hibition 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. 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. cyp 3a4 inhibitors: triamcinolone acetonide is a substrate of cyp3a4. ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to an increased risk of corticosteroid side effects. co-administration of other strong cyp3a4 inhibitors (e.g., ritonavir, atazanavir, clarithromycin, indinavir, itraconazole, nefazodone, nelfinavir, saquinavir, telithromycin, cobicistat-containing products) with triamcinolone acetonide injectable suspension may cause increased plasma concentration of triamcinolone leading to adverse reactions. (see adverse reactions .) during postmarketing use, there have been reports of clinically significant drug interactions in patients receiving triamcinolone acetonide and strong cyp3a4 inhibitors (e.g., ritonavir). (see warnings, endocrine and precautions, endocrine .) consider the benefit-risk of concomitant use and monitor for systemic corticosteroid side effects. 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. hepatic enzyme inducers (e.g., barbiturates, phenytoin, carbamazepine, rifampin): drugs which induce hepatic microsomal drug metabolizing enzyme activity may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. nonsteroidal anti-inflammatory drugs (nsaids): concomitant use of aspirin (or other nonsteroidal anti-inflammatory drugs) 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. skin tests: corticosteroids may suppress reactions to skin tests. vaccines: patients on prolonged 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: infections: vaccination ).

ia associated with cancer, nonsuppurative thyroiditis. gastrointestinal diseases: to tide the patient over a critical period of the disease in regional enteritis and ulcerative colitis. hematologic disorders: acquired (autoimmune) hemolytic anemia, diamond-blackfan anemia, pure red cell aplasia, selected cases of secondary thrombocytopenia. miscellaneous: trichinosis with neurologic or myocardial involvement, tuberculous meningitis with subarachnoid block or impending block when used with appropriate antituberculous chemotherapy. neoplastic diseases: for the palliative management of leukemias and lymphomas. nervous system: acute exacerbations of multiple sclerosis; cerebral edema associated with primary or metastatic brain tumor or craniotomy. ophthalmic diseases: sympathetic ophthalmia, temporal arteritis, uveitis, and ocular inflammatory conditions unresponsive to topical corticosteroids. renal diseases: to induce diuresis or remission of proteinuria in idiopathic nephrotic syndrome or that due to lupus erythematosus. respiratory diseases: berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy, idiopathic eosinophilic pneumonias, symptomatic sarcoidosis. rheumatic disorders: as adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in acute gouty arthritis; acute rheumatic carditis; ankylosing spondylitis; psoriatic arthritis; rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy). for the treatment of dermatomyositis, polymyositis, and systemic lupus erythematosus. intra-articular the intra-articular or soft tissue administration of triamcinolone acetonide injectable suspension is indicated as adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in acute gouty arthritis, acute and subacute bursitis, acute nonspecific tenosynovitis, epicondylitis, rheumatoid arthritis, synovitis of osteoarthritis.

