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Related Experiment Videos

Hyperfibrinogenaemia and hyperviscosity in sickle-cell crisis

S G Richardson, G R Breeze, J Stuart

    Journal of Clinical Pathology
    |October 1, 1976
    PubMed
    Summary

    Painful sickle-cell crisis is linked to higher plasma fibrinogen and blood viscosity. Increased interaction between fibrinogen and red blood cells may cause vaso-occlusive crises in sickle-cell disease patients.

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    Area of Science:

    • Hematology
    • Vascular Biology
    • Sickle Cell Disease Research

    Background:

    • Sickle cell disease is a genetic blood disorder characterized by abnormal hemoglobin.
    • Vaso-occlusive crisis is a hallmark complication, causing severe pain and organ damage.
    • Blood rheology, including viscosity and flow dynamics, plays a critical role in disease pathophysiology.

    Purpose of the Study:

    • To investigate the relationship between plasma fibrinogen levels, whole-blood viscosity, and sickle cell crisis.
    • To determine if elevated blood viscosity contributes to the precipitation of painful vaso-occlusive events.

    Main Methods:

    • Plasma fibrinogen concentration was measured.
    • Whole-blood viscosity was assessed at two shear rates (23 sec-1 and 230 sec-1).
    • Measurements were taken during sickle cell crisis episodes and compared to non-crisis states in patients with sickle cell anemia.

    Main Results:

    • A significant increase in plasma fibrinogen concentration was observed during painful sickle cell crisis.
    • Whole-blood viscosity was significantly elevated during crisis episodes compared to non-crisis periods.
    • These findings suggest a correlation between increased fibrinogen and heightened blood viscosity during sickle cell crisis.

    Conclusions:

    • Elevated plasma fibrinogen and increased whole-blood viscosity are associated with painful sickle cell crisis.
    • Enhanced interaction between fibrinogen and erythrocytes in vivo may be a key factor in increasing blood viscosity.
    • This heightened viscosity is a potential contributor to the precipitation of vaso-occlusive crises in sickle cell disease.

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