Cao S W
Department of Pathology, Shandong Academy of Medical Sciences, Jinan.
Zhonghua Bing Li Xue Za Zhi. 1990 Dec;19(4):294-6.
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.
我们使用来亨鸡建立碘致甲状腺肿模型，观察其病理变化，并测定甲状腺中一碘甲腺原氨酸（MIT）、二碘甲腺原氨酸（DIT）、三碘甲状腺原氨酸（T3）和甲状腺素（T4）的水平，血清中T3、T4和促甲状腺激素（TSH）的水平，以及甲状腺中碘转运和有机碘合成的量。结果显示，高碘摄入增强了甲状腺功能并促进了有机碘的合成。有机碘合成速率超过了T3、T4的分泌，滤泡中有机碘的积累对滤泡上皮产生压力抑制，进而血清T3和T4水平下降。对垂体的负反馈作用减弱，促甲状腺激素分泌增加，甲状腺上皮出现增生。因此，我们提出有机碘积累导致的滤泡扩张和TSH升高引起的上皮增生是碘致甲状腺肿发病机制的两个不同阶段。
