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Plasma haemoglobin and complement activation in sickle cell disease

K DeCeulaer, W A Wilson, A G Morgan

    Journal of Clinical & Laboratory Immunology
    |July 1, 1981
    PubMed
    Summary

    In sickle cell disease, haemolysis activates complement, leading to reduced levels of functional factor B and C3. This may impair the alternative pathway

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    Area of Science:

    • Hematology
    • Immunology
    • Biochemistry

    Background:

    • Sickle cell disease (SCD) is a genetic blood disorder characterized by abnormal hemoglobin.
    • Complement system plays a crucial role in immune function and host defense.
    • Haemolysis, the destruction of red blood cells, is a common complication in SCD.

    Purpose of the Study:

    • To investigate the role of haemolysis in complement dysfunction in asymptomatic patients with homozygous sickle cell disease.
    • To measure indices of complement activation and haemolysis in SCD patients.

    Main Methods:

    • Studied 30 asymptomatic patients with homozygous sickle cell disease.
    • Measured plasma concentrations of C3d (complement C3 breakdown product) as an index of complement activation.
    • Assessed serum concentrations of C3 and functional factor B, alongside plasma hemoglobin and reticulocyte counts.

    Main Results:

    • Elevated C3d levels were observed in 40% of patients, indicating increased complement turnover.
    • Modest decreases in serum C3 and functional factor B concentrations were found.
    • A positive correlation was identified between C3d levels and plasma hemoglobin concentration (r = 0.56, p < 0.005).

    Conclusions:

    • Intravascular haemolysis in sickle cell disease can activate the complement system.
    • This activation may lead to partial depletion of functional factor B and C3.
    • Reduced levels of these complement components could impair the immune function of the alternative pathway.

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