der close supervision and the need for respiratory support should be anticipated. anticoagulants, oral co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. antidiabetics because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. antitubercular drugs serum concentrations of isoniazid may be decreased. bupropion since systemic steroids, as well as bupropion, can lower the seizure threshold, concurrent administration should be undertaken only with extreme caution; low initial dosing and small gradual increases should be employed. cholestyramine cholestyramine may increase the clearance of corticosteroids. cyclosporine increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. convulsions have been reported with this concurrent use. digitalis glycosides patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. estrogens, including oral contraceptives estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. fluoroquinolones post-marketing surveillance reports indicate that the risk of tendon rupture may be increased in patients receiving concomitant fluoroquinolones (e.g., ciprofloxacin, levofloxacin ) and corticosteroids, especially in the elderly. tendon rupture can occur during or after treatment with quinolones. hepatic enzyme inducers, inhibitors and substrates drugs which induce cytochrome p450 3a4 (cyp 3a4) enzyme activity (e.g., barbiturates, phenytoin, carbamazepine, rifampin ) may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. drugs which inhibit cyp 3a4 (e.g., ketoconazole, itraconazole, ritonavir, indinavir, macrolide antibiotics such as erythromycin ) have the potential to result in increased plasma concentrations of corticosteroids. glucocorticoids are moderate inducers of cyp 3a4. co-administration with other drugs that are metabolized by cyp 3a4 (e.g., indinavir, erythromycin ) may increase their clearance, resulting in decreased plasma concentration. ketoconazole ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. in addition, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal. nonsteroidal anti-inflammatory agents (nsaids) concomitant use of aspirin (or other nonsteroidal anti-inflammatory agents ) and corticosteroids increases the risk of gastrointestinal side effects. aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. the clearance of salicylates may be increased with concurrent use of corticosteroids; this could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. phenytoin in post-marketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control. phenytoin has been demonstrated to increase the hepatic metabolism of corticosteroids, resulting in a decreased therapeutic effect of the corticosteroid. quetiapine increased doses of quetiapine may be required to maintain control of symptoms of schizophrenia in patients receiving a glucocorticoid, a hepatic enzyme inducer. skin tests corticosteroids may suppress reactions to skin tests. thalidomide co-administration with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use. vaccines patients on corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible (see warnings: infection: vaccination).

selected cases of: systemic lupus erythematosus, systemic dermatomyositis (polymyositis), acute rheumatic carditis. dermatologic diseases pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme (stevens-johnson syndrome); exfoliative dermatitis; mycosis fungoides; severe psoriasis; severe seborrheic dermatitis. allergic states control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment: seasonal or perennial allergic rhinitis; bronchial asthma; contact dermatitis; atopic dermatitis; serum sickness; drug hypersensitivity reactions. ophthalmic diseases severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: allergic corneal marginal ulcers, herpes zoster ophthalmicus, anterior segment inflammation, diffuse posterior uveitis and choroiditis, sympathetic ophthalmia, allergic conjunctivitis, keratitis, chorioretinitis, optic neuritis, iritis and iridocyclitis. respiratory diseases symptomatic sarcoidosis; loeffler’s syndrome not manageable by other means; berylliosis; fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy; aspiration pneumonitis. hematologic disorders idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults; acquired (autoimmune) hemolytic anemia; erythroblastopenia (rbc anemia); congenital (erythroid) hypoplastic anemia. neoplastic diseases for palliative management of: leukemias and lymphomas in adults, acute leukemia of childhood. edematous states to induce a diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus. gastrointestinal diseases to tide the patient over a critical period of the disease in: ulcerative colitis, regional enteritis. miscellaneous tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy; trichinosis with neurologic or myocardial involvement.

