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PredniSONE

Pronunciation

Pronunciation

(PRED ni sone)

Index Terms

  • Deltacortisone
  • Deltadehydrocortisone
  • Deltasone

Dosage Forms

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

Concentrate, Oral:

PredniSONE Intensol: 5 mg/mL (30 mL) [contains alcohol, usp; unflavored flavor]

Solution, Oral:

Generic: 5 mg/5 mL (5 mL [DSC], 120 mL, 500 mL)

Tablet, Oral:

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.

  • Deltasone
  • PredniSONE Intensol
  • Rayos

Pharmacologic Category

  • Corticosteroid, Systemic

Pharmacology

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)

Metabolism

Hepatic to metabolite prednisolone (active)

Excretion

Urine (as conjugates)

Time to Peak

Oral: Immediate-release tablet: 2 hours; Delayed-release tablet: 6 to 6.5 hours

Half-Life Elimination

2 to 3 hours

Protein Binding

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; in infancy, mineralocorticoid supplementation is of particular importance).

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; idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults.

Delayed-release only: Pure red cell aplasia.

Immediate-release only: Erythroblastopenia (red blood cell anemia).

Neoplastic diseases:

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.

Ophthalmic diseases:

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.

Rheumatic disorders:

Maintenance therapy:

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.

Short-term therapy:

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.

Use: Unlabeled

Autoimmune hepatitis; Bell's palsy, adjunctive therapy for pain management in immunocompetent patients with herpes zoster; Takayasu arteritis; giant cell arteritis; Grave’s ophthalmopathy prophylaxis; subacute thyroiditis; thyrotoxicosis (type II amiodarone-induced); acute exacerbation of chronic obstructive pulmonary disease (COPD) (immediate release products)

Contraindications

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.

Dosing: Adult

General dosing range: 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

Indication-specific dosing:

Acute asthma (NAEPP 2007): Oral: 40 to 60 mg per day for 3 to 10 days; administer as single or 2 divided doses

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).

Acute gout (ACR guidelines [Khanna 2012]): Oral: Initial: ≥0.5 mg/kg for 5 to 10 days

Anaphylaxis, adjunctive treatment (Lieberman 2005): Oral: 0.5 mg/kg

Antineoplastic: Oral: Usual range: 10 mg daily to 100 mg/m2/day (depending on indication). Note: Details concerning dosing in combination regimens should also be consulted.

Autoimmune hepatitis (off-label use; Czaja 2002): Oral: Initial treatment: 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

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 (Baugh 2013).

Crohn disease, moderate/severe (off-label use): 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: 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)

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)

Graves ophthalmopathy prophylaxis (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 (Bahn 2011)

Herpes zoster (off-label use; Dworkin 2007): Oral: 60 mg daily for 7 days, followed by 30 mg daily for 7 days, then 15 mg daily for 7 days

Immune thrombocytopenia (ITP) (American Society of Hematology, 1997): Oral: 1 to 2 mg/kg/day

Lupus nephritis, induction (Hahn 2012): 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

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

Multiple sclerosis, acute exacerbations: Oral: 200 mg daily for 1 week, followed by 80 mg every other day for 1 month.

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 (HHS [OI 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 (American College of Rheumatology 2002): Oral: ≤10 mg daily

Subacute thyroiditis (off-label use): Oral: 40 mg daily for 1 to 2 weeks; gradually taper over 2 to 4 weeks or longer depending on clinical response. Note: NSAIDs should be considered first-line therapy in such patients (Bahn 2011).

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 II amiodarone-induced; off-label use): Oral: 40 mg daily for 14 to 28 days; gradually taper over 2 to 3 months depending on clinical response (Bahn 2011)

Tuberculosis, severe, paradoxical reactions (off-label dose, AIDSinfo guidelines 2008): Oral: 1 mg/kg/day, gradually reduce after 1 to 2 weeks

Dosing: Geriatric

Refer to adult dosing; use the lowest effective dose.

Dosing: Pediatric

General dosing range: 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.

Indication-specific dosing:

Acute asthma (NAEPP 2007): Oral:

0 to 11 years 1 to 2 mg/kg/day for 3 to 10 days (maximum: 60 mg daily)

≥12 years: Refer to Adults dosing

Autoimmune hepatitis (off-label use; Czaja 2002): Oral: Initial treatment: 2 mg/kg/day for 2 weeks (maximum: 60 mg daily), followed by a taper over 6 to 8 weeks to a dose of 0.1 to 0.2 mg/kg/day or 5 mg daily

Bell palsy (off-label use): 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 (Baugh 2013).

Nephrotic syndrome (Pediatric Nephrology Panel recommendations [Hogg 2000]): Oral: Initial: 2 mg/kg daily or 60 mg/m2/day given every day in 1 to 3 divided doses (maximum: 80 mg daily) until urine is protein free or for 4 to 6 weeks; followed by maintenance dose: 2 mg/kg/dose or 40 mg/m2/dose given every other day in the morning; gradually taper and discontinue after 4 to 6 weeks. Note: No definitive treatment guidelines exist. Dosing is dependent on institution protocols and individual response.

Pneumocystis pneumonia (adjunctive therapy) in HIV-infected patients (off-label dose; AIDSinfo guidelines 2008): Oral:

Children: 1 mg/kg twice daily for 5 days, followed by 0.5 to 1 mg/kg twice daily for 5 days, followed by 0.5 mg/kg once daily for 11 to 21 days

Adolescents: Refer to adult dosing.

