AMIODARONE-INDUCED THYROID-DYSFUNCTION

Cases of hypothyroidism and hyperthyroidism associated with amiodarone therapy are described, and the mechanisms, clinical appearance, and m anagement of amiodarone-induced thyroid dysfunction are discussed. A 7 2-year-old man with a history of recurrent ventricular tachycardia unr esponsive to conventional antiarrhythmic drugs was started on amiodaro ne therapy. Initially he responded well, but after three months he beg an to have fatigue, dry skin, and intolerance of cold. His serum thyro id-stimulating hormone (TSH) concentration had risen from 4.4 muU/mL b efore amiodarone therapy began to 20 muU/mL, consistent with hypothyro idism. He was started on sodium levothyroxine for thyroid hormone repl acement; the dosage was adjusted in accordance with subsequent TSH mea surements. His hospital course was complicated by congestive heart fai lure. The second patient was a 43-year-old man with a history of atria l fibrillation who developed hyperthyroidism when placed on amiodarone therapy. He had persistent sweating, intolerance of heat, restlessnes s, and tachycardia. Thyroid function tests confirmed the presence of h yperthyroidism. The patient was treated with propylthiouracil and prop ranolol, and amiodarone was discontinued. He remained unresponsive to the propylthiouracil, which was discontinued, and was scheduled for ra dioactive iodine treatment. The mechanism of amiodarone-induced thyroi d dysfunction may involve the large iodine content of the drug. Amioda rone-induced hypothyroidism may range in severity from mild symptoms t o severe myxedema; the skin, hair, and nails are particularly affected . Persons with clinical hyperthyroidism secondary to amiodarone treatm ent show the signs and symptoms of a hypermetabolic state resulting fr om thyroid hormone excess. Amiodarone-induced hypothyroidism is treate d with levothyroxine and hyperthyroidism with antithyroid drugs. Amiod arone can cause thyroid dysfunction, which can have serious consequenc es.