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Elevated hematocrit enhances platelet accumulation following vascular injury

Bethany L. Walton, Marcus Lehmann, Tyler Skorczewski, Lori A. Holle, Joan D. Beckman, Jeremy A. Cribb, Micah J. Mooberry, Adam R. Wufsus, Brian C. Cooley, Jonathan W. Homeister, Rafal Pawlinski, Michael R. Falvo, Nigel S. Key, Aaron L. Fogelson, Keith B. Neeves and Alisa S. Wolberg

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  • RE: Hematocrit levels and sickle cell disease
    • Felicity N. E. Gavins, Department of Molecular & Cellular Physiology Louisiana State University Health Sciences Center Shreveport
    • Other Contributors:
      • Elena Senchenkova, Department of Molecular & Cellular Physiology

    RBC morphology and hematocrit increases risk of thrombosis: impact for sickle cell disease therapy

    Corresponding author:
    Felicity N. E. Gavins
    Department of Molecular & Cellular Physiology
    Louisiana State University Health Sciences Center Shreveport
    1501 Kings Highway
    Shreveport, LA 71103,
    USATel: +1318-675-4199
    Fax: +1318-675-6005
    Email: fgavin@lsuhsc.edu

    Walton and colleagues1 showed RBCs (RBCsHIGH) in healthy mice push platelets towards vessel walls thereby prolonging platelet-thrombi interaction time and increasing the rate of thrombus formation. Furthermore, their results indicated that hematocrit is a direct pro-thrombotic risk-factor promoting platelet communications in arterial thrombi. However, what these findings mean in the context of diseases such as Sickle-Cell-Disease (SCD) remain to be determined.

    SCD patients have low (due to anemia) and high hematocrit levels.2 Increased hematocrit levels cause increased blood viscosity and serve as a surrogate measure for the effect of increased viscosity in the disease pathogenesis.5 Additionally, increased hematocrit in SCD has been linked with acute-chest-syndrome, acute-multi-organ-syndrome, pain, ocular complications3 and stroke (11% of SCD patients have a stroke before 20-years, increasing to 24% by 45-years.2 In addition...

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    Conflict of Interest:
    None declared.