Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study

Study (n=68) found coagulation activation is common in hospitalised patients with COVID-19, with elevated plasma von Willebrand factor levels increasing with disease severity. Findings identify a potential prognostic role for measurement of endothelial markers in this setting.

SPS commentary:

A commentary notes that further studies will be required to define the different mechanisms through which SARS-CoV-2 infection causes such marked endothelial cell effects, particularly within the pulmonary microvasculature. It adds that given the diffuse nature of COVID-19 pneumonia, the large volume of alveolar cavity and proximity with the pulmonary microvasculature, local inflammation, and dysregulated pro-inflammatory cytokine generation are undoubtedly important in this context. It suggests other mechanisms might include complement activation, neutrophil extracellular trap activation and release, and significant hypoxia. Furthermore, endothelial cells express the ACE2 receptor that facilitates viral entry into cells, and electron microscopy studies have reported SARS-CoV-2 viral particles within the endothelium. It concludes that irrespective of the mechanisms of endothelial cell activation and associated pulmonary intravascular coagulopathy in COVID-19, it will be interesting to see whether immunosuppressive therapy including corticosteroids and tocilizumab actually improve endothelial cell function towards reversal of in-situ immunothrombosis and survival improvement.


The Lancet Haematology

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