IN THE past two decades, research on simple goiter has concentrated on the mechanisms which govern the adaptation of the thyroid gland to iodine deficiency. As a result of these investigations, the pathogenesis of goiters induced by shortage of iodine is rather well understood at the present time. The accumulated knowledge has been laid down in a number of easily accessible reviews (1–57). In contrast to previously published work, the present review is devoted to those aspects of simple goiter which have not been explained by the investigations on iodine deficiency. They include structural and functional heterogeneity between single follicles or between different regions of a goiter, the growth of goiters in spite of abundant iodine supply, the development of single and multiple nodules, the pathogenesis of cold and hot follicles, and the pathogenesis of hyperthyroidism in simple goiter. Simple goiter is a slowly developing diffuse or nodular enlargement of the thyroid gland resulting from excessive replication of epithelial cells with subsequent generation of new follicles of widely differing structure and function.
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Studer et al. (1982) studied this question.