Dosing: Renal Impairment

Dosing adjustment in renal impairment: There are no dosage adjustments provided in the manufacturer’s labeling.

Hemodialysis effects: Supplemental dose is not necessary.

Dosing: Hepatic Impairment

There are no dosage adjustments provided in the manufacturer’s labeling.

Administration

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.

Dietary Considerations

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

Storage

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.

Drug Interactions

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

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

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

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

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

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

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

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

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

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

NSAID (COX-2 Inhibitor): Corticosteroids (Systemic) may enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). Monitor therapy

NSAID (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of NSAID (Nonselective). Monitor therapy

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

Quinolone Antibiotics: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolone Antibiotics. 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

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 (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

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

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. Avoid combination

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

Test Interactions

Decreased response to skin tests

Adverse Reactions

Frequency not defined.

Cardiovascular: Congestive heart failure (in susceptible patients), hypertension

Central nervous system: Emotional instability, headache, intracranial pressure increased (with papilledema), psychic derangements (including euphoria, insomnia, mood swings, personality changes, severe depression), seizure, vertigo

Dermatologic: Bruising, facial erythema, petechiae, thin fragile skin, urticaria, wound healing impaired

Endocrine & metabolic: Adrenocortical and pituitary unresponsiveness (in times of stress), carbohydrate intolerance, Cushing’s syndrome, diabetes mellitus, fluid retention, growth suppression (in children), hypokalemic alkalosis, hypothyroidism enhanced, menstrual irregularities, negative nitrogen balance due to protein catabolism, potassium loss, sodium retention

Gastrointestinal: Abdominal distension, pancreatitis, peptic ulcer (with possible perforation and hemorrhage), ulcerative esophagitis

Hepatic: ALT increased, AST increased, alkaline phosphatase increased

Neuromuscular & skeletal: Aseptic necrosis of femoral and humeral heads, muscle mass loss, muscle weakness, osteoporosis, pathologic fracture of long bones, steroid myopathy, tendon rupture (particularly Achilles tendon), vertebral compression fractures

Ocular: Exophthalmos, glaucoma, intraocular pressure increased, posterior subcapsular cataracts

Miscellaneous: Allergic reactions, anaphylactic reactions, diaphoresis, hypersensitivity reactions, infections, Kaposi’s sarcoma

<1% (Limited to important or life-threatening): Venous thrombosis (Johannesdottir, 2013)

Warnings/Precautions

Concerns related to adverse effects:

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

• Adrenal suppression: May cause hypercorticism 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.

• 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 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). Amebiasis should be ruled out in any patient with recent travel to tropic climates or unexplained diarrhea prior to initiation of corticosteroids.

• 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 severe depression, euphoria, insomnia, mood swings, and personality changes, to frank psychotic manifestations. Pre-existing psychiatric conditions may be exacerbated by corticosteroid use.

Disease-related concerns:

• 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 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. Avoid ethanol may enhance gastric mucosal irritation.

• 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 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 ones.

Concurrent drug therapy issues:

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

Special populations:

• Elderly: Because of the risk of adverse effects, systemic corticosteroids should be used cautiously in the elderly in 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.

Monitoring Parameters

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)

Pregnancy Considerations

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 ~8-10 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 (Park-Wyllie 2000; Pradat 2003). Systemic corticosteroids may also influence fetal growth (decreased birth weight); however, information is conflicting (Lunghi 2010). Hypoadrenalism may occur in newborns following maternal use of corticosteroids in pregnancy; monitor.

When systemic corticosteroids are needed in pregnancy, it is generally recommended to use the lowest effective dose for the shortest duration of time, avoiding high doses during the first trimester (Leachman 2006; Lunghi 2010; Makol 2011; Østensen 2009). Inhaled corticosteroids are preferred for the treatment of asthma during pregnancy. Oral corticosteroids, such as prednisone, may be used for the treatment of severe persistent asthma if needed; the lowest dose administered on alternate days (if possible) should be used (NAEPP 2005). Prednisone may be used to treat lupus nephritis in pregnant women who have active nephritis or substantial extrarenal disease activity (Hahn 2012).

Pregnant women exposed to prednisone for antirejection therapy following a transplant may contact the National Transplantation Pregnancy Registry (NTPR) at 215-955-4820. Women exposed to prednisone during pregnancy for the treatment of an autoimmune disease (eg, rheumatoid arthritis) may contact the OTIS Autoimmune Diseases Study at 877-311-8972.

Patient Education

• 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, insomnia, or akathisia. Have patient report immediately to prescriber signs of infection, signs of hyperglycemia, signs of hypokalemia, signs of pancreatitis, severe asthenia, irritability, tremors, tachycardia, confusion, hyperhydrosis, dizziness, dyspnea, excessive weight gain, edema of extremities, skin changes, moon face, buffalo hump, significant headache, bradycardia, arrhythmia, angina, extremity discoloration, painful extremities, menstrual irregularities, arthralgia, osteodynia, vision changes, mood changes, behavioral changes, depression, paresthesia, considerable dyspepsia, ecchymosis, hemorrhaging, melena, or hematemesis (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 healthcare 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.

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