[Molecular aetiology of nodular goitre -- consequences for therapy?]

Up to 15 % of the adult German population display an enlarged thyroid gland and up to 30 % present thyroid nodules. Iodine deficiency is the most important factor in the etiology of nodular goiter. Insulin-like growth factor-I is overexpressed in thyroids in severely iodine deficient areas. There is evidence that iodolactones are mediators of thyroid hormone autoregulation. However familial and twin studies demonstrated a genetic component in the etiology of nodular goiter. Linkage analysis identified two chromosomal regions (MNG-1, Xp 22) in multinodular goiter. Other possible candidate genes or markers such as TG, TPO, NIS, PDS and TSH-R were not identified. Nodular goiter certainly comprises a number of genotypes. TSH receptor mutations result in activation of the cAMP cascade. Cells with a constitutively activated cAMP cascade have an increased growth advantage due to their TSH independent cAMP stimulation. Alimentary iodine supply should be the first choice in primary prevention of nodular thyroid disease in iodine deficient areas, because prevalence of nodular goiter is negative correlated with individual iodine status in epidemiological surveys. Surgical removal of nodular goiters should include nearly the hold thyroid tissue to avoid recurrent goiter.