(PRED ni sone)
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
PredniSONE Intensol: 5 mg/mL (30 mL) [contains alcohol, usp; unflavored flavor]
Generic: 5 mg/5 mL (5 mL [DSC], 120 mL, 500 mL)
Deltasone: 20 mg [scored; contains fd&c yellow #10 aluminum lake, fd&c yellow #6 aluminum lake]
Generic: 1 mg, 2.5 mg, 5 mg, 10 mg, 20 mg, 50 mg, 10 mg, 5 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)
Brand Names: U.S.
- PredniSONE Intensol
- Corticosteroid, Systemic
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.
50% to 90% (may be altered in hepatic failure, chronic renal failure, inflammatory bowel disease, hyperthyroidism, and in the elderly) (Frey 1990)
Hepatic to metabolite prednisolone (active)
Urine (as conjugates)
Time to Peak
Oral: Immediate-release tablet: 2 hours; Delayed-release tablet: 6 to 6.5 hours
2 to 3 hours
Concentration dependent: <50% (Frey 1990)
Special Populations: 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.
Use: Labeled Indications
Allergic states: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in drug hypersensitivity reactions, seasonal or perennial allergic rhinitis; serum sickness.
Dermatologic diseases: Atopic dermatitis; bullous dermatitis herpetiformis; contact dermatitis; exfoliative dermatitis/erythroderma; mycosis fungoides; pemphigus; severe erythema multiforme (Stevens-Johnson syndrome).
Immediate-release only: Severe psoriasis, severe seborrheic dermatitis.
Endocrine disorders: Congenital adrenal hyperplasia; hypercalcemia of malignancy; nonsuppurative thyroiditis; primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice; synthetic analogues may be used in conjunction with mineralocorticoids where applicable.
GI diseases: During acute episodes in regional enteritis (Crohn disease) and ulcerative colitis.
Hematologic disorders: Acquired (autoimmune) hemolytic anemia; congenital (erythroid) hypoplastic anemia/Diamond-Blackfan anemia; immune thrombocytopenia (formerly known as idiopathic thrombocytopenic purpura) in adults; secondary thrombocytopenia in adults.
Delayed-release only: Pure red cell aplasia.
Immediate-release only: Erythroblastopenia (red blood cell anemia).
Delayed-release only: Treatment of acute leukemia and aggressive lymphomas.
Immediate-release only: Palliative management of leukemias and lymphomas in adults; acute leukemia of childhood.
Nervous system (delayed-release only): Acute exacerbations of multiple sclerosis; cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Note: Treatment guidelines recommend the use of high dose IV or oral methylprednisolone for acute exacerbations of multiple sclerosis (Scott 2011; NICE 2014).
Delayed-release only: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa, such as sympathetic ophthalmia; uveitis and ocular inflammatory conditions unresponsive to topical steroids.
Immediate-release only: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa, such as allergic conjunctivitis, allergic corneal marginal ulcers, anterior segment inflammation, chorioretinitis, diffuse posterior uveitis and choroiditis, herpes zoster ophthalmicus, iridocyclitis, iritis, keratitis, optic neuritis, sympathetic ophthalmia.
Renal diseases: To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that is caused by lupus erythematosus.
Respiratory diseases: Aspiration pneumonitis; asthma; fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate chemotherapy; symptomatic sarcoidosis.
Delayed-release only: Acute exacerbations of chronic obstructive pulmonary disease (COPD); allergic bronchopulmonary aspergillosis; hypersensitivity pneumonitis; idiopathic bronchiolitis obliterans with organizing pneumonia; idiopathic eosinophilic pneumonias; idiopathic pulmonary fibrosis; Pneumocystis carinii pneumonia (PCP) associated with hypoxemia occurring in an HIV-positive individual who is also under treatment with appropriate anti-PCP antibiotics.
Immediate-release only: Berylliosis; Loeffler syndrome not manageable by other means.
Delayed-release only: During an exacerbation or as maintenance therapy in selected cases of ankylosing spondylitis, dermatomyositis/polymyositis, polymyalgia rheumatica, psoriatic arthritis, relapsing polychondritis, rheumatoid arthritis including juvenile rheumatoid arthritis, Sjögren syndrome, systemic lupus erythematosus, vasculitis.
Immediate-release only: During an exacerbation or as maintenance therapy in selected cases of acute rheumatic carditis, systemic dermatomyositis (polymyositis), systemic lupus erythematosus.
Delayed release only: As adjunctive therapy for short-term administration in acute gouty arthritis.
Immediate-release only: As adjunctive therapy for short-term administration in acute and subacute bursitis; acute gouty arthritis; acute nonspecific tenosynovitis; ankylosing spondylitis; epicondylitis; posttraumatic osteoarthritis; psoriatic arthritis; rheumatoid arthritis including juvenile rheumatoid arthritis; synovitis of osteoarthritis.
Miscellaneous: Trichinosis with neurologic or myocardial involvement; tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy.
Delayed-release only: Acute or chronic solid organ rejection.
Off Label Uses
Acute exacerbation of chronic obstructive pulmonary disease (COPD)
Based on the Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) guidelines, prednisone given for acute exacerbation of chronic obstructive pulmonary disease (COPD) is effective and recommended in the management of this condition.
