Altered fibrin clot structure and dysregulated fibrinolysis contribute to thrombosis risk in severe COVID-19.

ABSTRACT: The high incidence of thrombotic events suggests a possible role of the contact system pathway in COVID-19 pathology. In this study, we determined the altered levels of factor XII (FXII) and its activation products in critically ill patients with COVID-19 in comparison with patients with severe acute respiratory distress syndrome related to the influenza virus (acute respiratory distress syndrome [ARDS]-influenza). Compatible with those data, we found rapid consumption of FXII in COVID-19 but not in ARDS-influenza plasma. Interestingly, the lag phase in fibrin formation, triggered by the FXII activator kaolin, was not prolonged in COVID-19, as opposed to that in ARDS-influenza. Confocal and electron microscopy showed that increased FXII activation rate, in conjunction with elevated fibrino

SUBMITTER: Wygrecka M 

PROVIDER: S-EPMC8648369 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature