Anemia of Inflammation: A Review.
Anemia of Inflammation: A Review.
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DOI：
10.1016/j.mcna.2016.09.005
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发表时间：
2017-03
期刊：
影响因子：
--
通讯作者：
Fraenkel PG
中科院分区：
文献类型：
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作者：
Fraenkel PG
铁稳态受损和促炎细胞因子对红细胞生成的抑制作用，以及红细胞膜的改变损害其存活，导致炎症性贫血。最近的流行病学研究将炎症性贫血与危重疾病、肥胖、衰老和肾衰竭以及癌症、慢性感染和自身免疫性疾病联系起来。促炎细胞因子白细胞介素 6、铁调节激素铁调素和铁输出蛋白铁转运蛋白相互作用，在炎症环境中导致铁螯合。虽然严重贫血与危重疾病的不良后果相关，但实验模型表明，铁固存是针对病原体的自然防御的一部分。在动物模型和人类患者中，针对白细胞介素 6 或铁转运蛋白-铁调素轴的实验性治疗方法已显示出逆转贫血的功效，尽管这些药物尚未被批准用于治疗炎症性贫血。
Impaired iron homeostasis and the suppressive effects of proinflammatory cytokines on erythropoiesis, together with alterations of the erythrocyte membrane that impair its survival, cause the anemia of inflammation. Recent epidemiologic studies have connected inflammatory anemia with critical illness, obesity, aging, and kidney failure, as well as with cancer, chronic infection, and autoimmune disease. The proinflammatory cytokine, interleukin-6, the iron regulatory hormone, hepcidin, and the iron exporter, ferroportin, interact to cause iron sequestration in the setting of inflammation. While severe anemia is associated with adverse outcomes in critical illness, experimental models suggest that iron sequestration is part of a natural defense against pathogens. In animal models and human patients, experimental therapeutic approaches targeting interleukin-6 or the ferroportin-hepcidin axis have shown efficacy in reversing anemia, although these agents have not yet been approved for the treatment of the anemia of inflammation.