Risks of iodine-induced hyperthyroidism after correction of iodine deficiency by iodized salt

Abstract

Biochemical signs of hyperthyroidism, or even overt and possibly lethal clinical hyperthyroidism were reported in 2 severely iodine-deficient African countries (Zimbabwe and Democratic Republic of Congo, RDC) soon after the introduction of iodized salt. The 2 countries had access to iodized salt produced in Botswana, as well as 5 other countries in the region, namely Cameroon, Nigeria, Kenya, Tanzania, and Zambia. Therefore, a multicenter study was conducted in these 7 countries to evaluate whether the occurrence of iodine-induced hyperthyroidism (IIH) after the introduction of iodized salt was a general phenomenon or corresponded to specific local situations in the 2 affected countries. Two or 3 areas with a past history of severe iodine deficiency that had recently been supplemented with iodized salt were selected in each of the 7 countries. The prevalence of goiter was determined in 4423 schoolchildren in these areas and the concentration of urinary iodine in 2258. Salt factories and health structures were visited for the evaluation of the quality of iodized salt and the possible occurrence of IIH. The study showed that iodine deficiency had been eliminated in all areas investigated, and that the prevalence of goiter had markedly decreased since the introduction of iodized salt. This is a remarkable achievement in terms of public health. However, some areas were now exposed to iodine excess due mostly to a poor monitoring of the quality of the iodized salt and of the iodine intake of the population. In these areas or countries, IIH occurred only when the introduction of iodized salt had been of recent onset (<2 years), namely in Zimbabwe and RDC. In conclusion, the risk of IIH after correction of iodine deficiency is closely related to a recent excessive increment of iodine supply.