Name: Triamcinolone acetonide (Azmacort)
Class: Corticosteroid (Glucocorticoid)
Mechanism: PMNs in periph. blood, but decrease all other WBCs. Inhib. monocyte reactivity and secretion of IL-1 & TNF. Inhib. T cell activation, IgE-med. rxns, inducible cyclooxygenase II expression. Induces lipocortin ® inhibition of phospholipase A2.
Absorption: IM, aerosol, oral, topical, intraarticular.
Dist.: Metabolism.: Excretion, t½: 12-36 hr.
Toxicity/S.E.s: Cataracts, hypertension, osteoporosis, myopathy, obesity, acne, hirsutism, hyperglycemia, muscle atrophy/myopathy, convulsions, mood changes, derm. changes, ¯ cellular immunity. Glucocorticoid admin > equiv. of 20 mg hydrocortisone/d ® suppression of HPA axis. Sudden stop of chronic therapy ® impaired physiologic homeostasis. Drug Interactions—phenytoin, barbiturates, & rifampin induce catabolic enzymes; antacids ® ¯ bioavailability of prednisone; salicylate levels reduced; increased doses required for insulin, hypoglycemic agents, antihypertensives, and glaucoma meds; if hypokalemia occurs, increased toxicity of digoxin. Aerosol—oral candidiasis, dysphonia.
Special Features: Rel. anti-inflamm. potency of 5. Synth. agents have potent anti-inflamm. activity w/little (if any) mineralocorticoid effect.