Sathler PlÍnio C
Programa de Pós-graduação em Ciências Farmacêuticas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
An Acad Bras Cienc. 2020;92(4):e20200834. doi: 10.1590/0001-3765202020200834. Epub 2020 Aug 24.
The spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has already taken on pandemic proportions, affecting over 213 countries in a matter of weeks. In this context, several studies correlating hemostatic disorders with the infection dynamics of the new coronavirus have emerged. These studies have shown that a portion of the patients affected by Coronavirus Disease 2019 (COVID-19) have prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT), elevated D-dimer levels and other fibrinolytic products, antithrombin (AT) activity reduced and decrease of platelet count. Based on these hallmarks, this review proposes to present possible pathophysiological mechanisms involved in the hemostatic changes observed in the pathological progression of COVID-19. In this analysis, it is pointed the relationship between the downregulation of angiotensin-converting enzyme 2 (ACE2) and storm cytokines action with the onset of hypercoagulability state, other than the clinical events involved in thrombocytopenia and hyperfibrinolysis progression.
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的传播已呈大流行态势，在短短几周内就影响了213多个国家。在此背景下，出现了几项将止血障碍与新型冠状病毒感染动态相关联的研究。这些研究表明，一部分2019冠状病毒病（COVID-19）患者的凝血酶原时间（PT）和活化部分凝血活酶时间（APTT）延长，D-二聚体水平及其他纤维蛋白溶解产物升高，抗凝血酶（AT）活性降低，血小板计数减少。基于这些特征，本综述旨在阐述COVID-19病理进展过程中所观察到的止血变化可能涉及的病理生理机制。在该分析中，指出了血管紧张素转换酶2（ACE2）下调和细胞因子风暴作用与高凝状态的发生之间的关系，以及血小板减少和高纤维蛋白溶解进展所涉及的临床事件。