Based on the American Academy of Otolaryngology, Head and Neck Surgery, Clinical Practice Guideline: Bell's Palsy, prednisone given for Bell palsy is effective and recommended in the management of this condition.
Duchenne muscular dystrophy
Data from a meta-analysis, randomized controlled trials and retrospective cohort studies supports the use of prednisone for increasing muscular strength and function, improving pulmonary function, decreasing timed motor function, delaying development of scoliosis or cardiomyopathy, and delaying surgery for scoliosis in patients with Duchenne muscular dystrophy [Bonifati 2000], [King 2007], [Markham 2008], [Matthews 2016], [Schram 2013].
Based on the American Academy of Neurology guidelines for corticosteroid treatment of Duchenne muscular dystrophy, prednisone probably improves muscle strength and pulmonary function and possibly improves timed motor function, slows the development of scoliosis, reduces the need for scoliosis surgery by age 18, and delays the onset of cardiomyopathy [AAN [Gloss 2016]].
Glucocorticoid remediable aldosteronism, treatment
Based on the Endocrine Society guidelines for the management of primary aldosteronism, prednisone is an effective and recommended treatment to lower ACTH levels in patients with glucocorticoid remediable aldosteronism.
Based on the American Thyroid Association guidelines for the diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, glucocorticoids may be used in select patients being treated with radioiodine therapy to delay development or progression of Graves orbitopathy (GO). Glucocorticoids should be used in patients with active and mild GO who have additional risk factors for worsening GO and may be considered in patients with active and mild GO but without additional risk factors. In patients who smoke but who have no evidence of GO, there is insufficient evidence to recommend for or against prophylactic use of glucocorticoids. Glucocorticoids should not be used in patients with inactive GO or as prophylaxis in patients who do not smoke.
The use of corticosteroids in the treatment of pericarditis remains controversial and is dependent on the underlying cause of pericarditis, choice of steroid, dosing regimen, and route of administration. Current guidelines state that the use of systemic corticosteroids should be restricted to certain types of pericarditis, and published data demonstrate conflicting results regarding the efficacy of prednisone in pericarditis. Generally, prednisone should be reserved for cases of recurrent pericarditis when other therapies have failed. It is important to note that if prednisone is used, it should be started at the appropriate dose and tapered slowly.
Prostate cancer (metastatic)
Data from 2 large randomized phase III studies support the use of prednisone (in combination with abiraterone) in the treatment of metastatic castration-resistant prostate cancer [de Bono 2011], [Ryan 2015]. Data from a randomized phase III study supports the use of prednisone (in combination with cabazitaxel) in the treatment of metastatic castration-resistant prostate cancer which has progressed during or following docetaxel-based therapy [de Bono 2010]. Data from a randomized phase III study supports the use of prednisone (in combination with docetaxel) in the treatment of hormone-refractory metastatic prostate cancer [Berthold 2008], [Tannock 2004].
Based on the American Thyroid Association guidelines for the diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, corticosteroids are recommended for the treatment of subacute thyroiditis in patients who fail to respond to initial NSAID therapy or in patients with moderate to severe pain and/or thyrotoxic symptoms on initial presentation.
Thyrotoxicosis (type 2 amiodarone-induced)
Based on the American Thyroid Association guidelines for the diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, corticosteroid therapy is recommended in patients with overt thyrotoxicosis (type 2 amiodarone-induced). Use in combination with an antithyroid agent if etiology of thyrotoxicosis (eg type 1 or type 2) cannot be unequivocally determined or if patient is too clinically unstable to allow a trial of monotherapy.
Additional Off-Label Uses
Autoimmune hepatitis; Adjunctive therapy for pain management in immunocompetent patients with herpes zoster; Takayasu arteritis; Giant cell arteritis
Hypersensitivity to prednisone or any component of the formulation; administration of live or live attenuated vaccines with immunosuppressive doses of prednisone; systemic fungal infections
Documentation of allergenic cross-reactivity for corticosteroids is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
General dosing; anti-inflammatory/immunosuppressive/endocrine disorders: Oral: Initial: 5 to 60 mg daily:
Note: Dose depends upon condition being treated and response of patient. Consider alternate day therapy for long-term therapy. Discontinuation of long-term therapy requires gradual withdrawal by tapering the dose.
Prednisone taper (other regimens also available):
Day 1: 30 mg divided as 10 mg before breakfast, 5 mg at lunch, 5 mg at dinner, 10 mg at bedtime
Day 2: 5 mg at breakfast, 5 mg at lunch, 5 mg at dinner, 10 mg at bedtime
Day 3: 5 mg 4 times daily (with meals and at bedtime)
Day 4: 5 mg 3 times daily (breakfast, lunch, bedtime)
Day 5: 5 mg 2 times daily (breakfast, bedtime)
Day 6: 5 mg before breakfast
Acute asthma (off-label dose): Oral: 40 to 60 mg/day for 3 to 10 days; administer as single or 2 divided doses (NAEPP 2007).
Acute exacerbations of chronic obstructive pulmonary disease (COPD) (off-label use for immediate release products; off-label dose): Oral: 40 mg once daily for 5 days (GOLD 2014).
