Thyroxine treatment of benign goiter.

The conservative therapy of endemic as well as sporadic goiter is the TSH suppressive therapy with thyroxine. In the last decade, this therapeutic concept as well as the role of TSH in goiter development fell into disrepute. It has become evident that TSH mainly regulates thyroid function, induces hypertrophy of the follicular cells and increases the blood flow within the thyroid gland. The intrathyroidal iodine deficiency itself and the increased activity of local growth factors, however, may be the main causes of initiation, promotion and maintenance of hyperplasia. The clinical observation of a "shrinking" goiter during thyroxine therapy is now well established by ultrasound investigations as a decrease in goiter volume of maximal 30 to 40% within the first few months of treatment. Afterwards no further significant reduction in goiter size has been demonstrated so far. Stopping treatment results in an increase of goiter volume within a few weeks. These rapid changes can only be related to changes in the size of cells, follicles and vessels and not to growth or necrosis of thyroid cells. In comparison, treatment of endemic goiter with iodine also lead to a reduction of hypertrophy, but as demonstrated in rats, also to a reduction of hyperplasia. Treatment with iodine compared to thyroxine has a prolonged effect on reduction of goiter size even after withdrawal of the substitution. The main question that has to be discussed is whether the hyperplastic part of an endemic goiter in adults can be treated at all, either with thyroxine or iodine or both.(ABSTRACT TRUNCATED AT 250 WORDS)