Etiology of Simple Goiter

Etiology of Simple Goiter

Abstract

EDITORIALS AND COMMENTARY Etiology of Simple Goiter Laszlo Hegedus,1 Thomas H. Brix,1 and Ralf Paschke2 ¨ imple goiter (SG), that is an enlarged nontoxic thyroid gland which is not the result of an inflammatory or neoplastic process, although on the wane, remains a nearly global problem (1,2). Until increasingly employed iodization programs significantly reduces its prevalence, the etiology as well as the therapy of benign nontoxic goiter should remain in focus. It is well accepted that sporadic or endemic SG (2,3), along with the other common thyroid diseases co-existing with goiter including Graves’ disease (4), toxic multinodular goiter, and Hashimoto’s thyroiditis (5), is a complex disease. These are all common and multifactorial with the clinical phenotype representing the net effect of many contributing genetic and environmental factors. It has been difficult to disentangle environmental influences from genetic susceptibility, progress has been slow in revealing candidate genes, and little is known of the roles of gene–environment and gene–gene interaction. A role for genetic factors in the etiology of SG has long been recognized. Familial aggregation is illustrated by the 5–10 times greater prevalence of SG among the probands of first degree female relatives as compared with the background population