AUTHOR=Dechamps Mélanie , De Poortere Julien , Martin Manon , Gatto Laurent , Daumerie Aurélie , Bouzin Caroline , Octave Marie , Ginion Audrey , Robaux Valentine , Pirotton Laurence , Bodart Julie , Gerard Ludovic , Montiel Virginie , Campion Alessandro , Gruson Damien , Van Dievoet Marie-Astrid , Douxfils Jonathan , Haguet Hélène , Morimont Laure , Derive Marc , Jolly Lucie , Bertrand Luc , Dumoutier Laure , Castanares-Zapatero Diego , Laterre Pierre-François , Horman Sandrine , Beauloye Christophe TITLE=Inflammation-Induced Coagulopathy Substantially Differs Between COVID-19 and Septic Shock: A Prospective Observational Study JOURNAL=Frontiers in Medicine VOLUME=8 YEAR=2022 URL=https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2021.780750 DOI=10.3389/fmed.2021.780750 ISSN=2296-858X ABSTRACT=

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.