Abstract
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.
Highlights
The menacing SARS-CoV2 virus has caused a pandemic with over 6.9 million cases and around 400,000 deaths
As of to date (07/11/2020), there are more than 3.2 million confirmed cases and ~134,729 deaths in the U.S Clinical features of patients admitted to the hospital with the viral disease COVID-19 are bilateral pneumonia, systemic inflammation, endothelial dysfunction, coagulation activation, acute respiratory distress syndrome, and multi-organ failure
The infection risk of SARS-CoV2 has no remarkable correlation with age because the expression of the virus receptor ACE2 does not vary much between young and old; mortality is significantly higher in older people compared with the young, (Table 1)
Summary
The menacing SARS-CoV2 virus has caused a pandemic with over 6.9 million cases and around 400,000 deaths. As of to date (07/11/2020), there are more than 3.2 million confirmed cases and ~134,729 deaths in the U.S Clinical features of patients admitted to the hospital with the viral disease COVID-19 are bilateral pneumonia, systemic inflammation, endothelial dysfunction, coagulation activation, acute respiratory distress syndrome, and multi-organ failure. Huge increase in D-dimer in critically ill COVID patients
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