Antoniadou Christina, Gavriilidis Efstratios, Ritis Konstantinos, Tsilingiris Dimitrios
First Department of Internal Medicine, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece.
Laboratory of Molecular Hematology, Department of Medicine, Democritus University of Thrace, Alexandroupolis, Greece.
Metabol Open. 2025 Jan 4;25:100344. doi: 10.1016/j.metop.2024.100344. eCollection 2025 Mar.
Anemia is a frequent, yet increasingly recognized, comorbidity in diabetes mellitus (DM), with prevalence often driven by multifactorial mechanisms. Hematinic deficiencies, common in this population, may arise from associated comorbidities or medications, such as metformin, as well as other drugs commonly employed for DM-related conditions. Among contributing factors, diabetic kidney disease (DKD) plays a pivotal role, with anemia developing more frequently and being more pronounced in earlier stages, than in CKD of other causes. This enhanced susceptibility stems primarily from the combined impact of impaired renal oxygen sensing and deficient erythropoietin (EPO) production linked to tubulointerstitial fibrosis. Additional mechanisms comprise glomerular dysfunction, shortened erythrocyte lifespan, uremia-induced bone marrow suppression, and increased bleeding risk. DM is also recognized as a chronic low-grade inflammatory condition, with its inflammatory burden driving iron maldistribution, suppression of erythropoiesis, and resistance to EPO. The diagnostic approach of anemia in DM mirrors that in the general population. Addressing modifiable causes such as hematinic deficiencies, and other chronic conditions, such as DKD and bone marrow disorders, is paramount. In total, the underlying pathophysiology of anemia in DM primarily reflects a state of absolute or relative EPO deficiency and/or diminished bone marrow responsiveness, effectively corresponding to 'anemia of chronic disease. Early initiation of EPO therapy, even in DM patients without overt DKD, may mitigate disease progression and improve outcomes. Future research should focus on diabetes-specific strategies integrating optimal EPO use, potentially implementing targeted management of renal and inflammatory contributors to anemia.
贫血是糖尿病（DM）中一种常见但日益受到重视的合并症，其患病率通常由多因素机制驱动。该人群中常见的造血物质缺乏可能源于相关合并症或药物，如二甲双胍以及常用于治疗糖尿病相关病症的其他药物。在诸多促成因素中，糖尿病肾病（DKD）起着关键作用，与其他病因导致的慢性肾脏病相比，贫血在DKD早期更频繁且更明显地发生。这种易感性增强主要源于肾氧感应受损和与肾小管间质纤维化相关的促红细胞生成素（EPO）生成不足的综合影响。其他机制包括肾小球功能障碍、红细胞寿命缩短、尿毒症诱导的骨髓抑制以及出血风险增加。DM也被认为是一种慢性低度炎症性疾病，其炎症负荷导致铁分布异常、红细胞生成受抑制以及对EPO产生抵抗。DM患者贫血的诊断方法与普通人群相似。解决可改变的病因，如造血物质缺乏，以及其他慢性病症，如DKD和骨髓疾病，至关重要。总体而言，DM患者贫血的潜在病理生理学主要反映绝对或相对EPO缺乏状态和/或骨髓反应性降低，实际上相当于“慢性病贫血”。即使在没有明显DKD的DM患者中，早期启动EPO治疗也可能减轻疾病进展并改善预后。未来的研究应聚焦于整合最佳EPO使用的糖尿病特异性策略，可能实施针对贫血的肾脏和炎症促成因素的靶向管理。
