Lacour B, Basile C, Drüeke T
Nephrologie. 1980;1(1):9-14.
Red blood cell (RBC) production has been explored in hyperparathyroid as compared to normal rats. The hyperparathyroid state was obtained by feeding the rats a calcium-deficient diet during 30 days. A significant decrease (p less than 0.001) in reticulocyte count and in erythrocyte 59Fe incorporation was observed in hyperparathyroid rats when compared to control animals. A comparable inhibition of erythrocyte 59Fe incorporation in hyperparathyroid rats was found when the study was performed after stimulating bone marrow activity by acute arterial hemorrhage. These results of decreased RBC production using a model of endogenous hyperparathyroidism could be confirmed in additional experiments using a model of exogenous hyperparathyroidism. In this model, the rats received either parathyroid extract (3 x 10 USP/day during 8 days) or vehicle only. Again, a decrease in erythrocyte 59Fe incorporation was observed in hyperparathyroid animals when compared to control animals. It is concluded that the hyperparathyroid state is accompanied by a decrease of RBC production in the rat. It is probable that a similar pathogenesis underlies the anemia of patients with primary or secondary hyperparathyroidism.
与正常大鼠相比，已经对甲状旁腺功能亢进大鼠的红细胞（RBC）生成进行了研究。通过给大鼠喂食30天缺钙饮食来诱导甲状旁腺功能亢进状态。与对照动物相比，甲状旁腺功能亢进大鼠的网织红细胞计数和红细胞59Fe掺入量显著降低（p<0.001）。当通过急性动脉出血刺激骨髓活性后进行该研究时，在甲状旁腺功能亢进大鼠中发现了类似的红细胞59Fe掺入抑制。使用内源性甲状旁腺功能亢进模型降低RBC生成的这些结果可以在使用外源性甲状旁腺功能亢进模型的其他实验中得到证实。在该模型中，大鼠接受甲状旁腺提取物（8天内每天3×10 USP）或仅接受赋形剂。同样，与对照动物相比，甲状旁腺功能亢进动物的红细胞59Fe掺入量降低。结论是甲状旁腺功能亢进状态伴随着大鼠RBC生成的减少。原发性或继发性甲状旁腺功能亢进患者贫血的发病机制可能与此相似。
