Pathogenesis of Iodine-Induced Thyrotoxicosis: Studies in Northern Tasmania

Abstract

The increased incidence of thyrotoxicosis following bread iodation in Tasmania in 1966 was most evident in older age groups. Comparing the first 6 yr following iodation with the immediately preceding 6 yr, the number of thyrotoxic patients at Launceston General Hospital over the age of 50 yr increased by a factor of 3.8, the number in the fifth decade by a factor of 3.0, and the number under the age of 40 yr by a factor of 1.6; the number with exophthalmos did not change. In patients over the age of 50, LATS was detected in the serum of only 2 of 47 (4.3%) tested and in 3 of 22 (13.7%) assays on IgG concentrates. In patients under the age of 50, LATS was detected in the serum of 8 of 48 patients (17%) and in 11 of 16 (69%) assays on IgG concentrates. Antithyroglobulin antibodies (tanned red cell test) were detected in 4 of 38 tested over the age of 50 and 4 of 39 tested under the age of 50. Thyroid cytoplasmic antibodies were found in 13 of 37 tested over the age of 50 and in 23 of 42 tested under the age of 50. On thyroid scintiscanning of 88 patients, 17%, all over the age of 40, had autonomous nodules and only 16% had the uniform uptake of Graves' disease. The remaining 67% had diffusely irregular uptake equally compatible with Graves' disease or toxic autonomous goiter. It is concluded that the increase was mainly caused by an excess of patients with toxic autonomous goiter and not of Graves' disease. The hypothesis is presented that iodine-induced thyrotoxicosis is explained by the presence, in many euthyroid older persons with multinodular goiter, of autonomous thyroid tissue either in the form of discrete nodules or diffusely scattered micronodules. It is suggested that iodine is a regulator of hormone production in autonomous tissue and its administration in such persons results in an increase in hormone production, in some cases to thyrotoxic levels.