el Hassan A M, Saeed A M, Fandrey J, Jelkmann W
Department of Physiology, University of Khartoum, Sudan.
Eur J Haematol. 1997 Nov;59(5):299-304. doi: 10.1111/j.1600-0609.1997.tb01690.x.
One of the most serious manifestations of Plasmodium falciparum malaria is anaemia. Its established causes are increased red cell destruction and ineffective erythropoiesis. Since proinflammatory cytokines have been shown to suppress the in vitro synthesis of erythropoietin (Epo), we measured serum immunoreactive Epo in 90 Sudanese patients suffering from malaria. Even in severe cases of anaemia (blood haemoglobin < 80 g/l), serum Epo levels rarely exceeded 300 U/l. For comparison, serum Epo was increased up to 12,000 U/l in a reference group of Caucasian patients with anaemia not associated with infection. Moreover, the slope of the log Epo/haemoglobin regression line was less steep in malarial anaemia. Thus, as documented for other chronic inflammatory disorders, there is a relative lack of Epo in malaria-associated anaemia. Treatment with the antimalarial drug chloroquine may aggravate the defect in Epo production, because chloroquine inhibited Epo synthesis when tested in cell culture.
恶性疟原虫疟疾最严重的表现之一是贫血。其已确定的病因是红细胞破坏增加和红细胞生成无效。由于促炎细胞因子已被证明可抑制体外促红细胞生成素（Epo）的合成，我们检测了90名苏丹疟疾患者的血清免疫反应性Epo。即使在严重贫血病例（血血红蛋白<80g/l）中，血清Epo水平也很少超过300U/l。作为对比，在一组与感染无关的贫血白种人患者参考组中，血清Epo升高至12000U/l。此外，疟疾贫血患者中log Epo/血红蛋白回归线的斜率较平缓。因此，正如其他慢性炎症性疾病所证明的那样，疟疾相关性贫血中相对缺乏Epo。抗疟药物氯喹治疗可能会加重Epo产生的缺陷，因为在细胞培养试验中氯喹可抑制Epo合成。
