Amiodarone-induced thyroid gland dysfunction.
Of a population of 400 patients treated with amiodarone, 97 underwent thyroid function evaluation. Of these, 20 patients proved to be thyrotoxic and 16 hypothyroid. In thyrotoxic patients, symptoms developed 2 to 36 months after starting treatment with amiodarone, the most specific laboratory finding being a high total T3 (TT3). No antithyroid treatment proved useful. Thyroid function returned to normal 3 to 7 months after stopping amiodarone therapy. In the hypothyroid group, a high thyroid-stimulating hormone was the most specific laboratory finding. These patients were treated with substitute therapy with or without withdrawal of amiodarone. The iodine content of the thyroid gland in part of this population taking amiodarone was measured by in vivo x-ray fluorescence. Patients in whom thyrotoxicosis developed showed especially high iodine contents. During treatment with amiodarone, patients at high risk of thyrotoxicosis were recognized by increasing TT3 values and higher iodine thyroid levels. A reduction in maintenance dose should be considered in this specific population.
D000638:Amiodarone / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000139:chemically induced; D007455:Iodine / Q000378:metabolism; D008297:Male; D013610:Tachycardia / Q000188:drug therapy; D013959:Thyroid Diseases / Q000139:chemically induced* / Q000378:metabolism; D013961:Thyroid Gland / Q000378:metabolism; D013971:Thyrotoxicosis / Q000139:chemically induced; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D014284:Triiodothyronine; D013972:Thyrotropin; D007455:Iodine; D000638:Amiodarone; D013974:Thyroxine