Anemia of Chronic Disease
Anemia of Chronic Disease
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DOI：
10.1053/j.seminhematol.2013.06.006
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发表时间：
2013-07-01
影响因子：
3.6
通讯作者：
Wolanskyj, Alexandra P.
中科院分区：
文献类型：
--
作者：
Gangat, Naseema;Wolanskyj, Alexandra P.
慢性病贫血（ACD）或炎症可能继发于感染、自身免疫性疾病、慢性肾功能衰竭或恶性肿瘤。其特征是免疫激活，炎症细胞因子增加，从而导致铁调素水平增加。此外，促红细胞生成素水平不适当或对促红细胞生成素反应低下以及红细胞存活率降低也会导致贫血。铁调素是铁代谢的中心调节剂，在 ACD 的病理生理学中发挥着关键作用。铁调素与巨噬细胞、肝细胞和肠细胞上存在的铁输出蛋白铁转运蛋白结合，导致后者降解。这导致铁被困在巨噬细胞和肝细胞内，导致功能性缺铁。铁调素的产生反过来又通过 BMP-SMAD 和 JAK-STAT 信号通路受到铁储存、炎症和红细胞生成的调节。贫血的治疗应主要针对基础疾病，也可考虑常规治疗，如红细胞输注、铁剂、促红细胞生成素，以及针对铁调素-铁转运蛋白轴和参与铁调素产生的信号通路（BMP-SMAD、JAK-STAT）的新型药物。塞明血液学 50：232-238。 (C) 2013 Elsevier Inc. 保留所有权利。
Anemia of chronic disease (ACD) or inflammation may be secondary to infections, autoimmune disorders, chronic renal failure, or malignancies. It is characterized by an immune activation with an increase in inflammatory cytokines and resultant increase in hepcidin levels. In addition, inappropriate erythropoietin levels or hyporesponsiveness to erythropoietin and reduced red blood cell survival contribute to the anemia. Hepcidin being the central regulator of iron metabolism plays a key role in the pathophysiology of ACD. Hepcidin binds to the iron export protein, ferroportin, present on macrophages, hepatocytes, and enterocytes, causing degradation of the latter. This leads to iron trapping within the macrophages and hepatocytes, resulting in functional iron deficiency. Production of hepcidin is in turn regulated by iron stores, inflammation, and erythropoiesis via the BMP-SMAD and JAK-STAT signaling pathways. Treatment of anemia should primarily be directed at the underlying disease, and conventional therapy such as red blood cell transfusions, iron, erythropoietin, and novel agents targeting the hepcidin-ferroportin axis and signaling pathways (BMP-SMAD, JAK-STAT) involved in hepcidin production also may be considered. Semin Hematol 50:232-238. (C) 2013 Elsevier Inc. All rights reserved.