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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
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Autonomic nervous system dysfunction: implication in sickle cell disease.

Philippe Connes1, Thomas D Coates

  • 1Inserm UMR 665, Hôpital Ricou, CHU de Pointe-à-Pitre, 97157 Pointe-à-Pitre, Guadeloupe.

Comptes Rendus Biologies
|May 7, 2013
PubMed
Summary
This summary is machine-generated.

Sickle cell disease involves abnormal hemoglobin causing red blood cells to sickle, leading to pain crises. This review explores how blood flow issues and autonomic nervous system dysfunction may trigger these vaso-occlusive crises.

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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
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Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload

Published on: March 14, 2017

Area of Science:

  • Hematology
  • Vascular Biology
  • Autonomic Neuroscience

Background:

  • Sickle cell disease (SCD) is an inherited blood disorder characterized by abnormal hemoglobin.
  • This abnormality leads to red blood cell sickling, causing hemolytic anemia, tissue damage, and vaso-occlusive crises (VOC).
  • The precise triggers for VOC exacerbations remain unclear.

Purpose of the Study:

  • To review the interaction of blood rheological factors in sickle cell disease.
  • To explore the potential role of autonomic nervous system (ANS) dysfunction and vasoconstriction in triggering VOC.
  • To discuss the mechanisms underlying ANS dysfunction in SCD.

Main Methods:

  • Literature review of studies on blood rheology in SCD.
  • Analysis of research on the autonomic nervous system and its role in vaso-occlusion.
  • Synthesis of findings on cellular adhesion, inflammation, and coagulation in SCD pathophysiology.

Main Results:

  • Altered blood rheology, increased cellular adhesion, inflammation, and coagulation impair microvascular flow.
  • Autonomic nervous system dysfunction may contribute to vasoconstriction, increasing VOC risk.
  • Understanding these interactions is key to identifying VOC triggers.

Conclusions:

  • Blood rheological factors and ANS dysfunction are critical components in the pathophysiology of sickle cell disease.
  • Further research into the interplay between rheology and the ANS may reveal novel therapeutic targets for preventing VOC.
  • Addressing ANS dysfunction could be a strategy to mitigate VOC in sickle cell disease patients.