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The coagulopathy, endotheliopathy, and vasculitis of COVID-19.
Inflammation Research ( IF 6.7 ) Pub Date : 2020-09-12 , DOI: 10.1007/s00011-020-01401-6
Toshiaki Iba 1 , Jean Marie Connors 2 , Jerrold H Levy 3
Affiliation  

Background

COVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy.

Methods

The authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19.

Results

The primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed.

Conclusion

The endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease.



中文翻译:

COVID-19 的凝血功能障碍、内皮病变和血管炎。

背景

以 D-二聚体升高为特征的 COVID-19 相关凝血病(CAC)与各种血栓并发症和疾病严重程度相关。本综述的目的是阐明这种独特凝血病的病理生理学。

方法

作者使用 MeSH(医学主题词)术语“COVID-19”、“SARS-CoV-2”、“冠状病毒”、“凝血病”和“血栓”,通过 PubMed 对已发表的医学文献进行了在线搜索。然后,选择了 51 篇与 COVID-19 中的凝血病密切相关的文章。

结果

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 的主要靶标是肺细胞、免疫细胞和血管内皮细胞。肺泡损伤和肺微血管血栓形成是 COVID-19 急性肺损伤的主要原因。发生的内皮病变是由于直接感染 SARS-CoV-2 和其他途径的激活,包括免疫系统和血栓炎症反应,导致所谓的 CAC。结果,微血管和大血管血栓事件发生在动脉、毛细血管、小静脉和大静脉血管床中,从而产生多器官功能障碍和血栓并发症。除内皮损伤外,SARS-CoV-2 还可引起血管炎,表现为全身性炎症性血管疾病。

结论

SARS-COV-2直接内皮感染引起的内皮病变和炎症引起的间接损伤在CAC的发展中起主要作用。血栓炎症的强化控制对于改善这种高度有害的传染性疾病的结果是必要的。

更新日期:2020-09-12
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