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[Study of the pathogenesis of high iodine-induced goiter]
1Department of Pathology, Shandong Academy of Medical Sciences, Jinan.
We used Leghorn chickens to establish iodine-induced goiter. The pathologic changes were observed. The levels of MIT, DIT, T3 and T4 in the thyroid, and T3, T4 and TSH in serum, and the amount of iodine transport and synthesis of organic iodine in thyroid were determined. The results showed that high iodine intake strengthened the thyroid function and enhanced the synthesis of organic iodine. The rate of organic iodine synthesis exceeded T3,T4 secretion and the accumulation of organic iodine in the follicules exerted pressure inhibition on follicular epithelium, and then the levels of serum T3 and T4 dropped down. The negative feedback effect on the pituitary became weak. The secretion of thyrotropin rose and the hyperplasia of thyroid epithelium appeared. Therefore, we propose that the follicular distension resulting from the accumulation of organic iodine and the epithelial hyperplasia induced by rise of TSH are two different stages of the pathogenesis of iodine-induced goiter.
We used Leghorn chickens to establish iodine-induced goiter. The pathologic changes were observed. The levels of MIT, DIT, T3 and T4 in the thyroid, and T3, T4 and TSH in serum, and the amount of iodine transport and synthesis of organic iodine in thyroid were determined. The results showed that high iodine intake strengthened the thyroid function and enhanced the synthesis of organic iodine. The rate of organic iodine synthesis exceeded T3,T4 secretion and the accumulation of organic iodine in the follicules exerted pressure inhibition on follicular epithelium, and then the levels of serum T3 and T4 dropped down. The negative feedback effect on the pituitary became weak. The secretion of thyrotropin rose and the hyperplasia of thyroid epithelium appeared. Therefore, we propose that the follicular distension resulting from the accumulation of organic iodine and the epithelial hyperplasia induced by rise of TSH are two different stages of the pathogenesis of iodine-induced goiter.