rine corticosteroids can produce reversible hypothalamic-pituitary adrenal (hpa) axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment. adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage. this type of relative insufficiency may persist for up to 12 months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. if the patient is receiving steroids already, dosage may have to be increased. metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased in hyperthyroid patients. changes in thyroid status of the patient may necessitate adjustment in dosage. infection general patients who are on corticosteroids are more susceptible to infections than are healthy individuals. there may be decreased resistance and inability to localize infection when corticosteroids are used. infection with any pathogen (viral, bacterial, fungal, protozoan or helminthic) in any location of the body may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect cellular immunity, humoral immunity, or neutrophil function. 1 these infections may be mild, but may be severe and at times fatal. with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. 2 corticosteroids may also mask some signs of current infection. fungal infections corticosteroids may exacerbate systemic fungal infections and therefore should not be used in the presence of such infections unless they are needed to control life-threatening drug reactions. there have been cases reported in which concomitant use of amphotericin b and hydrocortisone was followed by cardiac enlargement and congestive heart failure (see precautions: drug interactions : amphotericin b injection and potassium-depleting agents). special pathogens latent disease may be activated or there may be an exacerbation of intercurrent infections due to pathogens, including those caused by amoeba, candida, cryptococcus, mycobacterium, nocardia, pneumocystis, toxoplasma . it is recommended that latent amebiasis or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent time in the tropics or any patient with unexplained diarrhea. similarly, corticosteroids should be used with great care in patients with known or suspected strongyloides (threadworm) infestation. in such patients, corticosteroid-induced immunosuppression may lead to strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia. corticosteroids should not be used in cerebral malaria. tuberculosis the use of prednisone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for management of the disease in conjunction with an appropriate antituberculous regimen. if corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. during prolonged corticosteroid therapy, these patients should receive chemoprophylaxis. vaccination administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. killed or inactivated vaccines may be administered. however, the response to such vaccines may be diminished and cannot be predicted . indicated immunization procedures may be undertaken in patients receiving nonimmunosuppressive doses of corticosteroids as replacement therapy (e.g., for addison’s disease). viral infections chickenpox and measles can have a more serious or even fatal course in pediatric and adult patients on corticosteroids. in pediatric and adult patients who have not had these diseases, particular care should be taken to avoid exposure. how the dose, route and duration of corticosteroid administration affect the risk of developing a disseminated infection is not known. the contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. if exposed to chickenpox, prophylaxis with varicella zoster immune globulin (vzig) may be indicated. if exposed to measles, prophylaxis with pooled intramuscular immunoglobulin (ig) may be indicated. (see the respective package inserts for complete vzig and ig prescribing information.) if chickenpox develops, treatment with antiviral agents may be considered. ophthalmic use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to bacteria, fungi or viruses. the use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. corticosteroids should not be used in active ocular herpes simplex because of possible corneal perforation.

sweating, karposi’s sarcoma (see precautions: general precautions ), lupus erythematosus-like lesions, perineal irritation, purpura, rash, striae, subcutaneous fat atrophy, suppression of reactions to skin tests, striae, telangiectasis, thin fragile skin, thinning scalp hair, urticaria. endocrine adrenal insufficiency-greatest potential caused by high potency glucocorticoids with long duration of action (associated symptoms include: arthralgias, buffalo hump, dizziness, life-threatening hypotension, nausea, severe tiredness or weakness), amenorrhea, postmenopausal bleeding or other menstrual irregularities, decreased carbohydrate and glucose tolerance, development of cushingoid state, diabetes mellitus (new onset or manifestations of latent), glycosuria, hyperglycemia, hypertrichosis, hyperthyroidism (see warnings: endocrine ), hypothyroidism, increased requirements for insulin or oral hypoglycemic agents in diabetics, lipids abnormal, moon face, negative nitrogen balance caused by protein catabolism, secondary adrenocortical and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery or illness) (see warnings: endocrine ), suppression of growth in pediatric patients. fluid and electrolyte disturbances congestive heart failure in susceptible patients, fluid retention, hypokalemia, hypokalemic alkalosis, metabolic alkalosis, hypotension or shock-like reaction, potassium loss, sodium retention with resulting edema. gastrointestinal abdominal distention, abdominal pain, anorexia which may result in weight loss, constipation, diarrhea, elevation in serum liver enzyme levels (usually reversible upon discontinuation), gastric irritation, hepatomegaly, increased appetite and weight gain, nausea, oropharyngeal candidiasis, pancreatitis, peptic ulcer with possible perforation and hemorrhage, perforation of the small and large intestine (particularly in patients with inflammatory bowel disease), ulcerative esophagitis, vomiting. hematologic anemia, neutropenia (including febrile neutropenia). metabolic negative nitrogen balance due to protein catabolism. musculoskeletal arthralgias, aseptic necrosis of femoral and humeral heads, increase risk of fracture, loss of muscle mass, muscle weakness, myalgias, osteopenia, osteoporosis (see precautions: musculoskeletal ), pathologic fracture of long bones, steroid myopathy, tendon rupture (particularly of the achilles tendon), vertebral compression fractures. neurological/psychiatric amnesia, anxiety, benign intracranial hypertension, convulsions, delirium, dementia (characterized by deficits in memory retention, attention, concentration, mental speed and efficiency, and occupational performance), depression, dizziness, eeg abnormalities, emotional instability and irritability, euphoria, hallucinations, headache, impaired cognition, incidence of severe psychiatric symptoms, increased intracranial pressure with papilledema (pseudotumor cerebri) usually following discontinuation of treatment, increased motor activity, insomnia, ischemic neuropathy, long-term memory loss, mania, mood swings, neuritis, neuropathy, paresthesia, personality changes, psychiatric disorders including steroid psychoses or aggravation of pre-existing psychiatric conditions, restlessness, schizophrenia, verbal memory loss, vertigo, withdrawn behavior. ophthalmic blurred vision, cataracts (including posterior subcapsular cataracts), central serous chorioretinopathy, establishment of secondary bacterial, fungal and viral infections, exophthalmos, glaucoma, increased intraocular pressure (see precautions: ophthalmic ), optic nerve damage, papilledema. other abnormal fat deposits, aggravation/masking of infections, decreased resistance to infection (see warnings: infection ), hiccups, immunosuppression, increased or decreased motility and number of spermatozoa, malaise, insomnia, moon face, pyrexia. to report suspected adverse reactions, contact west-ward pharmaceuticals corp. at 1-877-233-2001, or the fda at 1-800-fda-1088 or www.fda.gov/medwatch.

