Centre for Clinical Transfusion Medicine, University Hospital of Tübingen, Tübingen, Germany.
Institute for Clinical and Experimental Transfusion Medicine, Medical Faculty of Tübingen, University Hospital of Tübingen, Tübingen, Germany.
Hamostaseologie. 2022 Oct;42(S 01):S14-S23. doi: 10.1055/a-1797-0564. Epub 2022 Oct 26.
Coronavirus disease-2019 (COVID-19) is associated with increased thromboembolic complications. Long-term alteration in coagulation system after acute COVID-19 infection is still a subject of research. Furthermore, the effect of sera from convalescent subjects on platelets is not known. In this study, we investigated platelet phenotype, coagulation, and fibrinolysis in COVID-19 convalescent plasma (CCP) donors and analyzed convalescent sera-induced effects on platelets. We investigated CCP donors who had a history of mild COVID-19 infection and donors who did not have COVID-19 were used as controls. We analyzed phosphatidylserine (PS) externalization, CD62p expression, and glycoprotein VI (GPVI) shedding both in platelet-rich plasma (PRP) and after incubation of washed healthy platelets with donors' sera using flow cytometry. Coagulation and fibrinolysis systems were assessed with thromboelastometry. Forty-seven CCP donors (22 males, 25 females; mean age (±SD): 41.4 ± 13.7 years) with a history of mild COVID-19 infection were included. Median duration after acute COVID-19 infection was 97 days (range, 34-401). We did not find an increased PS externalization, CD62p expression, or GPVI shedding in platelets from CCP donors. Sera from CCP donors did not induce PS externalization or GPVI shedding in healthy platelets. Sera-induced CD62p expression was slightly, albeit statistically significantly, lower in CCP donors in plasma donors without a history of COVID-19. One patient showed increased maximum clot firmness and prolonged lysis time in thromboelastometry. Our findings suggest that procoagulant platelet phenotype is not present after mild COVID-19. Furthermore, CCP sera do not affect the activation status of platelets.
新型冠状病毒病-2019(COVID-19)与血栓栓塞并发症的增加有关。急性 COVID-19 感染后凝血系统的长期改变仍然是研究的主题。此外,恢复期患者血清对血小板的影响尚不清楚。在这项研究中,我们研究了 COVID-19 恢复期血浆(CCP)供体的血小板表型、凝血和纤溶,并分析了恢复期血清对血小板的影响。我们研究了有轻度 COVID-19 感染史的 CCP 供体,以及未感染 COVID-19 的供体作为对照。我们使用流式细胞术分析了富含血小板的血浆(PRP)中以及用供体血清孵育后的血小板中血小板磷脂酰丝氨酸(PS)外翻、CD62p 表达和糖蛋白 VI(GPVI)脱落。使用血栓弹性描记法评估凝血和纤溶系统。纳入了 47 名有轻度 COVID-19 感染史的 CCP 供体(22 名男性,25 名女性;平均年龄(±标准差):41.4±13.7 岁)。急性 COVID-19 感染后中位时间为 97 天(范围,34-401 天)。我们没有发现 CCP 供体的血小板 PS 外翻、CD62p 表达或 GPVI 脱落增加。CCP 供体的血清未诱导健康血小板的 PS 外翻或 GPVI 脱落。与无 COVID-19 病史的血浆供体相比,CCP 供体的血清诱导的 CD62p 表达略低,但具有统计学意义。一名患者在血栓弹性描记法中表现出最大凝块硬度增加和溶解时间延长。我们的研究结果表明,轻度 COVID-19 后不存在促凝血小板表型。此外,CCP 血清不会影响血小板的激活状态。