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Amniotic fluid embolism triggers disseminated intravascular coagulation (DIC). Procoagulant phosphatidylserine (PS) and tissue factor (TF)-exposing extracellular vesicles (EVs) in amniotic fluid significantly activate blood clotting, driving DIC pathogenesis.

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Area of Science:

  • Hematology
  • Obstetrics
  • Pathophysiology

Background:

  • Amniotic fluid (AF) embolism can cause disseminated intravascular coagulation (DIC).
  • Extracellular vesicles (EVs) exposing phosphatidylserine (PS) and tissue factor (TF) are implicated in AF embolism-induced DIC.
  • Understanding the procoagulant mechanisms of AF is crucial for managing this obstetric emergency.

Purpose of the Study:

  • To analyze the procoagulant properties of amniotic fluid (AF).
  • To investigate the role of PS- and TF-exposing extracellular vesicles (EVs) in AF-induced coagulopathy.
  • To elucidate the pathomechanisms underlying AF embolism-induced DIC.

Main Methods:

  • Functional coagulation assays including prothrombinase, EV-associated TF activity, fibrin, and thrombin generation assays.
  • Whole blood clotting model to assess clotting time.
  • Flow cytometry to identify and quantify PS+ and TF+ EVs in AF.
  • Comparison of AF with control plasma.

Main Results:

  • PS exposure on EVs was 21-fold higher in AF compared to plasma.
  • EV-associated TF activity was significantly increased in AF.
  • AF-derived EVs activated coagulation via PS and TF, significantly shortening clotting time in a whole blood model.
  • The contact activation pathway (FXII) was unaffected.
  • A subpopulation of PS+ and TF+ EVs was identified in AF but not in control plasma.

Conclusions:

  • PS- and TF-exposing EVs in amniotic fluid are key drivers of its procoagulant potential.
  • These EVs activate the blood coagulation cascade, contributing to DIC.
  • The findings provide further insight into the mechanisms of AF-induced coagulopathy.