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 冠状病毒病 (COVID-19) 中，多种血栓炎症事件促成了病理生理学，包括凝血系统激活、纤维蛋白溶解抑制、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。尽管血小板减少症并不是感染性凝血病的初始表现，但最近的研究表明血小板在 COVID-19 相关凝血病 SARS-CoV-2 中的重要作用，已知其刺突蛋白可直接或间接促进促血栓和炎症释放导致 COVID-19 相关凝血病的介质。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，