Anaphylaxis, adjunctive treatment (off-label dose): Oral: 0.5 mg/kg (Lieberman 2005)
Antineoplastic: Oral: Usual range: 10 mg daily to 100 mg/m2/day (depending on indication). Refer to specific protocol for dosing and administration details.
Autoimmune hepatitis (off-label use): Oral: Initial: 60 mg daily for 1 week, followed by 40 mg daily for 1 week, then 30 mg daily for 2 weeks, then 20 mg daily. Half this dose should be given when used in combination with azathioprine (AASLD [Manns 2010]).
Bell palsy (off-label use): Oral: 60 mg daily for 5 days, followed by a 5-day taper. Treatment should begin within 72 hours of onset of symptoms (OHNS [Baugh 2013]).
Crohn disease, moderate/severe (off-label dose): Oral: 40 to 60 mg daily until resolution of symptoms and resumption of weight gain (usual duration: 7 to 28 days) (Lichtenstein 2009).
Dermatomyositis/polymyositis (off-label dose): Oral: 1 mg/kg daily (range: 0.5 to 1.5 mg/kg/day), often in conjunction with steroid-sparing therapies; depending on response/tolerance, consider slow tapering after 2 to 8 weeks depending on response; taper regimens vary widely, but often involve 5 to 10 mg decrements per week and may require 6 to 12 months to reach a low once-daily or every-other-day dose to prevent disease flare (Briemberg 2003; Hengstman 2009; Iorizzo 2008; Wiendl 2008).
Duchenne muscular dystrophy (off-label use): Oral: 0.75 mg/kg/day or 10 mg/kg/weekend, divided over 2 days. When used daily, the dose may be decreased to 0.3 mg/kg/day in patients who experience adverse reactions. Doses as high as 1.5 mg/kg/day have been studied, but there is no evidence that doses above 0.75 mg/kg/day provide greater efficacy (AAN [Gloss 2016]; Escolar 2011; Matthews 2016).
Giant cell arteritis (off-label use): Oral: Initial: 40 to 60 mg daily; typically requires 1 to 2 years of treatment, but may begin to taper after 2 to 3 months; alternative dosing of 30 to 40 mg daily has demonstrated similar efficacy (Hiratzka 2010).
Glucocorticoid remediable aldosteronism, treatment (off-label use): Oral: Initial: 2.5 to 5 mg once daily preferably at bedtime to suppress early morning ACTH surge (Funder 2016)
Gout, treatment of acute flare (off-label): Oral: Initial: ≥0.5 mg/kg for 5 to 10 days (ACR guidelines [Khanna 2012]) or 30 to 35 mg daily for 3 to 5 days (EULAR [Richette 2017])
Graves orbitopathy (off-label use): Oral: 0.4 to 0.5 mg/kg/day, starting 1 to 3 days after radioactive iodine treatment, and continued for 1 month, then gradually taper over 2 months (Ross 2016).
Herpes zoster (off-label use): Oral: 60 mg daily for 7 days, followed by 30 mg daily for 7 days, then 15 mg daily for 7 days (Dworkin 2007).
Immune thrombocytopenia (off-label dose): Oral: 1 to 2 mg/kg/day (American Society of Hematology 1997).
Immune thrombocytopenia in pregnancy: Initial: 10 to 20 mg/day (ACOG 2016). 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 (ACOG 2016; Neunert 2011).
Lupus nephritis, induction (off-label dose): Oral:
Class III-IV lupus nephritis: 0.5 to 1 mg/kg/day (after glucocorticoid pulse) tapered after a few weeks to lowest effective dose, in combination with an immunosuppressive agent (Hahn 2012).
Class V lupus nephritis: 0.5 mg/kg/day for 6 months in combination mycophenolate mofetil; if not improved after 6 months, use 0.5 to 1 mg/kg/day (after a glucocorticoid pulse) for an additional 6 months in combination with cyclophosphamide (Hahn 2012).
Multiple sclerosis, acute exacerbations:
Note: Treatment guidelines recommend the use of high dose IV or oral methylprednisolone for acute exacerbations of multiple sclerosis (AAN [Scott 2011]; NICE 2014).
Oral: 200 mg daily for 1 week, followed by 80 mg every other day for 1 month.
Pericarditis (off-label use):
Recurrent pericarditis: Oral: 1 to 1.5 mg/kg once daily for at least 1 month; taper dose over a 3-month period (Maisch 2004)
Tuberculosis pericarditis: Oral: 1 to 2 mg/kg once daily for 5 to 7 days followed by 6 to 8 weeks of tapering (Maisch 2004) or 60 mg once daily for 4 weeks, followed by 30 mg once daily for 4 weeks, 15 mg once daily for 2 weeks, and 5 mg once daily for 1 week (Reuter 2006).
Pneumocystis pneumonia (adjunctive therapy) in HIV-infected patients (off-label dose): Oral: 40 mg twice daily for 5 days beginning as early as possible and within 72 hours of PCP therapy, followed by 40 mg once daily on days 6 through 10, followed by 20 mg once daily on days 11 through 21 (DHHS [adult] 2015).
