Hintze G, Köbberling J
Klin Wochenschr. 1987 Jul 1;65(13):583-9. doi: 10.1007/BF01726663.
The hypothesis that goitrogenesis in iodine deficiency can be attributed to the stimulatory effect of thyrotropin (TSH) on the thyroid gland and has long been held to be valid. The task of this review is to describe the reasons why this concept is being challenged. In addition, we report on the autoregulation of the thyroid gland and on in vitro investigations dealing with TSH as a growth factor, which have yielded conflicting results. Finally, we summarize preliminary studies comparing the therapeutic effect of thyroxine and iodine on goiter size. In comparison to thyroxine, iodine application in doses of 300-500 micrograms/day may represent an equally effective way of treatment in areas of endemic goiter, especially in younger patients. In this age group, the risk of side-effects, e.g., iodine-induced thyrotoxicosis, should be low.
长期以来,人们一直认为碘缺乏导致甲状腺肿的假说归因于促甲状腺激素(TSH)对甲状腺的刺激作用,该假说一直被认为是正确的。本综述的任务是描述这一概念受到挑战的原因。此外,我们报告了甲状腺的自动调节以及关于TSH作为生长因子的体外研究,这些研究得出了相互矛盾的结果。最后,我们总结了比较甲状腺素和碘对甲状腺肿大小治疗效果的初步研究。与甲状腺素相比,每天服用300 - 500微克剂量的碘可能是地方性甲状腺肿地区同样有效的治疗方法,尤其是对年轻患者。在这个年龄组中,副作用的风险,如碘诱发的甲状腺毒症,应该较低。