products Containing Ethanol. A disulfiram-like reaction may occur. Risk C: Monitor
MetyraPONE: Coadministration of Corticosteroids (Systemic) and MetyraPONE may alter diagnostic results. Management: Consider alternatives to the use of the metyrapone test in patients taking systemic corticosteroids. Risk D: Consider Therapy Modification
Mifamurtide: Corticosteroids (Systemic) may decrease therapeutic effects of Mifamurtide. Risk X: Avoid
MiFEPRIStone: May decrease therapeutic effects of Corticosteroids (Systemic). MiFEPRIStone may increase 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
Mumps- Rubella- or Varicella-Containing Live Vaccines: Corticosteroids (Systemic) may decrease therapeutic effects of Mumps- Rubella- or Varicella-Containing Live Vaccines. Corticosteroids (Systemic) may increase adverse/toxic effects of Mumps- Rubella- or Varicella-Containing Live Vaccines. Specifically, the risk of vaccine-associated infection may be increased. Risk X: Avoid
Nadofaragene Firadenovec: Corticosteroids (Systemic) may increase adverse/toxic effects of Nadofaragene Firadenovec. Specifically, the risk of disseminated adenovirus infection may be increased. Risk X: Avoid
Natalizumab: Corticosteroids (Systemic) may increase immunosuppressive effects of Natalizumab. Risk X: Avoid
Neuromuscular-Blocking Agents (Nondepolarizing): May increase adverse neuromuscular effects 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 increase adverse/toxic effects of Nicorandil. Gastrointestinal perforation has been reported in association with this combination. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): Corticosteroids (Systemic) may increase adverse/toxic effects of Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective). Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Nonselective): Corticosteroids (Systemic) may increase adverse/toxic effects of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Topical): May increase adverse/toxic effects of Corticosteroids (Systemic). Specifically, the risk of gastrointestinal bleeding, ulceration, and perforation may be increased. Risk C: Monitor
Ocrelizumab: Corticosteroids (Systemic) may increase immunosuppressive effects of Ocrelizumab. Risk C: Monitor
Ofatumumab: Corticosteroids (Systemic) may increase immunosuppressive effects of Ofatumumab. Risk C: Monitor
Ozanimod: Corticosteroids (Systemic) may increase immunosuppressive effects of Ozanimod. Risk C: Monitor
Pidotimod: Corticosteroids (Systemic) may decrease therapeutic effects of Pidotimod. Risk C: Monitor
Pimecrolimus: May increase immunosuppressive effects of Corticosteroids (Systemic). Risk X: Avoid
Pneumococcal Vaccines: Corticosteroids (Systemic) may decrease therapeutic effects of Pneumococcal Vaccines. Risk C: Monitor
Poliovirus Vaccine (Live/Trivalent/Oral): Corticosteroids (Systemic) may decrease therapeutic effects of Poliovirus Vaccine (Live/Trivalent/Oral). Corticosteroids (Systemic) may increase adverse/toxic effects of Poliovirus Vaccine (Live/Trivalent/Oral). Specifically, the risk of vaccine-associated infection may be increased. Risk X: Avoid
Polymethylmethacrylate: Corticosteroids (Systemic) may increase adverse/toxic effects 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 increase adverse/toxic effects of Quinolones. Specifically, the risk of tendonitis and tendon rupture may be increased. Risk C: Monitor
Rabies Vaccine: Corticosteroids (Systemic) may decrease therapeutic effects of Rabies Vaccine. Management: Complete rabies vaccination at least 2 weeks before initiation of immunosuppressant therapy if possible. If combined, check for rabies antibody titers, and if vaccination is for post exposure prophylaxis, administer a 5th dose of the vaccine. Risk D: Consider Therapy Modification
Ritlecitinib: Corticosteroids (Systemic) may increase immunosuppressive effects of Ritlecitinib. Risk X: Avoid
Ritodrine: Corticosteroids (Systemic) may increase adverse/toxic effects of Ritodrine. Risk C: Monitor
Ruxolitinib (Topical): Corticosteroids (Systemic) may increase immunosuppressive effects of Ruxolitinib (Topical). Risk X: Avoid
Salicylates: May increase adverse/toxic effects of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Risk C: Monitor
Sargramostim: Corticosteroids (Systemic) may increase therapeutic effects of Sargramostim. Specifically, corticosteroids may enhance the myeloproliferative effects of sargramostim. Risk C: Monitor
Secnidazole: Products Containing Ethanol may increase adverse/toxic effects of Secnidazole. Risk X: Avoid
