Iodine-induced hyperthyroidism is hyperthyroidism associated with increased iodine intake, referred to as iodine hyperthyroidism, also known as iodine-based Graves’ disease or iodine-induced thyrotoxicosis. Hyperthyroidism with iodine has been reported continuously since iodine supplementation to prevent endemic goiter. The first case of iodine hyperthyroidism was reported in 1821 (coindet reported hyperthyroidism in 6 of 150 people who were given 250 mg of iodine per day). Epidemiological data found in the Netherlands, Yugoslavia, Australia, Tasmania after iodine supplementation hyperthyroidism incidence was significantly higher than before iodine supplementation, in long-term iodine supplementation for 6 months, the incidence of hyperthyroidism rose, 1 ~ 3 years to reach the peak, and 6 ~ 10 years to recover to the level of iodine supplementation before the iodine, iodine-induced hyperthyroidism is most likely to occur in the functionally normal patients with endemic goiter after the sudden acceptance of excessive iodine therapy. Disease etiology Iodine has a close relationship with the thyroid gland; the former is the raw material for the synthesis of thyroid hormones, and the daily iodine requirement of those over 12 years of age is about 150 μg. The synthesis of thyroid hormones rises with the increase in iodine supply within a certain dosage range; however, the opposite result can occur if the iodine supply exceeds a certain limit. 1, short-term large doses of iodine supply, can make the release of thyroid hormones by acute inhibition, this inhibitory effect is also known as the Woff-Chaikoff effect, may be a temporary protective mechanism, so as to avoid the release and synthesis of excessive hormones; clinical also often use this effect to treat hyperthyroidism crisis. 2, long-term oversupply of iodine, Woff-Chaikoff effect will gradually disappear, the so-called “escape phenomenon”, escape after the synthesis and release of thyroid hormones can be restored to normal, or even accelerated, and sometimes occur in iodine hyperthyroidism. Symptoms and signs The clinical manifestations of iodine hyperthyroidism are similar to those of Graves’ disease, except that the former is older and occurs more often in the elderly and less often in children (it has been reported that none of the 50,000 cases of iodine-treated children had IIH), and the male-to-female ratio of 1:6 to 1:10 is similar to that of Graves’ disease (in iodine-deficient areas with IIH, the majority of the patients have nodules of the thyroid gland, and 15% to 30% of the patients have a smaller or no goiter. goiter, some patients have no nodules), the condition is relatively mild, no thyroid gland pressure pain, thyroid examination can be seen nodular goiter or single nodule, usually no protruding eyes, and rarely have the vascular murmur and tremor in the thyroid area, cardiovascular symptoms and signs are obvious, and the serum antithyroid antibody is negative. A thyroid scan may reveal the presence of “hot spots”. Characteristically, there is a decrease in iodine uptake by the thyroid gland, which is <3% in 24h. Because of the wide range of normal values for urinary iodine, measurement of urinary iodine is of little diagnostic help. Diagnostic tests Diagnosis: 1. Recent history of increased iodine intake, patient with hyperthyroidism manifestations: tachycardia, sweating, weight loss, lethargy and weakness in older age. 2.Laboratory examination of blood FT4 is elevated, FT3 is also elevated, but it is disproportionate to the elevation of T4, not as significant as T4, TSH is decreased, low or no response during TRH excitation test, and the characteristic test is the decrease of 131I uptake rate. 3, thyroid scanning can find the existence of "hot zone". 4. Other causes of hyperthyroidism should be excluded.