Amiodarone-treated patients with suppressed TSH test are at risk of thyrotoxicosis.

Therapeutic use of the potent antiarrhythmic drug amiodarone requires early detection of impending hyperthyroidism, a potentially life-threatening adverse reaction in cardiac patients. Since amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3), serum T4 and T3 levels become unreliable parameters of thyroid function. In 44 patients treated with amiodarone for a median period of 7.3 months, up to seven TRH-TSH tests were performed. The TSH response to TRH was normal in 23 patients, partially suppressed in eight, totally suppressed in eight and overshooting in five patients. Two of the eight patients with suppressed TRH-TSH tests were clinically hyperthyroid, in four others thyrotoxicosis developed within 1 to 2 1/2 months after the first observation of a suppressed TSH response, while two patients remained euthyroid. In all patients with negative TRH-TSH tests. TSH response to TRH returned to normal between 2 and 29 months after withdrawal of amiodarone. We conclude that the TRH-TSH test, repeated at intervals, is a reliable tool for assessing thyroid function in patients on long-term treatment with amiodarone. Patients with a suppressed response under amiodarone therapy are at risk of developing thyrotoxicosis. Normalization of the TSH response indicates that this risk is over.