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Related Experiment Videos

Coagulation factor XIII concentration in sickle-cell disease

R Ittyerah, N Alkjaersig, A Fletcher

    The Journal of Laboratory and Clinical Medicine
    |October 1, 1976
    PubMed
    Summary

    Plasma factor XIII levels in sickle-cell disease (SSD) patients are lower during crisis-free periods. Factor XIII concentration changes during SSD crises may indicate increased thrombosis risk and vascular occlusion.

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    Area of Science:

    • Hematology
    • Vascular Biology
    • Coagulation Science

    Background:

    • Sickle-cell disease (SSD) is characterized by vaso-occlusive crises.
    • The role of coagulation factors, specifically factor XIII, during SSD crises is not fully understood.
    • Previous research indicates complex interactions between red blood cells, platelets, and coagulation in SSD.

    Purpose of the Study:

    • To investigate serial changes in plasma factor XIII concentrations in patients with sickle-cell disease (SSD).
    • To correlate factor XIII levels with disease activity, platelet counts, and fibrinogen levels during SSD crises.
    • To evaluate the potential role of factor XIII in the pathophysiology of SSD crises.

    Main Methods:

    • Serial plasma factor XIII assays were performed over 1.5 to 2 years in four SSD patients.

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  • Platelet counts and fibrinogen concentrations were monitored concurrently.
  • Observations were made during both crisis-free periods and active SSD crises.

    • Main Results:

    • Plasma factor XIII concentrations were lower in SSD patients compared to normal subjects during crisis-free periods.
    • Crisis onset was associated with a decrease in platelets and factor XIII, followed by an increase in fibrinogen and platelet count.
    • Factor XIII levels rose post-crisis, peaking at 3 weeks, coinciding with the resolution of thrombocytosis.

    Conclusions:

    • Observed alterations in plasma factor XIII support its involvement in the thrombotic processes during SSD crises.
    • Changes in factor XIII may indicate enhanced fibrin deposition and/or thrombosis, contributing to vascular occlusion and organ infarction in SSD.
    • Further research is warranted to elucidate the precise mechanisms linking factor XIII dynamics to SSD pathophysiology.