medications is usually considered negligible compared to that received in flush solutions containing benzyl alcohol. administration of high dosages of medications containing this preservative must take into account the total amount of benzyl alcohol administered. the amount of benzyl alcohol at which toxicity may occur is not known. if the patient requires more than the recommended dosages or other medications containing this preservative, the practitioner must consider the daily metabolic load of benzyl alcohol from these combined sources (see precautions: pediatric use ). rare instances of anaphylaxis have occurred in patients receiving corticosteroid therapy (see adverse reactions ). cases of serious anaphylaxis, including death, have been reported in individuals receiving triamcinolone acetonide injection, regardless of the route of administration. because triamcinolone acetonide injectable suspension is a suspension, it should not be administered intravenously. unless a deep intramuscular injection is given, local atrophy is likely to occur. (for recommendations on injection techniques, see dosage and administration .) due to the significantly higher incidence of local atrophy when the material is injected into the deltoid area, this injection site should be avoided in favor of the gluteal area. increased dosage of rapidly acting corticosteroids is indicated in patients on corticosteroid therapy subjected to any unusual stress before, during, and after the stressful situation. triamcinolone acetonide injectable suspension is a long-acting preparation, and is not suitable for use in acute stress situations. to avoid drug-induced adrenal insufficiency, supportive dosage may be required in times of stress (such as trauma, surgery, or severe illness) both during treatment with triamcinolone acetonide injectable suspension and for a year afterwards. results from one multicenter, randomized, placebo-controlled study with methylprednisolone hemisuccinate, an intravenous corticosteroid, showed an increase in early (at 2 weeks) and late (at 6 months) mortality in patients with cranial trauma who were determined not to have other clear indications for corticosteroid treatment. high doses of systemic corticosteroids, including triamcinolone acetonide injectable suspension, should not be used for the treatment of traumatic brain injury. cardio-renal average and large doses of corticosteroids can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. these effects are less likely to occur with the synthetic derivatives except when they are used in large doses. dietary salt restriction and potassium supplementation may be necessary (see precautions ). all corticosteroids increase calcium excretion. literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction; therefore, therapy with corticosteroids should be used with great caution in these patients. endocrine corticosteroids can produce reversible hypothalamic-pituitary-adrenal (hpa) axis suppression with the potential for glucocorticosteroid insufficiency after withdrawal of treatment. 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.

xacerbations in the disease process, the patient's individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment. in this latter situation it may be necessary to increase the dosage of the corticosteroid for a period of time consistent with the patient's condition. if after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly. dosage systemic the suggested initial dose is 60 mg, injected deeply into the gluteal muscle . atrophy of subcutaneous fat may occur if the injection is not properly given. dosage is usually adjusted within the range of 40 mg to 80 mg, depending upon patient response and duration of relief. however, some patients may be well controlled on doses as low as 20 mg or less. hay fever or pollen asthma: patients with hay fever or pollen asthma who are not responding to pollen administration and other conventional therapy may obtain a remission of symptoms lasting throughout the pollen season after a single injection of 40 mg to 100 mg. in the treatment of acute exacerbations of multiple sclerosis, daily doses of 160 mg of triamcinolone for a week followed by 64 mg every other day for one month are recommended (see precautions: neuro-psychiatric ). in pediatric patients, the initial dose of triamcinolone may vary depending on the specific disease entity being treated. the range of initial doses is 0.11 to 1.6 mg/kg/day in 3 or 4 divided doses (3.2 to 48 mg/m 2 bsa/day). for the purpose of comparison, the following is the equivalent milligram dosage of the various glucocorticoids: cortisone, 25 triamcinolone, 4 hydrocortisone, 20 paramethasone, 2 prednisolone, 5 betamethasone, 0.75 prednisone, 5 dexamethasone, 0.75 methylprednisolone, 4 these dose relationships apply only to oral or intravenous administration of these compounds. when these substances or their derivatives are injected intramuscularly or into joint spaces, their relative properties may be greatly altered. local intra-articular administration: a single local injection of triamcinolone acetonide is frequently sufficient, but several injections may be needed for adequate relief of symptoms. initial dose: 2.5 mg to 5 mg for smaller joints and from 5 mg to 15 mg for larger joints, depending on the specific disease entity being treated. for adults, doses up to 10 mg for smaller areas and up to 40 mg for larger areas have usually been sufficient. single injections into several joints, up to a total of 80 mg, have been given.

