Iodide-induced thyrotoxicosis.
Iodide-induced thyrotoxicosis (IIT) occurs in patients with: 1) endemic goiter; 2) nonendemic goiter; 3) no previous thyroid disease. Iodine prophylaxis for endemic goiter caused transient increase of 0.01-0.04% over the basal incidence of hyperthyroidism peaking at 1-3 years and normalizing in 3-10 years despite continued iodide exposure. Elderly subjects with large nodular goiters of long standing are at greater risk. In nonendemic areas, iodine-containing drugs such as amiodarone, radiographic contrast media or iodochlorhydroxyquinoline are implicated in IIT more often than iodides. With nonendemic goiter, IIT occurs more commonly in women whereas, in the absence of preexisting thyroid disease, men are more often affected. In both groups, exophthalmos and antithyroid antibodies are absent, radioiodine uptake is low, there is no thyroid tenderness or pain, and the hyperthyroidism is self-limited (1-6 months) and should thus be treated conservatively. IIT occurs more frequently in areas of marginal iodine intake (Europe) than in the U.S. In view of the extensive exposure to iodine, it is a rare complication in this country. It is postulated that defective autoregulation of hormone biosynthesis may contribute to IIT.[1]References
- Iodide-induced thyrotoxicosis. Fradkin, J.E., Wolff, J. Medicine (Baltimore) (1983) [Pubmed]
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