COVID-19快速淀粉样蛋白形成和血栓形成(简要文献综述)

V. A. Kozlov, S. Sapozhnikov
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引用次数: 1

摘要

COVID-19患者的病程常伴有高凝和大血管血栓形成。在多例患者中接种ChAdOx1 nCoV-19(阿斯利康)疫苗可导致不典型(脑静脉窦、门静脉、腹腔和肝静脉)和典型(股深静脉和腓肠静脉、肺动脉血栓栓塞、急性动脉血栓形成)部位血小板减少和血栓形成。mRNA疫苗(Moderna和Pfizer)的使用有时伴有血小板减少和出血,但没有血栓形成。这种情况促使人们在使用以前从未使用过的针对COVID-19的疫苗时寻找血栓形成的机制。本文的目的是让医学界了解COVID-19血栓形成的机制;探讨淀粉样蛋白快速形成和淀粉样蛋白刺激凝血止血系统的可能病因。迄今为止完成的唯一一项研究提供了关于通过COVID-19病毒衣壳刺突蛋白在健康人和处于COVID-19疾病急性期的人的全血中形成致密大纤维蛋白凝块的快速淀粉样蛋白形成的信息。作者发现了刺突蛋白对血凝块形成的直接影响,但没有研究刺突蛋白触发血栓形成的可能的致病途径。由于作者直接指出了淀粉样蛋白快速形成在触发凝血中的作用,其机制尚不为从业者所知,因此讨论血管床淀粉样蛋白快速形成以及淀粉样蛋白作为触发凝血止血因素的作用是有意义的。其他作者先前关于b -淀粉样蛋白和AA -淀粉样蛋白对阿尔茨海默病和系统性淀粉样变性血凝块形成的影响的研究证实了正在讨论的出版物。根据所研究的文献来源,我们认为一些从COVID-19严重形式中康复的患者可能随后发生全身性淀粉样变性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RAPID AMYLOID FORMATION AND THROMBI FORMATION IN COVID-19 (A BRIEF LITERATURE REVIEW)
The course of COVID-19 in patients is often complicated by hypercoagulation and thrombosis of the great vessels. Vaccination against COVID-19 with ChAdOx1 nCoV-19 (AstraZeneca) in a number of patients turned out to cause thrombocytopenia and thrombi formation in atypical (cerebral venous sinus, portal, abdominal, and hepatic veins) and typical (deep femoral and sural veins, pulmonary artery thromboembolia, acute arterial thrombosis) places. And the use of mRNA vaccines (Moderna and Pfizer) was sometimes accompanied by thrombocytopenia and hemorrhage, but without thrombi formation. This circumstance gave rise to the search for mechanisms of thrombi formation when using previously never-used vaccines developed against COVID-19. The purpose of the paper is to inform the medical community about the mechanisms of thrombi formation in COVID-19; to discuss possible pathogenetic ways of rapid amyloid formation and amyloidogenic stimulation of the coagulation hemostasis system. The only study completed to date provides information on the launch of rapid amyloid formation with the formation of dense large fibrin clots in the whole blood of both healthy people and those who were in the acute period of COVID‑19 disease by the spike protein of the COVID-19 virus capsid. The authors, having discovered the fact of the direct influence of spike protein on the formation of blood clots, nevertheless did not investigate possible pathogenetic ways of triggering thrombi formation by the spike protein. Since the authors directly pointed out the role of rapid amyloid formation in triggering coagulation, the mechanism of which is unknown to practitioners, it makes sense to discuss the issues of rapid amyloid formation in the vascular bed and the role of amyloid as a factor in triggering coagulation hemostasis. The publication under discussion is confirmed by previous studies of other authors on the influence of b‑amyloid and AA‑amyloid on the formation of blood clots in Alzheimer's disease and systemic amyloidosis. Based on the literature sources studied, we suggested that some of the patients who recovered from COVID-19 in its severe form may subsequently develop systemic amyloidosis.
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