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Hypercoagulable state in sickle cell disease.

Camille Faes1, Erica M Sparkenbaugh2, Rafal Pawlinski3

  • 1Interuniversity Laboratory of Human Movement Biology EA7424, Vascular biology and Red Blood Cell Team, University Claude Bernard Lyon1, Villeurbanne, France; Laboratory of Excellence "GR-Ex, " Paris, France.

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|April 5, 2018
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Summary
This summary is machine-generated.

Sickle cell disease (SCD) involves chronic coagulation activation, increasing thrombotic risks. This complex interplay between coagulation, hemolysis, and inflammation contributes to SCD

Keywords:
Sickle cell anaemiaclothaemolysismicroparticlesprocoagulant state

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Area of Science:

  • Hematology
  • Vascular Biology
  • Thrombosis Research

Background:

  • Sickle cell disease (SCD) is characterized by chronic coagulation activation.
  • Key procoagulant factors like tissue factor and thrombin generation are elevated in SCD.
  • Natural anticoagulant levels are decreased, and RBC morphology is altered in SCD.

Purpose of the Study:

  • To investigate the role of coagulation activation in the pathophysiology of sickle cell disease.
  • To explore the complex interactions between coagulation, hemolysis, and inflammation in SCD.

Main Methods:

  • Review of clinical data from SCD patients.
  • Analysis of results from SCD mouse models.
  • Examination of coagulation dynamics and RBC morphology in SCD.

Main Results:

  • Consistent evidence of chronic coagulation activation in SCD patients and models.
  • SCD patients exhibit increased susceptibility to thrombotic complications.
  • Altered sickle red blood cell morphology impacts clot formation dynamics.

Conclusions:

  • Coagulation activation is a significant feature contributing to SCD pathophysiology.
  • Complex interactions between coagulation, hemolysis, and inflammation are central to SCD.
  • Targeting coagulation pathways may offer therapeutic strategies for SCD complications.