Rifampin
Salicylates
Toxoids
Vaccines
Vitamin D analogs
Triamcinolone (Nasacort® AQ; Kenalog®) Interactions
NOTE: The interactions listed below refer to systemic triamcinolone. There are no known interactions between topical triamcinolone preparations and other drugs.
Hepatic microsomal enzyme inducers, including barbiturates, bosentan, ethotoin, phenytoin or fosphenytoin, carbamazepine, and rifampin, can increase the metabolism of corticosteroids. Dosages of systemic triamcinolone may require adjustment if these agents are initiated or withdrawn during corticosteroid therapy.
Estrogens have been associated with elevated serum concentrations of corticosteroid binding globulin (CBG), leading to increased circulating corticosteroids. Patient response to corticosteroids should be monitored, with doses adjusted as necessary, if estrogen is added to or withdrawn during therapy.
Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs such as diuretics and amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly.
Glucocorticoids may interact with cholinesterase inhibitors, including ambenonium, neostigmine, and pyridostigmine, occasionally causing severe muscle weakness in patients with myasthenia gravis. Glucocorticoids are occasionally used therapeutically, however, in the treatment of some patients with myasthenia gravis. In such patients it is recommended that corticosteroid therapy be initiated at low dosages (i.e., 10 - 25 mg/day of prednisone or equivalent) and with close clinical monitoring. The dosage should be increased gradually as tolerated, with continued careful monitoring of the patient’s clinical status.
Killed or inactivated vaccines and toxoids do not represent a danger to immunocompromised persons and generally should be administered as recommended for healthy persons. The immune response of immunocompromised persons to vaccines is not as good as healthy persons; higher doses or more frequent boosters may be required, although the immune response still may be suboptimal. Live-virus vaccines should not be given to immunocompromised individuals due to the potentiation of virus replication and adverse reactions to the virus. Those undergoing high-dose corticosteroid therapy should not be exposed to others who have recently received the oral poliovirus vaccine (OPV). Measles-mumps-rubella (MMR) vaccination is not contraindicated for the close contacts, including health care professionals, of immunocompromised patients. Passive immunoprophylaxis with immune globulins may be indicated for immunocompromised persons instead of, or in addition to, vaccination. When exposed to a vaccine-preventable disease such as measles, severely immunocompromised children should be considered susceptible regardless of their vaccination history.
Systemic corticosteroids increase blood glucose levels. Because of this action, a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
Concomitant use of L-asparaginase or pegaspargase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase or pegaspargase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions.
Patients receiving cardiac glycosides and corticosteroids concomitantly are at an increased risk for developing arrhythmias or digitalis toxicity due to corticosteroid-induced hypokalemia. Corticosteroid-induced hypokalemia could also enhance the proarrhythmic effects of dofetilide.
Corticosteroids can cause increases in blood pressure, sodium and water retention, and hypokalemia, predisposing patients to interactions with certain other medications. Hypokalemia is known to potentiate neuromuscular blockade associated with nondepolarizing neuromuscular blockers. In addition, case reports and clinical studies have reported myopathy and weakness, sometimes prolonged, with the combined use of neuromuscular blocking agents with corticosteroids in critically ill patients. Many cases involved patients with no underlying risk factors. The term ‘blocking agent-corticosteroid myopathy’ (BACM) has been applied to this syndrome. When given concomitantly for prolonged periods these agents appear to confer a greater risk of myopathy versus the use of either agent alone, and the pathology of the effect is not known. When combined use is necessary for prolonged periods, careful monitoring of the patient is recommended.
Corticosteroids administered systemically prior to or concomitantly with photosensitizing agents may decrease the efficacy of photodynamic therapy.
The risk of cardiac toxicity with isoproterenol in asthma patients appears to be increased with the coadministration of corticosteroids or methylxanthines. Intravenous infusions of isoproterenol in refractory asthmatic children at rates of 0.05 - 2.7 ug/kg/min have caused clinical deterioration, myocardial infarction (necrosis), congestive heart failure and death.
Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. While therapy is designed to take advantage of this effect, patients may be predisposed to over-immunosuppression resulting in an increased risk for the development of severe infections. Close clinical monitoring is advised with concurrent use; in the presence of serious infections, continuation of the corticosteroid or immunosuppressive agent may be necessary but should be accompanied by appropriate antimicrobial therapies as indicated.
Vitamin D plus calcium supplements are generally recommended for the prevention of osteoporosis in patients taking long-term corticosteroids. A relationship of functional antagonism exists between vitamin D analogs, which promote calcium absorption, and corticosteroids, which inhibit calcium absorption. Therapeutic effect of vitamin D analogs should be monitored when used concomitantly with corticosteroids.
Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function.
Mifepristone, RU-486 exhibits antiglucocorticoid activity that may antagonize the corticosteroids. In rats, the activity of dexamethasone was inhibited by oral mifepristone doses of 10 - 25 mg/kg. A mifepristone dose of 4.5 mg/kg in humans resulted in compensatory increases in ACTH and cortisol. Mifepristone is contraindicated in patients on long-term corticosteroid therapy. Although specific drug interactions have not been studied, dexamethasone may lower serum levels of mifepristone by induction of mifepristone metabolism via CYP3A4.
Additional monitoring may be required when coadministering systemic or inhaled corticosteroids with mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored.
[ Last revised: 11/7/2005 2:06:00 PM ]
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