McMaster Center for Transfusion Research, McMaster University, Hamilton, Ontario, Canada.
Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada.
Transfus Med Rev. 2021 Jul;35(3):22-28. doi: 10.1016/j.tmrv.2021.06.001. Epub 2021 Jun 15.
Anemia is not only a consequence of bleeding, but also a modifiable risk factor for bleeding in patients with thrombocytopenia or platelet function defects. In this review we outline the mechanism of anemia-induced bleeding in patients with platelet disorders, which involves a disturbance in normal red blood cell (RBC) rheology and reduced platelet margination to the endothelial surface due to a decrease in RBC mass, leading to impaired primary hemostasis and bleeding. Biologically, anemia reduces the mass of RBCs in the central column of flowing blood through a vessel resulting in fewer platelets coming into contact with the endothelial surface at the periphery of the flowing blood column. Thus, anemia results in impaired primary hemostasis. Von Willebrand factor (vWF) is another component of primary hemostasis and vWF deficiency, especially a deficiency of the highest vWF multimers, can also manifest with bleeding when concomitant anemia occurs. Clinically, patients at greatest risk for anemia-induced bleeding include patients with hematological malignancies in whom anemia and thrombocytopenia occur as a result of the underlying disease or the myelotoxic effects of treatment; patients with renal insufficiency with uremic thrombocytopathy and hypoproliferative anemia; and patients with inherited or acquired bleeding disorders affecting primary hemostasis (eg, Bernard-Soulier syndrome, von Willebrand disease) with chronic blood loss and iron deficiency anemia. Underlying abnormalities of any components of primary hemostasis plus concomitant anemia may result in major bleeding disorders; therefore, correction of remediable abnormalities-most notably, correction of the anemia- would be expected to have important clinical benefit. In this review we discuss how the correction of the anemia may lead to improvement of bleeding outcomes in patients with a primary hemostatic defect, supported by evidence from animal models, clinical trials and clinical experience.
贫血不仅是出血的结果，也是血小板减少或血小板功能缺陷患者出血的可改变的危险因素。在这篇综述中，我们概述了血小板疾病患者贫血引起出血的机制，该机制涉及由于红细胞（RBC）质量减少导致正常 RBC 流变学紊乱和血小板向内皮表面的边缘性减少，从而导致初级止血和出血受损。从生物学上讲，贫血通过血管中流动血液的中央柱减少 RBC 的质量，导致较少的血小板与流动血液柱的外周内皮表面接触。因此，贫血会导致初级止血受损。血管性血友病因子（von Willebrand factor，vWF）是初级止血的另一个组成部分，vWF 缺乏，特别是最高 vWF 多聚体的缺乏，也会在同时发生贫血时表现为出血。临床上，最容易发生贫血引起出血的患者包括血液系统恶性肿瘤患者，其贫血和血小板减少是由于基础疾病或治疗的骨髓毒性作用引起的；肾功能不全伴有尿毒症性血小板减少症和低增生性贫血的患者；以及影响初级止血（如伯纳德-苏利耶综合征、血管性血友病）的遗传性或获得性出血性疾病患者，存在慢性失血和缺铁性贫血。任何初级止血成分的基础异常加上同时存在的贫血可能导致严重的出血性疾病；因此，纠正可纠正的异常——尤其是纠正贫血——有望带来重要的临床获益。在这篇综述中，我们讨论了纠正贫血如何改善有原发性止血缺陷的患者的出血结局，这得到了来自动物模型、临床试验和临床经验的证据的支持。
