与COVID-19相关的血细胞的定量和定性变化

N. Evtugina, S. S. Sannikova, A. Peshkova, S. Safiullina, I. Andrianova, G. R. Tarasova, R. R. Khismatullin, S. M. Abdullaeva, R. Litvinov
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摘要

目的探讨血液学疾病与新冠肺炎发病机制、病程及转归的关系方法对235例接受抗凝及免疫抑制药物治疗的中重度急性新冠肺炎住院患者进行全血细胞计数、形态学及血小板功能检测,并与临床特征及炎症标志物合成进行比较。结果溶血性贫血、嗜中性粒细胞和淋巴细胞减少症与未成熟红细胞和白细胞相关,表明COVID-19患者造血功能激活受损,特别是在严重和致命病例中,以及存在合并症时,血栓收缩功能受损。在男性患者中,凝块收缩的变化更为明显,凝块收缩的抑制与贫血和凝血功能障碍直接相关,包括高d -二聚体水平;血小板收缩能力下降是由于中度血小板减少症合并慢性血小板活化和继发性血小板功能障碍所致。血凝块的结构和细胞组成取决于其收缩程度,收缩受损的血凝块具有多孔性;结论发生定量和质变的血细胞参与了COVID-19的发病机制,血小板驱动的体内血块收缩受到抑制可能是血栓形成前机制的一部分©2021作者(s)这是一篇开放获取的文章,遵循知识共享署名40国际许可(CC-BY 40)的条款分发。允许在任何媒介上不受限制地使用、分发和复制,前提是要注明原作者和来源。参见http://creativecommons org/ licenses/by/4 0/
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Quantitative and qualitative changes in blood cells associated with COVID-19
Aim To establish the relationship of hematological disorders with the pathogenesis, course and outcomes of COVID-19 Methods We examined 235 hospitalized patients with moderate and severe forms of acute COVID-19 receiving anticoagulants and immunosuppressive drugs We studied the full blood cell counts and morphology along with the platelet function by flow cytometry in comparison with the clinical features and synthesis of inflammatory markers To assess platelet contractility, blood clot contraction (retraction) kinetics was used in combination with scanning electron microscopy of platelets and blood clots Results Hemolytic anemia, neutrophilia and lymphopenia were associated with immature erythrocytes and leukocytes, indicating activation of hematopoiesis Contraction of blood clots in COVID-19 was impaired, especially in severe and lethal cases, as well as in the presence of comorbidities, including myeloproliferative and coronary heart diseases and acute cerebrovascular disease In male patients, the changes in clot contraction were more pronounced Suppression of clot contraction correlated directly with anemia and coagulopathy, including a high D-dimer level, which confirms the pathogenetic significance of blood clot contraction in COVID-19 A decrease in platelet contractility was due to moderate thrombocytopenia in combination with chronic platelet activation and secondary platelet dysfunction The structure and cellular composition of blood clots depended on the extent of contraction;clots with impaired contraction were porous, had a low content of deformed polyhedral erythrocytes (polyhedrocytes) and an even distribution of fibrin Conclusion Blood cells undergoing both quantitative and qualitative changes are involved in the pathogenesis of COVID-19;the suppressed platelet-driven contraction of intravital blood clots may be a part of the prothrombotic mechanisms © 2021 The Author(s) This is an open-access article distributed under the terms of the Creative Commons Attribution 4 0 International License (CC-BY 4 0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited See http://creativecommons org/ licenses/by/4 0/
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