Bános C, Takó J, Salamon F, Györgyi S, Czikkely R
Acta Med Acad Sci Hung. 1979;36(4):381-94.
The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.
在7名使用含雌激素口服避孕药的甲状腺功能正常女性和8名对照组中，于肌内注射促肾上腺皮质激素（2mg长效合成促皮质素）之前（及之后），静脉注射0.4mg促甲状腺激素释放激素（TRH），检测血清促甲状腺激素（TSH）、甲状腺素（T4）、三碘甲状腺原氨酸（T3）及反三碘甲状腺原氨酸（rT3）的反应，结果如下：（1）内源性糖皮质激素分泌增加与TSH对TRH反应的抑制有关；（2）生成量减少的TSH仍能刺激甲状腺分泌；（3）血清皮质激素水平升高未能影响甲状腺对TSH的分泌反应；（4）血清甲状腺素结合球蛋白（TBG）水平升高时，垂体 - 甲状腺轴的调控仍保持正常。在另一组研究中，对6名未接受治疗的正常对照者、6名使用口服避孕药的正常女性及10名未接受治疗的甲状腺功能亢进患者，研究了促肾上腺皮质激素诱导的内源性糖皮质激素分泌过多作用下的血清TBG、T4、T3、rT3及皮质醇水平。在治疗后的4天内，血清TBG水平下降，口服避孕药使用者下降幅度最大，对照组下降幅度最小。发现血清T4在2至4天内下降，血清T3与血清rT3升高平行，持续1至2天，随后进行促肾上腺皮质激素负荷试验。在甲状腺功能正常的病例中，血清TSH水平也出现短暂下降。结论为，在内源性糖皮质激素分泌过多的情况下：（1）T4向T3的单碘脱失减少，T4向rT3的转化增加，与血清皮质醇水平的变化平行；（2）内源性糖皮质激素抑制TBG合成；（3）血清TBG水平的变化伴随着血清T4浓度的降低。
