Microparticles are new biomarkers of septic shock-induced disseminated intravascular coagulopathy
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Updated: May 10, 2026
Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
Published on: August 4, 2023
Xavier Delabranche1, Julie Boisramé-Helms, Pierre Asfar
1Service de Réanimation Médicale, Nouvel Hôpital Civil, Hôpitaux Universitaires de Strasbourg, 1, Place de l'Hôpital, 67091, Strasbourg Cedex, France.
Purpose:
Septic shock-induced disseminated intravascular coagulopathy (DIC) contributes to multiple organ failure. Mechanisms governing vascular responses to open occurrence of DIC have not yet been established. Circulating plasma microparticles (MPs), released upon cell stress, constitute a catalytic procoagulant surface and are surrogates of vascular cell activation/injury. Herein, MPs were assessed as possible markers of haemostatic and vascular dysfunction in the DIC time course.
Methods:
One hundred patients with septic shock from three ICUs were enrolled and their haemostatic status evaluated at admission (D1), D2, D3 and D7. Circulating procoagulant MPs were isolated, quantified by prothrombinase assay and their cellular origin determined. DIC diagnosis was made according to the JAAM 2006 score.
Results:
Ninety-two patients were analysed and 40 had DIC during the first 24 h. Routine clotting times and factor/inhibitor activity did not allow assessing vascular cell involvement. At admission, thrombin generation and fibrinolysis were observed in both groups while impaired fibrin polymerisation was evidenced only in DIC patients. Sustained thrombin generation persisted over time in both groups at D7. While total microparticle concentrations were in the same range regardless of DIC diagnosis, specific phenotypes were already detected at admission in DIC patients. Endothelial- and leucocyte-derived MPs were higher in DIC while an increased soluble glycoprotein V/platelet ratio was delayed, underscoring the first involvement of endothelial cells and leucocytes whereas platelet activation was delayed. Endothelium-derived CD105-MPs (OR 6.55) and CD31-MPs (OR 0.49) were strongly associated with early DIC in multivariate analysis.
Conclusion:
Endothelial-derived microparticles are relevant biomarkers of septic shock-induced DIC and could be used to evaluate early vascular injury.
Insights
Septic shock-induced disseminated intravascular coagulopathy (DIC) involves early vascular injury. Endothelial-derived microparticles (MPs) are key biomarkers, helping assess this early damage and potential organ failure in critically ill patients.
Area of Science:
- Critical Care Medicine
- Hematology
- Vascular Biology
Background:
- Septic shock frequently causes disseminated intravascular coagulopathy (DIC), a major contributor to multiple organ failure.
- The precise mechanisms of vascular damage during DIC remain unclear.
- Circulating plasma microparticles (MPs) are released during cellular stress and indicate vascular activation or injury.
Purpose of the Study:
- To investigate circulating MPs as potential biomarkers for hemostatic and vascular dysfunction in septic shock-induced DIC.
- To determine the cellular origin and temporal dynamics of MPs during the course of DIC.
Main Methods:
- One hundred septic shock patients were enrolled, with hemostatic status assessed on days 1, 2, 3, and 7.
- Procoagulant MPs were isolated and quantified using a prothrombinase assay.
- Cellular origin of MPs was identified, and DIC diagnosis was based on the JAAM 2006 score.
Main Results:
- Forty of 92 analyzed patients developed DIC within 24 hours.
- While total MP levels were similar, DIC patients showed higher endothelial- and leukocyte-derived MPs at admission.
- Endothelium-derived CD105-MPs and CD31-MPs were significantly associated with early DIC onset.
Conclusions:
- Endothelial-derived microparticles serve as valuable biomarkers for septic shock-induced DIC.
- These MPs can effectively indicate early vascular injury in patients with septic shock.
- Monitoring MPs may aid in evaluating the severity and progression of DIC.
