期刊
THORAX
卷 76, 期 4, 页码 412-420出版社
BMJ PUBLISHING GROUP
DOI: 10.1136/thoraxjnl-2020-216243
关键词
pulmonary embolism; innate immunity; viral infection; cytokine biology; respiratory infection
Thrombotic events in COVID-19, especially venous thromboemboli, are associated with disease severity and poor clinical outcomes. Distinctive microvascular abnormalities include endothelial inflammation, disruption of intercellular junctions, and microthrombi formation. COVID-19 can lead to immunothrombosis, and a better understanding of the pathobiological mechanisms is crucial for developing new treatments.
Thrombotic events that frequently occur in COVID-19 are predominantly venous thromboemboli (VTE) and are associated with increasing disease severity and worse clinical outcomes. Distinctive microvascular abnormalities in COVID-19 include endothelial inflammation, disruption of intercellular junctions and microthrombi formation. A distinct COVID-19-associated coagulopathy along with increased cytokines and activation of platelets, endothelium and complement occur in COVID-19, which is more frequent with worsening disease severity. This proinflammatory milieu may result in immunothrombosis, a host defence mechanism that can become dysregulated, leading to excess formation of immunologically mediated thrombi which predominantly affect the microvasculature. The haemostatic and immune systems are intricately linked, and multifactorial processes are likely to contribute to VTE and immunothrombosis in COVID-19. This state-of-the-art review will explore the pathobiological mechanisms of immunothrombosis and VTE in COVID-19 focusing on: COVID-19-associated coagulopathy, pathology, endothelial dysfunction and haemostasis, the immune system and thrombosis, genetic associations and additional thrombotic mechanisms. An understanding of the complex interplay between these processes is necessary for developing and assessing how new treatments affect VTE and immunothrombosis in COVID-19.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据