Lanser Lukas, Weiss Günter
Department of Internal Medicine II (Infectiology, Immunology, Rheumatology, Pneumology), Medical University of Innsbruck, Innsbruck, Austria.
Adv Exp Med Biol. 2025;1480:179-195. doi: 10.1007/978-3-031-92033-2_13.
Anemia of inflammation (AI), also known as anemia of chronic disease, is the most common anemia in hospitalized patients and considered to be the second most common anemia worldwide after iron deficiency anemia (IDA). The hallmark of AI is iron restriction within macrophages of the mononuclear phagocyte system (MPS) resulting in hypoferremia and hyperferritinemia together with suppression of erythropoiesis and shortened erythrocyte lifespan. Symptoms are comparable to other anemia entities and often related to the underlying disease. Patients usually present with normocytic, normochromic, hypoproliferative, mild-to-moderate anemia, reduced circulating iron levels (transferrin saturation), and increased stored iron (serum ferritin). However, AI is often associated with true iron deficiency on the basis of inflammatory diseases and blood losses of different reasons, which is why the correct identification of these patients, and their iron needs is a diagnostic challenge. Treatment of the underlying disease that causes immune activation is the primary therapeutic approach for AI which normally results in its resolution over time. Concomitant pathologies and factors contributing to the AI severity should be considered and, when feasible, specifically corrected. Iron supplementation is the first-line therapy for AI+IDA patients, while intravenously applied iron is trapped in macrophages of the MPS during advanced inflammation in patients with solely AI, whereas orally supplemented iron is not properly absorbed. Effectiveness of erythropoiesis-stimulating agents is limited in AI due to inflammation-mediated suppression of erythropoietin (Epo) signaling and impaired erythroid cell proliferation and differentiation, while red blood cell transfusion should primarily be used in life-threatening anemia. Clinical studies on hypoxia-inducible factor prolyl hydroxylase inhibitors seem promising although concerns about their safety and efficacy in AI arose within recent years. New treatment strategies aim to modify the hepcidin-ferroportin axis, yet clinical trials are still outstanding.
炎症性贫血（AI），也称为慢性病贫血，是住院患者中最常见的贫血类型，被认为是全球仅次于缺铁性贫血（IDA）的第二常见贫血。AI的标志是单核吞噬细胞系统（MPS）巨噬细胞内的铁限制，导致低铁血症和高铁蛋白血症，同时伴有红细胞生成受抑制和红细胞寿命缩短。其症状与其他贫血类型相似，且常与基础疾病相关。患者通常表现为正细胞、正色素、增生低下的轻至中度贫血，循环铁水平降低（转铁蛋白饱和度），储存铁增加（血清铁蛋白）。然而，基于炎症性疾病和不同原因的失血，AI常与真正的缺铁相关，这就是为什么正确识别这些患者及其铁需求是一项诊断挑战。治疗引起免疫激活的基础疾病是AI的主要治疗方法，通常随着时间推移可使其缓解。应考虑导致AI严重程度的伴随病理和因素，并在可行时进行针对性纠正。铁补充是AI合并IDA患者的一线治疗方法，而在单纯AI患者的晚期炎症期间，静脉注射的铁会被困在MPS的巨噬细胞中，而口服补充的铁吸收不佳。由于炎症介导的促红细胞生成素（Epo）信号抑制以及红系细胞增殖和分化受损，促红细胞生成刺激剂在AI中的有效性有限，而红细胞输血主要应用于危及生命的贫血。关于缺氧诱导因子脯氨酰羟化酶抑制剂的临床研究似乎前景乐观，尽管近年来对其在AI中的安全性和有效性存在担忧。新的治疗策略旨在改变铁调素 - 铁转运蛋白轴，但临床试验仍在进行中。