Polymyalgia rheumatica (off-label dose): Oral: Evidence to support an optimal dose and duration are lacking; recommendations provided are general guidelines only. Individualize therapy using the minimum effective dose and duration (Dejaco [EULAR/ACR 2015]):
Initial: Dosage range: 12.5 to 25 mg daily; consider higher doses within this range for patients at high risk of relapse and low risk of adverse events; consider lower doses within this range for patients with high risk factors for side effects (eg, diabetes, osteoporosis, glaucoma). Single daily doses are preferred over divided daily doses. Avoid initial doses ≤7.5 mg/day or >30 mg/day.
Tapering: For initial dosing, taper to a dose of 10 mg/day within 4 to 8 weeks. If relapse occurs, increase dosing to the prerelapse dose and gradually taper back to the dose which relapse occurred within 4 to 8 weeks. Once remission is achieved (initial or relapse therapy), taper daily dose by 1 mg every 4 weeks (or by 1.25 mg decrements if using schedules such as 10 mg and 7.5 mg on alternate days) until discontinuation.
Prostate cancer, metastatic (off-label use): Oral: 5 mg twice daily (in combination with abiraterone) until disease progression or unacceptable toxicity (de Bono 2011; Ryan 2015) or 10 mg once daily (in combination with cabazitaxel) for up to 10 cycles (de Bono 2010) or 5 mg twice daily (in combination with docetaxel) for up to 10 cycles (Berthold 2008; Tannock 2004).
Rheumatoid arthritis (off-label dose): Oral: ≤10 mg daily (American College of Rheumatology 2002).
Subacute thyroiditis (off-label use): Oral: Initial: 40 mg/day for 1 to 2 weeks; gradually taper over 2 to 4 weeks or longer depending on clinical response (Ross 2016).
Takayasu arteritis (off-label use): Oral: Initial: 40 to 60 mg daily; taper to lowest effective dose when ESR and CRP levels are normal; usual duration: 1 to 2 years (Hiratzka 2010).
Thyrotoxicosis, type 2 amiodarone-induced (off-label use): Oral: 40 mg once daily for 14 to 28 days; gradually taper over 2 to 3 months depending on clinical response. Note: Use in combination with an antithyroid agent if etiology of thyrotoxicosis (eg type 1 or type 2) cannot be unequivocally determined or if patient is too clinically unstable to allow a trial of monotherapy (Ross 2016).
Tuberculosis, severe, paradoxical reactions (off-label dose): Oral: 1 mg/kg/day, gradually reduce after 1 to 2 weeks (AIDSinfo guidelines 2008).
Refer to adult dosing; use the lowest effective dose.
General dosing; anti-inflammatory/immunosuppressive/endocrine disorders: Children and Adolescents: Oral: Refer to adult dosing.
Note: Dose depends upon condition being treated and response of patient; dosage for infants and children should be based on severity of the disease and response of the patient rather than on strict adherence to dosage indicated by age, weight, or body surface area. Consider alternate day therapy for long-term therapy. Discontinuation of long-term therapy requires gradual withdrawal by tapering the dose.
Acute asthma (off-label dose): Oral:
Infants and Children <12 years: 1 to 2 mg/kg/day for 3 to 10 days (maximum: 60 mg/day) (NAEPP 2007).
Children ≥12 years and Adolescents: Refer to adult dosing.
Antineoplastic: Children and Adolescents: Oral: Refer to adult dosing or to specific protocol.
Autoimmune hepatitis (monotherapy or in combination with azathioprine) (off-label use): Infants, Children, and Adolescents: Oral: Initial: 1 to 2 mg/kg/day for 2 weeks (maximum: 60 mg/day), followed by a taper over 6 to 8 weeks to a dose of 0.1 to 0.2 mg/kg/day or 2.5 to 5 mg daily (AASLD [Manns 2010]; Della Corte 2012).
Bell palsy (off-label use):
Infants, Children, and Adolescents <16 years: Oral: 1 mg/kg/day for 1 week, then taper over 1 week; ideally start within the 72 hours of onset of symptoms; maximum daily dose: 60 mg/day
Adolescents ≥16 years: Oral: Refer to adult dosing.
Duchenne muscular dystrophy (off-label use): Children ≥ 4 years and Adolescents: Oral: 0.75 mg/kg/day or 10 mg/kg/weekend, divided over 2 days. The dose may be decreased to 0.3 mg/kg/day in patients who experience adverse reactions. Doses as high as 1.5 mg/kg/day have been studied, but there is no evidence that doses above 0.75 mg/kg/day provide greater efficacy (AAN [Gloss 2016]; Escolar 2011; Matthews 2016).
Nephrotic syndrome; steroid sensitive (SSNS) (off-label dose): Children and Adolescents: Oral:
Initial episode: 2 mg/kg/day or 60 mg/m2/day once daily, maximum daily dose: 60 mg/day for 4 to 6 weeks; then adjust to an alternate-day schedule of 1.5 mg/kg/dose or 40 mg/m2/dose on alternate days as a single dose, maximum dose: 40 mg/dose (Gipson 2009; KDIGO 2012; KDOQI 2013); duration of therapy based on patient response.
