Amiodarone-induced thyrotoxicosis associated with thyrotropin receptor antibody.

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