Iodine-induced hyperthyroidism: occurrence and epidemiology.

We have critically reviewed the available information on iodine-induced hyperthyroidism (IIH) from published sources and other reports as well as the experience of the authors in Tasmania, Zaire, Zimbabwe, and Brazil. Administration of iodine in almost any chemical form may induce an episode of thyrotoxicosis (IIH). This has been observed in epidemic incidence in several countries when iodine has been given as prophylaxis in a variety of vehicles, but the attack rate as recorded has been low. IIH is most commonly encountered in older persons with long standing nodular goiter and in regions of chronic iodine deficiency, but instances in the young have been recorded. It customarily occurs after an incremental rise in mean iodine intake in the course of programs for the prevention of iodine deficiency, or when iodine-containing drugs such as radiocontrast media or amiodarone are administered. The biological basis for IIH appears most often to be mutational events in thyroid 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 localized foci within the gland or in the process of nodule formation. IIH may also occur with an increase in iodine intake in those whose hyperthyroidism (Graves' disease) is not expressed because of iodine deficiency. The risks of IIH are principally to the elderly who may have heart disease, and to those who live in regions where there is limited access to medical care. More information is needed on the long-term health impact of IIH or "subclinical" IIH, especially in the course of prophylaxis programs with iodized salt or iodinated oil in regions where access to health care is limited.

Thyrotoxicosis induced by iodine contamination of food--a common unrecognised condition?

The incidence of thyrotoxicosis in northern Tasmania rose significantly in 1964, two years before an epidemic of iodine-induced thyrotoxicosis was precipitated by the addition of iodate to bread to prevent goitre. Each time older patients accounted for most of the increase. The 1964 increase was probably iodine-induced as the use of iodophor disinfectants on dairy farms, which causes iodine residues in milk, began in 1963 and a fall in the prevalence of goitre in young children suggested an increase in dietary iodine at about that time. A further small increase in thyrotoxicosis in 1971 may also have been iodine-induced as it followed an extension of the use of iodophors. Dietary iodine is rising substantially in many places because of high iodine levels in milk and the use of iodine compounds in automated bread making, and this may be causing unsuspected iodine-induced thyrotoxicosis. Dietary iodine should be monitored regularly and clinicans alerted to any rise. Contamination of common foods with iodine should be more strictly controlled.

Hyperthyroidism in Tasmania following iodide supplementation: measurements of thyroid-stimulating autoantibodies and thyrotropin.

Serum thyroid-stimulating autoantibodies (LATS and LATS protector) and thyrotropin (TSH) concentrations were measured in the serum of 30 patients with hyperthyroidism living in Tasmania who developed their disease following correction of iodine deficiency by addition of iodate to the bread. Patients were grouped according to thyroid scan results. None of 8 patients with autonomous thyroid nodules had thyroid-stimulating autoantibodies. These were present in both of the patients with uniform thyroid scans and 14 of 20 patients (70%) with irregular scans without demonstrated localized autonomy. Serum TSH, measured by immunoassay of concentrated serum extracts, was 0.15 muU/ml or less in all patients, below the range of 0.35 to 2.60 muU/ml found in normal subjects. Only 6 (20%) of the 30 patients failed to show either localized autonomy or thyroid-stimulating autoantibodies. In most regards these patients resembled those with antonomous nodules. The findings support the conclusion that the increased incidence of phyerthyroidism in Tasmania was due to an increased supply of iodine to patients with latent hyperthyroidism whose thyroid glands, due to the presence of toxid nodule(s) or thyroid-stimulating autoantibodies, were unresponsive to control by TSH deprivation. There was no evidence for additional pathogenic mechanisms