Iodine solutions, such as saturated potassium iodide solutions (SSKI) or potassium iodide-iodine (Lugol's solution), replaced burnt sponge extract in the 19th century as treatment for endemic goiter. By extension, they were sometimes used to treat Graves’ disease, but by the end of the century they were considered to be a dangerous form of therapy. They returned to favor in the 1920s as preoperative treatment for hyperthyroidism and were for a time in the 1930s thought to be useful as the sole therapy for mild hyperthyroidism. Today, iodine continues to have a minor role in the treatment of hyperthyroidism.
The role of iodine in the treatment of hyperthyroidism will be reviewed here. The treatment of hyperthyroidism in general is reviewed in detail elsewhere. (See "Treatment of Graves' hyperthyroidism in adults" and "Beta blockers in the treatment of hyperthyroidism" and "Thionamides in the treatment of Graves' disease" and "Radioiodine in the treatment of hyperthyroidism".)
MECHANISM OF ACTION
Iodine has several effects on thyroid function. In hyperthyroid patients, iodine acutely inhibits hormonal secretion within hours , but the responsible mechanisms are uncertain. This is the most acute effect of iodine on thyroid status, occurring within one to two days of the start of therapy.
A second effect involves inhibition of thyroid hormone synthesis. In normal subjects, the administration of pharmacologic amounts of iodine leads to temporary inhibition of iodine organification in the thyroid gland, thereby diminishing thyroid hormone biosynthesis, a phenomenon called the Wolff-Chaikoff effect . However, within two to four weeks of continued exposure to excess iodine, organification and thyroid hormone biosynthesis resume in a normal fashion. This is called escape from the Wolff-Chaikoff effect. (See "Iodine-induced thyroid dysfunction" and "Thyroid hormone synthesis and physiology".)
In patients with autoimmune thyroid disease, there is abnormal autoregulation of iodine economy. Iodine-induced blockade of iodine organification persists and can result in or exacerbate hypothyroidism in patients with Hashimoto's thyroiditis, or ameliorate hyperthyroidism in Graves’ disease. Thus, patients with Graves’ hyperthyroidism are more sensitive to the inhibitory effect of pharmacologic doses of iodine than normal subjects, making iodine treatment effective in some patients. In addition, pharmacologic amounts of iodine may acutely ameliorate hyperthyroidism by blocking thyroid hormone release.