Relapse: 2 mg/kg/day or 60 mg/m2/day once daily, maximum daily dose: 60 mg/day, continue until complete remission for at least 3 days; then adjust to an alternate-day schedule of 1.5 mg/kg/dose or 40 mg/m2/dose on alternate days as a single dose, maximum dose: 40 mg/dose, recommended duration of alternate day dosing is variable: may continue for at least 4 weeks then taper. Longer duration of treatment may be necessary in patients who relapse frequently, some patients may require up to 3 months of treatment (Gipson 2009; KDIGO 2012; KDOQI 2013).
Maintenance therapy for frequently relapsing SSNS: Taper previous dose down to lowest effective dose which maintains remission using an alternate day schedule; usual effective range: 0.1 to 0.5 mg/kg/day on alternating days; other patients may require doses up to 0.7 mg/kg/dose every other day (KDIGO 2012; KDOQI 2013).
Pneumocystis pneumonia (adjunctive therapy) in HIV-infected patients (off-label dose): Oral:
Infants and Children: 1 mg/kg twice daily on days 1 to 5, followed by 0.5 to 1 mg/kg twice daily on days 6 to 10, followed by 0.5 mg/kg once daily on days 11 through 21 (DHHS [pediatric] 2013).
Adolescents: Refer to adult dosing.
Dosing: Renal Impairment
There are no dosage adjustments provided in the manufacturer’s labeling.
Hemodialysis: Supplemental dose is not necessary.
Dosing: Hepatic Impairment
There are no dosage adjustments provided in the manufacturer's labeling.
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.
Oral solution, concentrate: Administer only with provided calibrated dropper.
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
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.
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Monitor therapy
Aldesleukin: Corticosteroids may diminish the antineoplastic effect of Aldesleukin. Avoid combination
Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Monitor therapy
Androgens: Corticosteroids (Systemic) may enhance the fluid-retaining effect of Androgens. Monitor therapy
Antacids: May decrease the bioavailability of Corticosteroids (Oral). Management: Consider separating doses by 2 or more hours. Budesonide enteric coated tablets could dissolve prematurely if given with drugs that lower gastric acid, with unknown impact on budesonide therapeutic effects. Consider therapy modification
Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Monitor therapy
Aprepitant: May increase the serum concentration of Corticosteroids (Systemic). Management: No dose adjustment is needed for single 40 mg aprepitant doses. For other regimens, reduce oral dexamethasone or methylprednisolone doses by 50%, and IV methylprednisolone doses by 25%. Antiemetic regimens containing dexamethasone reflect this adjustment. Consider therapy modification
Axicabtagene Ciloleucel: Corticosteroids (Systemic) may diminish the therapeutic effect of Axicabtagene Ciloleucel. Management: Avoid use of corticosteroids as premedication before axicabtagene ciloleucel. Corticosteroids may, however, be required for treatment of cytokine release syndrome or neurologic toxicity. Consider therapy modification
BCG (Intravesical): Immunosuppressants may diminish the therapeutic effect of BCG (Intravesical). Avoid combination
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Monitor therapy
Boceprevir: May increase the serum concentration of PredniSONE. Monitor therapy
Calcitriol (Systemic): Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol (Systemic). Monitor therapy
Ceritinib: Corticosteroids may enhance the hyperglycemic effect of Ceritinib. Monitor therapy
Coccidioides immitis Skin Test: Immunosuppressants may diminish the diagnostic effect of Coccidioides immitis Skin Test. Monitor therapy
Corticorelin: Corticosteroids may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Monitor therapy
CycloSPORINE (Systemic): May increase serum concentrations of the active metabolite(s) of PredniSONE. PredniSONE may decrease the serum concentration of CycloSPORINE (Systemic). PredniSONE may increase the serum concentration of CycloSPORINE (Systemic). Monitor therapy
CYP3A4 Inducers (Strong): May decrease the serum concentration of PredniSONE. Monitor therapy
CYP3A4 Inhibitors (Strong): May increase the serum concentration of PredniSONE. Monitor therapy
Deferasirox: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Monitor therapy
Deferasirox: Corticosteroids may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Monitor therapy
Denosumab: May enhance the adverse/toxic effect of Immunosuppressants. Specifically, the risk for serious infections may be increased. Monitor therapy
Desirudin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Desirudin. More specifically, corticosteroids may increase hemorrhagic risk during desirudin treatment. Management: Discontinue treatment with systemic corticosteroids prior to desirudin initiation. If concomitant use cannot be avoided, monitor patients receiving these combinations closely for clinical and laboratory evidence of excessive anticoagulation. Consider therapy modification
Desmopressin: Corticosteroids (Systemic) may enhance the hyponatremic effect of Desmopressin. Avoid combination
DilTIAZem: May increase the serum concentration of Corticosteroids (Systemic). Monitor therapy
Echinacea: May diminish the therapeutic effect of Immunosuppressants. Consider therapy modification
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Monitor therapy
Fingolimod: Immunosuppressants may enhance the immunosuppressive effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and other immunosuppressants when possible. If combined, monitor patients closely for additive immunosuppressant effects (eg, infections). Consider therapy modification
Fluconazole: May increase the serum concentration of PredniSONE. Monitor therapy
Fosaprepitant: May increase the serum concentration of Corticosteroids (Systemic). The active metabolite aprepitant is likely responsible for this effect. Consider therapy modification
Hyaluronidase: Corticosteroids may diminish the therapeutic effect of Hyaluronidase. Management: Patients receiving corticosteroids (particularly at larger doses) may not experience the desired clinical response to standard doses of hyaluronidase. Larger doses of hyaluronidase may be required. Consider therapy modification
Indacaterol: May enhance the hypokalemic effect of Corticosteroids (Systemic). Monitor therapy
Indium 111 Capromab Pendetide: Corticosteroids (Systemic) may diminish the diagnostic effect of Indium 111 Capromab Pendetide. Avoid combination
