Anagnostou A, Miller M, Westenfelder C, Clemons G, Baranowski R
Division of Hematologic Research, Brown University, Pawtucket, Rhode Island 02860.
Exp Hematol. 1988 Feb;16(2):159-62.
Patients and/or experimental animals with chronic renal failure have decreased serum levels of triiodothyronine (T3), a hormone well known for its erythropoietic activity. The following studies were designed in order to determine whether this observed abnormality in T3 metabolism is an important contributory factor to the etiology of the anemia of uremia. Groups of rats were made chronically uremic by a standard 5/6 nephrectomy technique and received slightly above physiological doses of T3 either by intermittent S.C. injections (twice daily) or by continuous infusion from intraperitoneally implanted osmotic minipumps. After 2 weeks of such treatment, and despite a normalization of serum T3 levels, there were no significant changes in the hematocrit, individual red cell mass, or serum erythropoietin levels of the uremic animals given T3 compared to control rats. We conclude that (1) the decreased serum T3 levels observed in uremia are not an important contributory factor to the pathogenesis of the anemia, and (2) treatment with replacement doses of T3 does not result in significant improvement of erythropoiesis.
患有慢性肾衰竭的患者和/或实验动物血清三碘甲状腺原氨酸(T3)水平降低,T3是一种因具有促红细胞生成活性而广为人知的激素。开展以下研究以确定观察到的T3代谢异常是否是尿毒症贫血病因的一个重要促成因素。通过标准的5/6肾切除术使大鼠慢性尿毒症化,并通过间歇性皮下注射(每日两次)或通过腹腔植入的渗透微型泵持续输注给予略高于生理剂量的T3。经过2周的这种治疗后,尽管血清T3水平恢复正常,但与对照大鼠相比,给予T3的尿毒症动物的血细胞比容、个体红细胞量或血清促红细胞生成素水平均无显著变化。我们得出结论:(1)尿毒症中观察到的血清T3水平降低不是贫血发病机制的一个重要促成因素,(2)用替代剂量的T3治疗不会导致红细胞生成显著改善。