e tolerance, development of cushingoid state, glycosuria, hirsutism, hypertrichosis, increased requirements for insulin or oral hypoglycemic agents in diabetes, manifestations of latent diabetes mellitus, menstrual irregularities, postmenopausal vaginal hemorrhage, secondary adrenocortical and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery, or illness), suppression of growth in pediatric patients. fluid and electrolyte disturbances: congestive heart failure in susceptible patients, fluid retention, hypokalemic alkalosis, potassium loss, sodium retention. gastrointestinal: abdominal distention, bowel/bladder dysfunction (after intrathecal administration [see warnings: neurologic ]), elevation in serum liver enzyme levels (usually reversible upon discontinuation), hepatomegaly, increased appetite, nausea, pancreatitis, peptic ulcer with possible perforation and hemorrhage, perforation of the small and large intestine (particularly in patients with inflammatory bowel disease), ulcerative esophagitis. metabolic: negative nitrogen balance due to protein catabolism. musculoskeletal: aseptic necrosis of femoral and humeral heads, calcinosis (following intra-articular or intralesional use), charcot-like arthropathy, loss of muscle mass, muscle weakness, osteoporosis, pathologic fracture of long bones, post injection flare (following intra-articular use), steroid myopathy, tendon rupture, vertebral compression fractures. neurologic/psychiatric: convulsions, depression, emotional instability, euphoria, headache, increased intracranial pressure with papilledema (pseudotumor cerebri) usually following discontinuation of treatment, insomnia, mood swings, neuritis, neuropathy, paresthesia, personality changes, psychiatric disorders, vertigo. arachnoiditis, meningitis, paraparesis/paraplegia, and sensory disturbances have occurred after intrathecal administration. spinal cord infarction, paraplegia, quadriplegia, cortical blindness, and stroke (including brainstem) have been reported after epidural administration of corticosteroids (see warnings: serious neurologic adverse reactions with epidural administration and warnings: neurologic ). ophthalmic: exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts, rare instances of blindness associated with periocular injections. other: abnormal fat deposits, decreased resistance to infection, hiccups, increased or decreased motility and number of spermatozoa, malaise, moon face, weight gain. to report suspected adverse reactions, contact long grove pharmaceuticals, llc at 1-855-642-2594 or fda at 1-800-fda-1088 or www.fda.gov/medwatch.

hibition 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. 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. cyp 3a4 inhibitors: triamcinolone acetonide is a substrate of cyp3a4. ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to an increased risk of corticosteroid side effects. co-administration of other strong cyp3a4 inhibitors (e.g., ritonavir, atazanavir, clarithromycin, indinavir, itraconazole, nefazodone, nelfinavir, saquinavir, telithromycin, cobicistat-containing products) with triamcinolone acetonide injectable suspension may cause increased plasma concentration of triamcinolone leading to adverse reactions. (see adverse reactions .) during postmarketing use, there have been reports of clinically significant drug interactions in patients receiving triamcinolone acetonide and strong cyp3a4 inhibitors (e.g., ritonavir). (see warnings, endocrine and precautions, endocrine .) consider the benefit-risk of concomitant use and monitor for systemic corticosteroid side effects. 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. hepatic enzyme inducers (e.g., barbiturates, phenytoin, carbamazepine, rifampin): drugs which induce hepatic microsomal drug metabolizing enzyme activity may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. nonsteroidal anti-inflammatory drugs (nsaids): concomitant use of aspirin (or other nonsteroidal anti-inflammatory drugs) 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. skin tests: corticosteroids may suppress reactions to skin tests. vaccines: patients on prolonged 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: infections: vaccination ).

occur is not known. premature and low-birth-weight infants, as well as patients receiving high dosages, may be more likely to develop toxicity. practitioners administering this and other medications containing benzyl alcohol should consider the combined daily metabolic load of benzyl alcohol from all sources. the efficacy and safety of corticosteroids in the pediatric population are based on the well- established course of effect of corticosteroids which is similar in pediatric and adult populations. published studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic syndrome (>2 years of age), and aggressive lymphomas and leukemias (>1 month of age). other indications for pediatric use of corticosteroids, e.g., severe asthma and wheezing, are based on adequate and well-controlled trials conducted in adults, on the premises that the course of the diseases and their pathophysiology are considered to be substantially similar in both populations. the adverse effects of corticosteroids in pediatric patients are similar to those in adults (see adverse reactions ). like adults, pediatric patients should be carefully observed with frequent measurements of blood pressure, weight, height, intraocular pressure, and clinical evaluation 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 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.