[Thyroid hormones in the treatment of iodine deficiency goiter. Superfluous like goiter?].

In recent years, the widespread use of iodized salt in households and industrially produced foods has considerably improved the shortage of iodine in the German diet. Recent epidemiologic studies have shown that we are now at the threshold of adequacy. Over the last decade, views on the pathogenesis of iodine deficiency goiter have changed: while TSH was previously assumed to be the major factor underlying this form of goiter, experimental data now finger the activation of local growth factors, in particular IGF1. Iodinated organic compounds, in particular iodolacton produced by iodination of unsaturated fatty acids in the thyrocyte, are the key regulators of IGF1 activity by inhibitory action, and iodine is now the therapeutic agent of first choice for iodine deficiency goiter; long-term thyroxine treatment in TSH suppressive doses has been abandoned. The recommended daily dose of iodine is 200 micrograms; higher doses may induce or aggravate autoimmune thyroiditis, and should not be used for a length of time. In pregnant women, an adequate supply of iodine is of critical importance for optimal neurophysiological development, and the general use of iodine supplementation in pregnancy therefore remains mandatory in Germany.