der close supervision and the need for respiratory support should be anticipated. anticoagulants, oral co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. antidiabetics because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. antitubercular drugs serum concentrations of isoniazid may be decreased. bupropion since systemic steroids, as well as bupropion, can lower the seizure threshold, concurrent administration should be undertaken only with extreme caution; low initial dosing and small gradual increases should be employed. cholestyramine cholestyramine may increase the clearance of corticosteroids. cyclosporine increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. convulsions have been reported with this concurrent use. digitalis glycosides patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. estrogens, including oral contraceptives estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. fluoroquinolones post-marketing surveillance reports indicate that the risk of tendon rupture may be increased in patients receiving concomitant fluoroquinolones (e.g., ciprofloxacin, levofloxacin ) and corticosteroids, especially in the elderly. tendon rupture can occur during or after treatment with quinolones. hepatic enzyme inducers, inhibitors and substrates drugs which induce cytochrome p450 3a4 (cyp 3a4) enzyme activity (e.g., barbiturates, phenytoin, carbamazepine, rifampin ) may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. drugs which inhibit cyp 3a4 (e.g., ketoconazole, itraconazole, ritonavir, indinavir, macrolide antibiotics such as erythromycin ) have the potential to result in increased plasma concentrations of corticosteroids. glucocorticoids are moderate inducers of cyp 3a4. co-administration with other drugs that are metabolized by cyp 3a4 (e.g., indinavir, erythromycin ) may increase their clearance, resulting in decreased plasma concentration. ketoconazole ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. in addition, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal. nonsteroidal anti-inflammatory agents (nsaids) concomitant use of aspirin (or other nonsteroidal anti-inflammatory agents ) and corticosteroids increases the risk of gastrointestinal side effects. aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. the clearance of salicylates may be increased with concurrent use of corticosteroids; this could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. phenytoin in post-marketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control. phenytoin has been demonstrated to increase the hepatic metabolism of corticosteroids, resulting in a decreased therapeutic effect of the corticosteroid. quetiapine increased doses of quetiapine may be required to maintain control of symptoms of schizophrenia in patients receiving a glucocorticoid, a hepatic enzyme inducer. skin tests corticosteroids may suppress reactions to skin tests. thalidomide co-administration with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use. vaccines patients on corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible (see warnings: infection: vaccination).

aluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis. pediatric patients who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in their growth velocity. this negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of hypothalamic-pituitary-adrenal (hpa) axis suppression (i.e., cosyntropin stimulation and basal cortisol plasma levels). growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of hpa axis function. the linear growth of pediatric patients treated with corticosteroids should be monitored, and the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of treatment alternatives. in order to minimize the potential growth effects of corticosteroids, pediatric patients should be titrated to the lowest effective dose.