In order to evaluate the development of thyroid dysfunction during chronic amiodarone treatment in an area deficient in iodine and endemic for Chagas 'disease, a group of 24patients wasprospectively studied. Clinical examination and measurement of serum T4, T3, rT3, TSH and antithyroglobulin antibodies were performed before and at 3 and 9 months of use of amiodarone. A TSH response 30 minutes after IV injection of 200µg of TRH was also compared to TSH basal levels before and during amiodarone treatment. Thyroid radioative uptake and scan were obtained before and nine months after amiodarone was started. Elevated rT3 concentrations were unexpectedly found in two thirds of the patients before treatment. Thyroid dysfunction developed during amiodarone administration in 20,8% of the patients; 12,5% became hyperthyroid and 8,3%, hypothyroid (with negative antithyroglobulin antibodies). Positive RA1 uptake was seen in one patient with hyperthyroidism and diffuse goiter. Since T3 levels were not found to increase, the diagnosis of amiodarone-related hyperthyroidism was better evidenced by the reduced or blocked TSH response to TRH. Elevated TSH concentration was the best evidence of amiodarone- inducedhypothyroidism. Increase in TSH levels since the beginning of amiodarone therapy may predispose to the growth of a goiter. In conclusion, amiodarone treatment in an iodine deficient area as above should be judiciously decided and thyroidfunction carefully monitored before and during the use of the drug.
Amiodarone; Thyroidfunction; Chagas ' disease; Iodine deficiency