Inflammation-Induced Coagulopathy Substantially Differs Between COVID-19 and Septic Shock: A Prospective Observational Study

Mélanie Dechamps, Julien De Poortere, Manon Martin, Laurent Gatto, Aurélie Daumerie, Caroline Bouzin, Marie Octave, Audrey Ginion, Valentine Robaux, Laurence Pirotton, Julie Bodart, Ludovic Gerard, Virginie Montiel, Alessandro Campion, Damien Gruson, Marie-Astrid Van Dievoet, Jonathan Douxfils, Hélène Haguet, Laure Morimont, Marc DeriveLucie Jolly, Luc Bertrand, Laure Dumoutier, Diego Castanares-Zapatero, Pierre-François Laterre, Sandrine Horman, Christophe Beauloye

Research output: Contribution to journalArticlepeer-review


Critical COVID-19, like septic shock, is related to a dysregulated systemic inflammatory reaction and is associated with a high incidence of thrombosis and microthrombosis. Improving the understanding of the underlying pathophysiology of critical COVID-19 could help in finding new therapeutic targets already explored in the treatment of septic shock. The current study prospectively compared 48 patients with septic shock and 22 patients with critical COVID-19 regarding their clinical characteristics and outcomes, as well as key plasmatic soluble biomarkers of inflammation, coagulation, endothelial activation, platelet activation, and NETosis. Forty-eight patients with matched age, gender, and co-morbidities were used as controls. Critical COVID-19 patients exhibited less organ failure but a prolonged ICU length-of-stay due to a prolonged respiratory failure. Inflammatory reaction of critical COVID-19 was distinguished by very high levels of interleukin (IL)-1β and T lymphocyte activation (including IL-7 and CD40L), whereas septic shock displays higher levels of IL-6, IL-8, and a more significant elevation of myeloid response biomarkers, including Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) and IL-1ra. Subsequent inflammation-induced coagulopathy of COVID-19 also differed from sepsis-induced coagulopathy (SIC) and was characterized by a marked increase in soluble tissue factor (TF) but less platelets, antithrombin, and fibrinogen consumption, and less fibrinolysis alteration. In conclusion, COVID-19 inflammation-induced coagulopathy substantially differs from SIC. Modulating TF release and activity should be evaluated in critical COVID-19 patients.

Original languageEnglish
Article number780750
Pages (from-to)780750
JournalFrontiers in Medicine
Publication statusPublished - 11 Jan 2021


  • coagulopathy
  • COVID-19
  • endothelium
  • inflammation
  • NETosis
  • platelet
  • septic shock


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