[Efficacy of propylthiouracil in the treatment of amiodarone-induced hyperthyroidism].

Amiodarone is a benzofuranic derivative widely used in cardiologic practice because of its excellent antiarrhythmic properties. Due to its high iodine content, it interferes with thyroid physiology and can cause either hyper or hypothyroidism. Amiodarone-induced hyperthyroidism should be considered as a serious complication since it develops in cardiac patients, the clinical diagnosis can be difficult and because conventional methods of therapy are said to be often ineffective. We analyze the outcome of 10 pts, chronically treated with Amiodarone (16-60 mo, mean 37.6 mo) who develop hyperthyroidism during the antiarrhythmic therapy. All patients had multinodular goiter. Overt clinical picture for thyrotoxicosis was seen in 7 of them and lab tests showed: rT3 = 101.1 +/- 14.9 ng/dl; T3 = 220.2 +/- 25 ng/dl; T4 = 15.6 +/- 1.9 micrograms/dl, TSH = 0.8 +/- 0.2 microU/ml and TRH response 0.0 microU/ml. Thyroid microsomal antibodies were negative in 3 pts studied. After Amiodarone was discontinued, patients were followed-up monthly. In 2, normalization of clinical and laboratory indexes were obtained at 40-60 d and no other medication was given. In the remaining, due to the intensity of clinical manifestations, PTU treatment was started (300 mg/d) After 4 mo, euthyroidism was achieved in 6 and it persisted after discontinuation of PTU has patient failed to respond to PTU, 131I was administered with excellent results. Patients have been followed-up up to 3 years after therapy without observing thyrotoxic relapses nor deterioration of their cardiological condition.2+ conventional therapies (PTU or 131I) have been, very effective.