García-Ortega Alberto, de la Rosa David, Oscullo Grace, Castillo-Villegas Diego, López-Reyes Raquel, Martínez-García Miguel Ángel
Pneumology Department, Hospital Universitario and Politécnico La Fe, 46026 Valencia, Spain.
Medical Research Institute Hospital La Fe (IISLAFE), 46026 Valencia, Spain.
J Thorac Dis. 2021 Feb;13(2):1239-1255. doi: 10.21037/jtd-20-3062.
The new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been an unprecedented global health problem, causing more than 20 million infections and more than 900,000 deaths (September 2020). The SARS-CoV-2 infection, known as COVID-19, has various clinical presentations, from asymptomatic or mild catarrhal processes to severe pneumonia that rapidly progresses to acute respiratory distress syndrome (ARDS) and multiple organ failure. In the last few months, much scientific literature has been devoted to descriptions of different aspects of the coagulation disorders and arterial and venous thrombotic complications associated with COVID-19, particularly venous thromboembolism (VTE). These studies have revealed that SARS-CoV-2 could lead to a prothrombotic state reflecting the high cumulative incidence of associated thrombotic events, particularly in patients admitted to intensive care units (ICUs). As regards the coagulopathy observed in association with SARS-CoV-2 infection, the mechanisms that activate coagulation have been hypothesized as being linked to immune responses, through the release of pro-inflammatory mediators that interact with platelets, stimulate the expression of tissue factor, induce an upregulation of plasminogen activator inhibitor-1, suppress the fibrinolytic system and lead to endothelial dysfunction, triggering thrombogenesis. D-dimer elevation has been recognized as a useful biomarker of poor prognosis, although the best cut-off point for predicting VTE in COVID-19 patients has still not been clarified. This review will try to update all the available scientific information on this important topic with enormous clinical and therapeutic implications.
新型严重急性呼吸综合征冠状病毒2（SARS-CoV-2）已成为一个前所未有的全球健康问题，导致超过2000万例感染和90多万人死亡（2020年9月）。SARS-CoV-2感染，即2019冠状病毒病（COVID-19），有多种临床表现，从无症状或轻微的卡他性症状到严重肺炎，后者可迅速发展为急性呼吸窘迫综合征（ARDS）和多器官功能衰竭。在过去几个月里，许多科学文献致力于描述与COVID-19相关的凝血障碍以及动脉和静脉血栓形成并发症的不同方面，尤其是静脉血栓栓塞（VTE）。这些研究表明，SARS-CoV-2可导致血栓前状态，这反映了相关血栓事件的高累积发生率，特别是在入住重症监护病房（ICU）的患者中。关于与SARS-CoV-2感染相关的凝血病，激活凝血的机制被推测与免疫反应有关，通过释放与血小板相互作用的促炎介质，刺激组织因子的表达，诱导纤溶酶原激活物抑制剂-1上调，抑制纤维蛋白溶解系统并导致内皮功能障碍，从而引发血栓形成。D-二聚体升高已被认为是预后不良的有用生物标志物，尽管预测COVID-19患者VTE的最佳临界值仍未明确。本综述将尝试更新关于这一重要主题的所有现有科学信息，该主题具有巨大的临床和治疗意义。
