{"title":"COVID - 19凝血功能障碍和血栓形成:系统综述","authors":"R. Asrani, W. Bahou","doi":"10.17925/ohr.2022.18.1.78","DOIUrl":null,"url":null,"abstract":"Introduction: Since the onset of the SARS-CoV-2 pandemic, haematological laboratory abnormalities and thrombotic complications have been observed among infected patients. We aimed to highlight key pathophysiological mechanisms of COVID-19-associated coagulopathy and to summarize incidence rates of venous and arterial thrombotic events, comorbidities conferring risk, and current treatment guidelines including data from ongoing clinical trials. Methods: A systematic review was performed according to PRISMA recommendations of case–control studies, cohort studies, observational studies and randomized clinical trials (RCTs) published between 1 December 2019 and 30 September 2021 within PubMed and Web of Science. Inclusion criteria were English language, adult patients and at least one coagulation parameter described. Results: 2,554 records were screened, from which 59 studies were included. Abnormalities in several laboratory parameters were associated with worse clinical outcomes including elevations in prothrombin time, activated partial thromboplastin time, D-dimer, fibrinogen, von Willebrand factor antigen/activity and lupus anticoagulant antibodies. Rates of venous and arterial thromboembolism varied significantly among studies performed early in the pandemic and across different nations. Pathophysiological mechanisms included vascular endotheliopathy, increased inflammation and macrophage activation, neutrophil extracellular traps, antiphospholipid antibody production and obesity/adipose tissue signalling. Current recommendations for management of COVID coagulopathy from various societies include the use and dosing of systemic anticoagulation to prevent thrombotic sequelae in the outpatient, inpatient and critical care settings. The optimal anticoagulant dose for thromboprophylaxis in the inpatient and critical care settings is currently not well established. Conclusions: SARS-CoV-2 infection can cause a distinct form of coagulopathy, with thromboembolic complications leading to significant morbidity and mortality. The optimal treatment requires further refinement pending the results from key ongoing RCTs","PeriodicalId":249239,"journal":{"name":"Oncology & Haematology","volume":"75 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"COVID Coagulopathy and Thrombosis: A Systematic Review\",\"authors\":\"R. Asrani, W. Bahou\",\"doi\":\"10.17925/ohr.2022.18.1.78\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction: Since the onset of the SARS-CoV-2 pandemic, haematological laboratory abnormalities and thrombotic complications have been observed among infected patients. We aimed to highlight key pathophysiological mechanisms of COVID-19-associated coagulopathy and to summarize incidence rates of venous and arterial thrombotic events, comorbidities conferring risk, and current treatment guidelines including data from ongoing clinical trials. Methods: A systematic review was performed according to PRISMA recommendations of case–control studies, cohort studies, observational studies and randomized clinical trials (RCTs) published between 1 December 2019 and 30 September 2021 within PubMed and Web of Science. Inclusion criteria were English language, adult patients and at least one coagulation parameter described. Results: 2,554 records were screened, from which 59 studies were included. Abnormalities in several laboratory parameters were associated with worse clinical outcomes including elevations in prothrombin time, activated partial thromboplastin time, D-dimer, fibrinogen, von Willebrand factor antigen/activity and lupus anticoagulant antibodies. Rates of venous and arterial thromboembolism varied significantly among studies performed early in the pandemic and across different nations. Pathophysiological mechanisms included vascular endotheliopathy, increased inflammation and macrophage activation, neutrophil extracellular traps, antiphospholipid antibody production and obesity/adipose tissue signalling. Current recommendations for management of COVID coagulopathy from various societies include the use and dosing of systemic anticoagulation to prevent thrombotic sequelae in the outpatient, inpatient and critical care settings. The optimal anticoagulant dose for thromboprophylaxis in the inpatient and critical care settings is currently not well established. Conclusions: SARS-CoV-2 infection can cause a distinct form of coagulopathy, with thromboembolic complications leading to significant morbidity and mortality. 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引用次数: 2
摘要
自SARS-CoV-2大流行开始以来,在感染患者中观察到血液学实验室异常和血栓并发症。我们旨在强调covid -19相关凝血病的关键病理生理机制,并总结静脉和动脉血栓形成事件的发生率、具有风险的合并症以及目前的治疗指南,包括来自正在进行的临床试验的数据。方法:根据PRISMA的建议,对2019年12月1日至2021年9月30日在PubMed和Web of Science上发表的病例对照研究、队列研究、观察性研究和随机临床试验(rct)进行系统评价。纳入标准为英语、成年患者和至少描述一个凝血参数。结果:2554份记录被筛选,其中包括59项研究。一些实验室参数的异常与较差的临床结果相关,包括凝血酶原时间、活化的部分凝血活酶时间、d -二聚体、纤维蛋白原、血管性血友病因子抗原/活性和狼疮抗凝抗体的升高。在大流行早期和不同国家进行的研究中,静脉和动脉血栓栓塞率差异很大。病理生理机制包括血管内皮病变、炎症和巨噬细胞活化增加、中性粒细胞胞外陷阱、抗磷脂抗体产生和肥胖/脂肪组织信号传导。目前来自不同学会的关于COVID - 19凝血病管理的建议包括在门诊、住院和重症监护环境中使用和剂量全身性抗凝治疗以预防血栓后遗症。在住院和重症监护环境中预防血栓的最佳抗凝剂量目前还没有很好地确定。结论:SARS-CoV-2感染可引起不同形式的凝血功能障碍,伴有血栓栓塞并发症,导致显著的发病率和死亡率。在关键的随机对照试验结果出来之前,最佳治疗方案需要进一步完善
COVID Coagulopathy and Thrombosis: A Systematic Review
Introduction: Since the onset of the SARS-CoV-2 pandemic, haematological laboratory abnormalities and thrombotic complications have been observed among infected patients. We aimed to highlight key pathophysiological mechanisms of COVID-19-associated coagulopathy and to summarize incidence rates of venous and arterial thrombotic events, comorbidities conferring risk, and current treatment guidelines including data from ongoing clinical trials. Methods: A systematic review was performed according to PRISMA recommendations of case–control studies, cohort studies, observational studies and randomized clinical trials (RCTs) published between 1 December 2019 and 30 September 2021 within PubMed and Web of Science. Inclusion criteria were English language, adult patients and at least one coagulation parameter described. Results: 2,554 records were screened, from which 59 studies were included. Abnormalities in several laboratory parameters were associated with worse clinical outcomes including elevations in prothrombin time, activated partial thromboplastin time, D-dimer, fibrinogen, von Willebrand factor antigen/activity and lupus anticoagulant antibodies. Rates of venous and arterial thromboembolism varied significantly among studies performed early in the pandemic and across different nations. Pathophysiological mechanisms included vascular endotheliopathy, increased inflammation and macrophage activation, neutrophil extracellular traps, antiphospholipid antibody production and obesity/adipose tissue signalling. Current recommendations for management of COVID coagulopathy from various societies include the use and dosing of systemic anticoagulation to prevent thrombotic sequelae in the outpatient, inpatient and critical care settings. The optimal anticoagulant dose for thromboprophylaxis in the inpatient and critical care settings is currently not well established. Conclusions: SARS-CoV-2 infection can cause a distinct form of coagulopathy, with thromboembolic complications leading to significant morbidity and mortality. The optimal treatment requires further refinement pending the results from key ongoing RCTs