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Monitor therapy
Leflunomide: Immunosuppressants may enhance the adverse/toxic effect of Leflunomide. Specifically, the risk for hematologic toxicity such as pancytopenia, agranulocytosis, and/or thrombocytopenia may be increased. Management: Consider not using a leflunomide loading dose in patients receiving other immunosuppressants. Patients receiving both leflunomide and another immunosuppressant should be monitored for bone marrow suppression at least monthly. Consider therapy modification
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Monitor therapy
Mifamurtide: Corticosteroids (Systemic) may diminish the therapeutic effect of Mifamurtide. Avoid combination
MiFEPRIStone: May diminish the therapeutic effect of Corticosteroids (Systemic). MiFEPRIStone may increase the serum concentration of Corticosteroids (Systemic). Management: Avoid mifepristone in patients who require long-term corticosteroid treatment of serious illnesses or conditions (e.g., for immunosuppression following transplantation). Corticosteroid effects may be reduced by mifepristone treatment. Avoid combination
Mitotane: May decrease the serum concentration of Corticosteroids (Systemic). Consider therapy modification
Natalizumab: Immunosuppressants may enhance the adverse/toxic effect of Natalizumab. Specifically, the risk of concurrent infection may be increased. Avoid combination
Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse neuromuscular effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Consider therapy modification
Nicorandil: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nicorandil. Gastrointestinal perforation has been reported in association with this combination. Monitor therapy
Nivolumab: Immunosuppressants may diminish the therapeutic effect of Nivolumab. Consider therapy modification
Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective). Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Monitor therapy
Ocrelizumab: May enhance the immunosuppressive effect of Immunosuppressants. Monitor therapy
Pidotimod: Immunosuppressants may diminish the therapeutic effect of Pidotimod. Monitor therapy
Pimecrolimus: May enhance the adverse/toxic effect of Immunosuppressants. Avoid combination
Quinolones: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolones. Specifically, the risk of tendonitis and tendon rupture may be increased. Monitor therapy
Ritonavir: May increase the serum concentration of PredniSONE. Monitor therapy
Roflumilast: May enhance the immunosuppressive effect of Immunosuppressants. Consider therapy modification
Salicylates: May enhance the adverse/toxic effect of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease the serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Monitor therapy
Sargramostim: Corticosteroids (Systemic) may enhance the therapeutic effect of Sargramostim. Specifically, corticosteroids may enhance the myeloproliferative effects of sargramostim. Monitor therapy
Sipuleucel-T: Immunosuppressants may diminish the therapeutic effect of Sipuleucel-T. Monitor therapy
Somatropin: May diminish the therapeutic effect of PredniSONE. Growth hormone may reduce the conversion of prednisone to the active prednisolone metabolite. Consider therapy modification
Tacrolimus (Systemic): Corticosteroids (Systemic) may decrease the serum concentration of Tacrolimus (Systemic). Conversely, when discontinuing corticosteroid therapy, tacrolimus concentrations may increase. Monitor therapy
Tacrolimus (Topical): May enhance the adverse/toxic effect of Immunosuppressants. Avoid combination
Telaprevir: Corticosteroids (Systemic) may decrease the serum concentration of Telaprevir. Telaprevir may increase the serum concentration of Corticosteroids (Systemic). Management: Concurrent use of telaprevir and systemic corticosteroids is not recommended. When possible, consider alternatives. If used together, employ extra caution and monitor closely for excessive corticosteroid effects and diminished telaprevir effects. Consider therapy modification
Tertomotide: Immunosuppressants may diminish the therapeutic effect of Tertomotide. Monitor therapy
Tesamorelin: May decrease serum concentrations of the active metabolite(s) of PredniSONE. Consider therapy modification
Thiazide and Thiazide-Like Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. Monitor therapy
Tisagenlecleucel: Corticosteroids (Systemic) may diminish the therapeutic effect of Tisagenlecleucel. Management: Avoid use of corticosteroids as premedication or at any time during treatment with tisagenlecleucel, except in the case of life-threatening emergency (such as resistant cytokine release syndrome). Consider therapy modification
Tofacitinib: Immunosuppressants may enhance the immunosuppressive effect of Tofacitinib. Management: Concurrent use with antirheumatic doses of methotrexate or nonbiologic disease modifying antirheumatic drugs (DMARDs) is permitted, and this warning seems particularly focused on more potent immunosuppressants. Consider therapy modification
Trastuzumab: May enhance the neutropenic effect of Immunosuppressants. Monitor therapy
Urea Cycle Disorder Agents: Corticosteroids (Systemic) may diminish the therapeutic effect of Urea Cycle Disorder Agents. More specifically, Corticosteroids (Systemic) may increase protein catabolism and plasma ammonia concentrations, thereby increasing the doses of Urea Cycle Disorder Agents needed to maintain these concentrations in the target range. Monitor therapy
Vaccines (Inactivated): Immunosuppressants may diminish the therapeutic effect of Vaccines (Inactivated). Management: Vaccine efficacy may be reduced. Complete all age-appropriate vaccinations at least 2 weeks prior to starting an immunosuppressant. If vaccinated during immunosuppressant therapy, revaccinate at least 3 months after immunosuppressant discontinuation. Consider therapy modification
Vaccines (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Vaccines (Live). Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Live). Management: Doses equivalent to less than 2 mg/kg or 20 mg per day of prednisone administered for less than 2 weeks are not considered sufficiently immunosuppressive to create vaccine safety concerns. Higher doses and longer durations should be avoided. Consider therapy modification
Warfarin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Warfarin. Monitor therapy
Decreased response to skin tests
Frequency not defined.
