PMC:7381711 / 6453-7631 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7381711","sourcedb":"PMC","sourceid":"7381711","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7381711","text":"Taken together, it is likely that COVID-19-associated coagulopathy and thromboses contribute to the morbidity and mortality of the disease. However, it is important to recognize that other non-COVID-19 critical illnesses have demonstrated similar evidence of coagulopathy, yet failed to benefit from anticoagulation treatment in randomized controlled studies. For example, coagulopathy has been widely recognized as a contributor to organ failure in sepsis, a disease characterized by circulating D-dimer concentrations that approximate levels observed in patients with COVID-19 (Fig. 2; 10, 32, 38, 40). However, studies that have targeted this coagulopathy in sepsis with thrombomodulin (40), AT3 (42), tissue factor pathway inhibitor (1), and activated protein C (31) have all failed to improve mortality, despite improving laboratory indexes of coagulopathy. These studies suggest that coagulopathy may simply be a consequence of sepsis, as opposed to a key pathogenic driver of disease. Alternatively, as discussed below, coagulation may impart both harmful and protective effects within the injured lung, negating any clinical benefit (or harm) from anticoagulant 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