Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Hongo Bunkyo-ku, Tokyo, Japan.
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Trends Cardiovasc Med. 2022 Jan;32(1):1-9. doi: 10.1016/j.tcm.2021.08.012. Epub 2021 Aug 27.
In coronavirus disease 2019 (COVID-19), multiple thromboinflammatory events contribute to the pathophysiology, including coagulation system activation, suppressed fibrinolysis, vascular endothelial cell injury, and prothrombotic alterations in immune cells such as macrophages and neutrophils. Although thrombocytopenia is not an initial presentation as an infectious coagulopathy, recent studies have demonstrated the vital role of platelets in COVID-19-associated coagulopathy SARS-CoV-2 and its spike protein have been known to directly or indirectly promote release of prothrombotic and inflammatory mediators that lead to COVID-19-associated coagulopathy. Although clinical features of vaccine-induced immune thrombotic thrombocytopenia include uncommon locations of thrombosis, including cerebral venous sinus, we speculate coronavirus spike-protein-initiated prothrombotic pathways are involved in the pathogenesis of vaccine-induced immune thrombotic thrombocytopenia, as current evidence suggests that the spike protein is the promotor and other cofactors such as perturbed immune response and inflammatory reaction enhance the production of anti-platelet factor 4 antibody.
在 2019 年冠状病毒病（COVID-19）中，多种血栓炎症事件导致其病理生理学变化，包括凝血系统激活、纤溶抑制、血管内皮细胞损伤以及巨噬细胞和中性粒细胞等免疫细胞的促血栓形成改变。虽然血小板减少症不是感染性凝血障碍的初始表现，但最近的研究表明血小板在 COVID-19 相关凝血障碍中的重要作用。SARS-CoV-2 及其刺突蛋白已被证实可直接或间接促进促血栓形成和炎症介质的释放，从而导致 COVID-19 相关凝血障碍。尽管疫苗诱导的免疫性血栓性血小板减少症的临床特征包括不常见的血栓形成部位，包括脑静脉窦，但我们推测冠状病毒刺突蛋白引发的促血栓形成途径参与了疫苗诱导的免疫性血栓性血小板减少症的发病机制，因为目前的证据表明刺突蛋白是促进因子，而其他因素，如免疫反应紊乱和炎症反应，增强了抗血小板因子 4 抗体的产生。