Cardiovascular: Cardiac failure (in susceptible patients), hypertension
Central nervous system: Emotional lability, headache, increased intracranial pressure (with papilledema), myasthenia, psychiatric disturbance (including euphoria, insomnia, mood swings, personality changes, severe depression), seizure, vertigo
Dermatologic: Diaphoresis, facial erythema, skin atrophy, urticaria
Endocrine & metabolic: Cushing’s syndrome, decreased serum potassium, diabetes mellitus, fluid retention, growth suppression (children), hypokalemic alkalosis, hypothyroidism (enhanced), menstrual disease, negative nitrogen balance (due to protein catabolism), sodium retention
Gastrointestinal: Abdominal distention, carbohydrate intolerance, pancreatitis, peptic ulcer (with possible perforation and hemorrhage), ulcerative esophagitis
Hematologic & oncologic: Bruise, Kaposi’s sarcoma, petechia
Hepatic: Increased serum alkaline phosphatase, increased serum ALT, increased serum AST
Hypersensitivity: Anaphylaxis, hypersensitivity reaction
Neuromuscular & skeletal: Amyotrophy, aseptic necrosis of bones (femoral and humeral heads), osteoporosis, pathological fracture (long bones), rupture of tendon (particularly Achilles tendon), steroid myopathy, vertebral compression fracture
Ophthalmic: Exophthalmos, glaucoma, increased intraocular pressure, subcapsular posterior cataract
Miscellaneous: Wound healing impairment
<1% (Limited to important or life-threatening): Venous thrombosis (Johannesdottir 2013)
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children or in patients receiving high doses for prolonged periods. HPA axis suppression may lead to adrenal crisis. Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully. Particular care is required when patients are transferred from systemic corticosteroids to inhaled products due to possible adrenal insufficiency or withdrawal from steroids, including an increase in allergic symptoms. Patients receiving >20 mg per day of prednisone (or equivalent) may be most susceptible. Fatalities have occurred due to adrenal insufficiency in asthmatic patients during and after transfer from systemic corticosteroids to aerosol steroids; aerosol steroids do not provide the systemic steroid needed to treat patients having trauma, surgery, or infections.
• Anaphylactoid reactions: Rare cases of anaphylactoid reactions have been observed in patients receiving corticosteroids.
• Immunosuppression: Prolonged use of corticosteroids may increase the incidence of secondary infection, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to killed or inactivated vaccines. Exposure to chickenpox or measles should be avoided. Corticosteroids should not be used to treat viral hepatitis or cerebral malaria. Close observation is required in patients with latent tuberculosis and/or TB reactivity; restrict use in active TB (only fulminating or disseminated TB in conjunction with antituberculosis treatment). Latent or active amebiasis should be ruled out in any patient with recent travel to tropic climates or unexplained diarrhea prior to corticosteroid initiation. Use with extreme caution in patients with Strongyloides infections; hyperinfection, dissemination and fatalities have occurred.
• Kaposi sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi sarcoma (case reports); if noted, discontinuation of therapy should be considered (Goedert 2002).
• Myopathy: Acute myopathy has been reported with high dose corticosteroids, usually in patients with neuromuscular transmission disorders; may involve ocular and/or respiratory muscles; monitor creatine kinase; recovery may be delayed.
• Psychiatric disturbances: Corticosteroid use may cause psychiatric disturbances, including euphoria, insomnia, mood swings, personality changes, severe depression or frank psychotic manifestations. Pre-existing psychiatric conditions may be exacerbated by corticosteroid use.
• Cardiovascular disease: Use with caution in patients with HF and/or hypertension; long-term use has been associated with electrolyte disturbances, fluid retention, and hypertension. Use with caution in patients with a recent history of myocardial infarction (MI); left ventricular free wall rupture has been reported after the use of corticosteroids.
• Diabetes: Use corticosteroids with caution in patients with diabetes mellitus; may alter glucose production/regulation leading to hyperglycemia.
