Phenomenon of Iodide Inhibition in Various States of Thyroid Function with Observations on One Mechanism of Its Occurrence

Abstract

The 24-hr thyroidal 131I uptake in Hashimoto's thyroiditis is significantly depressed from control values if 2 mg of potassium iodide carrier is added to the diagnostic 131I dose (iodide inhibition). The phenomenon of iodide inhibition has been studied in 100 patients. Eleven were normal controls, 12 had Hashimoto's disease, 11 were thyrotoxic and 23 had been rendered euthyroid by 131I therapy. Thirteen had undergone thyroidectomy for thyrotoxicosis, 22 had a nontoxic goiter and 5 had been thyroidectomized for nontoxic goiter. Two patients had discontinued carbimazole therapy for thyrotoxicosis 1 yr prior to study and one patient had Pendred's syndrome. The results confirm that iodide inhibition occurs in Hashimoto's disease and show in addition that patients rendered euthyroid by 131I or by thyroidectomy, patients thyroidectomized for nontoxic goiter and the carbimazole-treated patients demonstrated inhibition. Studies of 131I kinetics and of stable iodine metabolism have demonstrated one mechanism of iodide inhibition whereby the initial thyroidal 131I uptake is followed by rapid discharge of accumulated radioactivity from the thyroid gland. This discharge has been seen in patients with Hashimoto's disease and in patients who had undergone thyroidectomy for thyrotoxicosis.