IODINE-INDUCED HYPERTHYROIDISM - OCCURRENCE AND EPIDEMIOLOGY

We have critically reviewed the available information on iodine-induce d hyperthyroidism (IIH) from published sources and other reports as we ll as the experience of the authors in Tasmania, Zaire, Zimbabwe, and Brazil. Administration of iodine in almost any chemical form may induc e an episode of thyrotoxicosis (IIH). This has been observed in epidem ic incidence in several countries when iodine has been given as prophy laxis in a variety of vehicles, but the attack rate as recorded has be en low. IIH is most commonly encountered in older persons with long st anding nodular goiter and in regions of chronic iodine deficiency, but instances in the young have been recorded. It customarily occurs afte r an incremental rise in mean iodine intake in the course of programs for the prevention of iodine deficiency, or when iodine-containing dru gs such as radiocontrast media or amiodarone are administered. The bio logical basis for IIH appears most often to be mutational events in th yroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient and iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localize d foci within the gland or in the process of nodule formation. IIH may also occur with an increase in iodine intake in those whose hyperthyr oidism (Graves' disease) is not expressed because of iodine deficiency . The risks of IIH are principally to the elderly who may have heart d isease, and to those who live in regions where there is limited access to medical care. More information is needed on the long-term health i mpact of IIH or ''subclinical'' IIH, especially in the course of proph ylaxis programs with iodized salt or iodinated oil in regions where ac cess to health care is limited.