Sipuleucel-T: Corticosteroids (Systemic) may decrease therapeutic effects 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
Sitafloxacin: Corticosteroids (Systemic) may increase adverse/toxic effects of Sitafloxacin. Specifically, the risk of tendonitis and tendon rupture may be increased. Management: Consider alternatives to coadministration of corticosteroids and sitafloxacin unless the benefits of coadministration outweigh the risk of tendon disorders. Risk D: Consider Therapy Modification
Sodium Benzoate: Corticosteroids (Systemic) may decrease therapeutic effects of Sodium Benzoate. Risk C: Monitor
Sphingosine 1-Phosphate (S1P) Receptor Modulators: May increase immunosuppressive effects of Corticosteroids (Systemic). Risk C: Monitor
Succinylcholine: Corticosteroids (Systemic) may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor
Tacrolimus (Systemic): Corticosteroids (Systemic) may decrease serum concentration of Tacrolimus (Systemic). Conversely, when discontinuing corticosteroid therapy, tacrolimus concentrations may increase. Risk C: Monitor
Tacrolimus (Topical): Corticosteroids (Systemic) may increase immunosuppressive effects of Tacrolimus (Topical). Risk X: Avoid
Talimogene Laherparepvec: Corticosteroids (Systemic) may increase adverse/toxic effects 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
Tertomotide: Corticosteroids (Systemic) may decrease therapeutic effects of Tertomotide. Risk X: Avoid
Tesamorelin: May decrease active metabolite exposure of PredniSONE. Risk C: Monitor
Thiazide and Thiazide-Like Diuretics: Corticosteroids (Systemic) may increase hypokalemic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor
Tofacitinib: Corticosteroids (Systemic) may increase immunosuppressive effects 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 decrease therapeutic effects of Typhoid Vaccine. Corticosteroids (Systemic) may increase adverse/toxic effects of Typhoid Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Risk X: Avoid
Ublituximab: Corticosteroids (Systemic) may increase immunosuppressive effects of Ublituximab. Risk C: Monitor
Upadacitinib: Corticosteroids (Systemic) may increase immunosuppressive effects 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 decrease therapeutic effects 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
Vaccines (Live): Corticosteroids (Systemic) may increase adverse/toxic effects of Vaccines (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may decrease therapeutic effects of Vaccines (Live). Management: Avoid live vaccines during and for 1 month after therapy with immunosuppressive doses of corticosteroids (equivalent to prednisone > 2 mg/kg or 20 mg/day in persons over 10 kg for at least 2 weeks). Give live vaccines 4 weeks prior to therapy if possible. Risk D: Consider Therapy Modification
Vaccines (Non-Live/Inactivated/Non-Replicating): Corticosteroids (Systemic) may decrease therapeutic effects of Vaccines (Non-Live/Inactivated/Non-Replicating). Management: Administer vaccines at least 2 weeks prior to immunosuppressive corticosteroids if possible. If patients are vaccinated less than 14 days prior to or during such therapy, repeat vaccination at least 3 months after therapy if immunocompetence restored. Risk D: Consider Therapy Modification
Vitamin K Antagonists: Corticosteroids (Systemic) may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor
Yellow Fever Vaccine: Corticosteroids (Systemic) may increase adverse/toxic effects of Yellow Fever Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may decrease therapeutic effects of Yellow Fever Vaccine. Risk X: Avoid
Zoster Vaccine (Live/Attenuated): Corticosteroids (Systemic) may increase adverse/toxic effects of Zoster Vaccine (Live/Attenuated). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may decrease therapeutic effects of Zoster Vaccine (Live/Attenuated). Risk X: Avoid
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
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. Maternal asthma symptoms should be monitored every 4 to 6 weeks during pregnancy (ERS/TSANZ [Middleton 2020]; GINA 2024).
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).
Blood pressure; weight; serum glucose; electrolytes; growth in pediatric patients; bone mineral density; assess hypothalamic-pituitary-adrenal (HPA) axis suppression (eg, ACTH stimulation test, morning plasma cortisol test, urinary free cortisol test); hemoglobin, occult blood loss. Monitor intraocular pressure with therapy >6 weeks.
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.
