Erythropoiesis and erythropoietin in hypo- and hyperthyroidism.
Erythropoiesis and erythropoietin in hypo- and hyperthyroidism.
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甲状腺功能减退症和甲状腺功能亢进症中的红细胞生成和促红细胞生成素。
DOI：
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发表时间：
1975
影响因子：
5.8
通讯作者：
G. Rastogi
中科院分区：
文献类型：
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作者：
K. C. Das;M. Mukherjee;T. K. Sarkar;R. Dash;G. Rastogi
对23例甲减和21例甲亢患者的红细胞生成进行了定性和定量研究，包括常规血液学评价、骨髓形态、血清铁、B12和叶酸状态、红细胞质量和血浆容量的放射性同位素法、红细胞动力学和血浆促红细胞生成素的放射生物测定法。大多数甲状腺功能低下的患者每公斤体重的红细胞质量显著降低。由于伴随的血浆容量减少，从血红蛋白和红细胞压积的数值来看，许多患者贫血的存在并不明显。甲减患者的红细胞动力学数据为骨髓的红细胞生成活性显著下降提供了证据。~3H-胸腺嘧啶核苷标记指数降低表明，骨髓中的红系细胞被耗尽，增殖活性也降低。血浆促红细胞生成素水平降低，通常不能通过小鼠红细胞增多症生物测定技术检测到。甲状腺功能低下状态下红细胞生成的这些变化似乎是对由于基础代谢率降低而导致的组织需氧量减少的生理调整的一部分。类似的研究显示，甲亢患者中有相当一部分出现轻度红细胞增多症。在本组其他患者中，由于缺乏铁、维生素B12和叶酸等造血营养素而导致的红细胞生成障碍与红细胞生成失败有关。这些患者的平均血浆促红细胞生成素水平明显升高，其中4例患者的血浆促红细胞生成素水平处于正常上限，其余患者的血浆促红细胞生成素水平均高于正常范围。所有甲亢患者的骨髓均呈甲状旁腺增生。甲亢患者红细胞平均~3H-胸腺嘧啶核苷标记指数也明显高于正常，其中8例在正常范围内，13例在正常范围以上。红细胞动力学研究也提供了骨髓中红细胞生成活性增加的证据。据推测，甲状腺激素刺激红血球生成，有时会导致红血球增多，但前提是不缺乏造血营养物质。类甲状腺激素对红细胞生成的刺激似乎是通过促红细胞生成素来实现的。
Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin. A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow. Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H-thymidine labeling index. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique. These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate. The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow. It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients. Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.