Platzer S, Groebner P, Hausen A, Obendorf L, Riccabona G
Wien Klin Wochenschr. 1980 Feb 1;92(3):88-91.
According to several reports we suspected that the pathogenesis of endemic goitre cannot be explained by iodine deficiency only, but that other--partially endogenous--goitrogenic factors must be present. We therefore studied 16 cases of "euthyroid" endemic goitre from the endemic goitre area of the province of Bolzano in Italy. After fractionation of tissue homogenates, T 4 and T 3 were measured by RIA and the I concentration was also termined. Thyroglobulin and its fractions were measured by ultracentrifuge procedures after assessment of the total protein concentration. Evaluation of the present results suggests that an insufficient synthesis of thyroglobulin in the examined goitres induces an inadequate adaptation of the organism to iodine deficiency, which, in turn, decreases the thyroid hormone concentration in thyroid tissue and enhances goitrogenesis. Considering the normal iodine content of the examined tissues, there obviously seems to be two intrathyroidal iodine pools, one of which supplies the body with thyroid hormones under pituitary stimulation even though its thyroglobulin pool is reduced, while a significant amount of the thyroidal iodine pool is bound in metabolically inert protein molecules and therefore increases the goitrogenic effect of iodine deficiency.
根据几份报告,我们怀疑地方性甲状腺肿的发病机制不能仅用碘缺乏来解释,还必须存在其他(部分为内源性的)致甲状腺肿因素。因此,我们研究了来自意大利博尔扎诺省地方性甲状腺肿病区的16例“甲状腺功能正常”的地方性甲状腺肿病例。组织匀浆分级分离后,用放射免疫分析法测定T4和T3,并测定碘浓度。在评估总蛋白浓度后,通过超速离心法测定甲状腺球蛋白及其组分。对目前结果的评估表明,在所检查的甲状腺肿中,甲状腺球蛋白合成不足导致机体对碘缺乏的适应性不足,进而降低甲状腺组织中的甲状腺激素浓度并增强甲状腺肿的发生。考虑到所检查组织的碘含量正常,甲状腺内显然存在两个碘池,其中一个即使其甲状腺球蛋白池减少,在垂体刺激下仍能为身体提供甲状腺激素,而大量的甲状腺碘池则与代谢惰性的蛋白质分子结合,因此增加了碘缺乏的致甲状腺肿作用。