Amiodarone-induced thyrotoxicosis associated with thyrotropin receptor antibody

Since amiodarone was first marketed in 1992 in Japan, the incidence of amio darone-induced thyrotoxicosis (AIT) has been increasing. Among 12 thyrotoxi c patients, a patient with arrhythmogenic right ventricular dysplasia, who had been taking amiodarone for 4 years, developed thyrotoxicosis with subac ute onset, accompanied by transiently positive thyrotropin (TSH) receptor a ntibody (TRAb), or thyrotropin-binding inhibiting immunoglobulin (TBII). Th e immunoglobulin G (IgG) obtained from the TRAb-positive serum of the patie nt elicited no thyroid hormone-releasing activity in cultured human thyroid follicles, whereas all IgGs obtained from untreated Graves' disease elicit ed positive results. These in vitro findings and clinical course suggest th at TRAb/TBII without thyroid-stimulating activity may develop in patients w ith amiodarone-induced destructive thyroiditis, as reported in patients wit h destructive thyroiditis, such as subacute and silent thyroiditis.