• Gastrointestinal disease: Use with caution in patients with GI diseases (diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, ulcerative colitis [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 with caution in patients with myasthenia gravis; exacerbation of symptoms has occurred especially during initial treatment with corticosteroids.
• Ocular disease: Use with caution in patients with cataracts and/or glaucoma; increased intraocular pressure, open-angle glaucoma, and cataracts have occurred with prolonged use. Use with caution in patients with a history of ocular herpes simplex; corneal perforation has occurred; do not use in active ocular herpes simplex. Consider routine eye exams in chronic users.
• Osteoporosis: Use with caution in patients with or who are at risk for osteoporosis; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures.
• Renal impairment: Use with caution in patients with renal impairment; fluid retention may occur.
• Seizure disorders: Use corticosteroids with caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis.
• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid patients.
Concurrent drug therapy issues:
• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.
• Elderly: Use with caution in the elderly 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).
• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.
• Stress: Patients may require higher doses when subject to stress (ie, trauma, surgery, severe infection).
Blood pressure; weight; serum glucose; electrolytes; growth in pediatric patients; presence of infection, bone mineral density; assess HPA axis suppression (eg, ACTH stimulation test, morning plasma cortisol test, urinary free cortisol test); Hgb, occult blood loss; chest x-ray (at regular intervals during prolonged therapy); IOP with therapy >6 weeks.
Pregnancy Risk Factor
C/D (product specific)
Adverse events have been observed with corticosteroids in animal reproduction studies. Prednisone and its metabolite, prednisolone, cross the human 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 or decreased birth weight; however, information is conflicting and may be influenced by maternal dose/indication for use (Lunghi 2010; Park-Wyllie 2000; Pradat 2003). Hypoadrenalism may occur in newborns following maternal use of corticosteroids in pregnancy; monitor.
When systemic corticosteroids are needed in pregnancy for rheumatic disorders, it is generally recommended to use the lowest effective dose for the shortest duration of time, avoiding high doses during the first trimester (Götestam Skorpen 2016; Makol 2011; Østensen 2009).
For dermatologic disorders in pregnant women, systemic corticosteroids are generally not preferred for initial therapy; should be avoided during the first trimester; and used during the second or third trimester at the lowest effective dose (Bae 2012; Leachman 2006). Prednisone is preferred by some guidelines when an oral corticosteroid is needed because placental enzymes limit passage to the embryo (Murase 2014).
Pregnant women with poorly controlled asthma or asthma exacerbations may have a greater fetal/maternal risk than what is associated with appropriately used medications. Uncontrolled asthma is associated with an increased risk of perinatal mortality, preeclampsia, preterm birth, and low birth weight infants. Inhaled corticosteroids are recommended for the treatment of asthma during pregnancy; however, systemic corticosteroids, including prednisone, should be used to control acute exacerbations or treat severe persistent asthma (ACOG 2008; GINA 2016; Namazy 2016).
Prednisone may be used to treat lupus nephritis in pregnant women who have active nephritis or substantial extrarenal disease activity (Hahn 2012). Prednisone is recommended for use in fetal-neonatal alloimmune thrombocytopenia and pregnancy-associated immune thrombocytopenia (ACOG 2016). Prednisone may be used (alternative agent) to treat primary adrenal insufficiency (PAI) in pregnant women. Pregnant women with PAI should be monitored at least once each trimester (Bornstein 2016).
The National Transplantation Pregnancy Registry (NTPR) is a registry which follows pregnancies which occur in maternal transplant recipients or those fathered by male transplant recipients. The NTPR encourages reporting of pregnancies following solid organ transplant by contacting them at 877-955-6877 or NTPR@giftoflifeinstitute.org.
• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
• Patient may experience nausea, vomiting, insomnia, or agitation. Have patient report immediately to prescriber signs of infection; signs of high blood sugar (confusion, fatigue, increased thirst, increased hunger, polyuria, flushing, fast breathing, or breath that smells like fruit); signs of adrenal gland problems (severe nausea, vomiting, severe dizziness, passing out, muscle weakness, severe fatigue, mood changes, lack of appetite, or weight loss); signs of low potassium (muscle pain or weakness, muscle cramps, or an abnormal heartbeat); signs of pancreatitis (severe abdominal pain, severe back pain, severe nausea, or vomiting); signs of skin changes (acne, stretch marks, slow healing, or hair growth); signs of DVT (edema, warmth, numbness, change in color, or pain in the extremities); severe loss of strength and energy; irritability; tremors; tachycardia; confusion; sweating a lot; dizziness; shortness of breath; excessive weight gain; swelling of arms or legs; round face; buffalo hump; severe headache; bradycardia; abnormal heartbeat; angina; menstrual changes; joint pain; bone pain; vision changes; mood changes; behavioral changes; depression; seizures; burning or numbness feeling; bruising; bleeding; severe abdominal pain; black, tarry, or bloody stools; or vomiting blood (HCAHPS).
• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.
More about prednisone
- Side Effects
- During Pregnancy or Breastfeeding
- Dosage Information
- Drug Images
- Drug Interactions
- Compare Alternatives
- Support Group
- Pricing & Coupons
- En Español
- 427 Reviews – Add your own review/rating
- Drug class: glucocorticoids