Jacob Giris, Aharon Anat, Brenner Benjamin
Medicine F and Recanati Research Center, Tel Aviv Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Hematologic Research Laboratory, Hematologic Department, Tel Aviv Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Front Physiol. 2020 Dec 16;11:596057. doi: 10.3389/fphys.2020.596057. eCollection 2020.
The emerging novel coronavirus disease (COVID-19), which is caused by the SARS-CoV-2 presents with high infectivity, morbidity and mortality. It presenting a need for immediate understanding of its pathogenicity. Inflammation and coagulation systems are over-activated in COVID-19. SARS-CoV-2 damages endothelial cell and pneumocyte, resulting in hemostatic disorder and ARDS. An influential biomarkers of poor outcome in COVID-19 are high circulating cytokines and D-dimer level. This latter is due to hyper-fibrinolysis and hyper-coagulation. Plasmin is a key player in fibrinolysis and is involved in the cleavage of many viruses envelop proteins, including SARS-CoV. This function is similar to that of TMPRSS2, which underpins the entry of viruses into the host cell. In addition, plasmin is involved in the pathophysiology of ARDS in SARS and promotes secretion of cytokine, such as IL-6 and TNF, from activated macrophages. Here, we suggest an out-of-the-box treatment for alleviating fibrinolysis and the ARDS of COVID-19 patients. This proposed treatment is concomitant administration of an anti-fibrinolytic drug and the anticoagulant.
由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引起的新型冠状病毒病（COVID-19）具有高传染性、发病率和死亡率。这表明需要立即了解其致病性。COVID-19中炎症和凝血系统过度激活。SARS-CoV-2损害内皮细胞和肺细胞，导致止血障碍和急性呼吸窘迫综合征（ARDS）。COVID-19预后不良的一个有影响力的生物标志物是循环细胞因子和D-二聚体水平升高。后者是由于过度纤维蛋白溶解和高凝状态。纤溶酶是纤维蛋白溶解的关键参与者，参与许多病毒包膜蛋白的裂解，包括SARS-CoV。该功能类似于跨膜丝氨酸蛋白酶2（TMPRSS2），后者是病毒进入宿主细胞的基础。此外，纤溶酶参与SARS中ARDS的病理生理学，并促进活化巨噬细胞分泌细胞因子，如白细胞介素-6（IL-6）和肿瘤坏死因子（TNF）。在此，我们提出一种非传统的治疗方法，以减轻COVID-19患者的纤维蛋白溶解和ARDS。该提议的治疗方法是同时给予抗纤维蛋白溶解药物和抗凝剂。
