COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy

The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called “cytokine storm” and coagulopathy. Hypoxia is also associated w...

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Detalles Bibliográficos
Autores principales: Chatterjee, Sabyasachi, Sengupta, Tanusree, Majumder, Samarpan, Majumder, Rinku
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485709/
https://www.ncbi.nlm.nih.gov/pubmed/32826388
http://dx.doi.org/10.18632/aging.103869
Descripción
Sumario:The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called “cytokine storm” and coagulopathy. Hypoxia is also associated with COVID-19. So far overlooked is the fact that both IL6 and hypoxia depress the abundance of a key anticoagulant, Protein S. We speculate that the IL6-driven cytokine explosion plus hypoxemia causes a severe drop in Protein S level that exacerbates the thrombotic risk in COVID-19 patients. Here we highlight a mechanism by which the IL6-hypoxia curse causes a deadly hypercoagulable state in COVID-19 patients, and we suggest a path to therapy.

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