Brenner B, Fandrey J, Jelkmann W
Institute of Physiology I, University of Bonn, Germany.
Eur J Haematol. 1994 Jul;53(1):6-10. doi: 10.1111/j.1600-0609.1994.tb00171.x.
Laboratory experiments have demonstrated that tetra- and triiodothyronine (T4, T3) enhance hypoxia-induced erythropoietin (Epo) production. In the present study serum immunoreactive Epo was measured in 29 patients with hyperthyroidism and in 10 patients with hypothyroidism. Epo levels were inversely correlated to the blood haemoglobin concentration [Hb] in both groups of patients. However, Epo levels at given [Hb] were significantly higher in the hyperthyroid state. In vitro studies confirmed that T4 and T3 stimulate Epo synthesis in the human liver cell line HepG2. This stimulating effect persisted for at least 1 day after the removal of T4 and T3 from the cultures. Thus, while thyroidal disorders affect steady-state levels of circulating Epo, it seems unlikely that thyroid hormones play a major role in abrupt adjustments of Epo production, such as the diurnal changes.
实验室实验已证明，四碘甲状腺原氨酸和三碘甲状腺原氨酸（T4、T3）可增强缺氧诱导的促红细胞生成素（Epo）的产生。在本研究中，对29例甲状腺功能亢进患者和10例甲状腺功能减退患者的血清免疫反应性Epo进行了检测。两组患者的Epo水平均与血红蛋白浓度[Hb]呈负相关。然而，在给定的[Hb]水平下，甲状腺功能亢进状态下的Epo水平显著更高。体外研究证实，T4和T3可刺激人肝癌细胞系HepG2中的Epo合成。从培养物中去除T4和T3后，这种刺激作用至少持续1天。因此，虽然甲状腺疾病会影响循环Epo的稳态水平，但甲状腺激素似乎不太可能在Epo产生的突然调节（如昼夜变化）中起主要作用。
