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Thromboembolism in Hageman trait

R A McPherson

    American Journal of Clinical Pathology
    |September 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    Severe Hageman factor (factor XII) deficiency in a patient led to lower extremity arterial thrombosis. This case highlights factor XII's crucial role in clot dissolution, not just blood clotting initiation.

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    Area of Science:

    • Hematology
    • Vascular Biology
    • Thrombosis Research

    Background:

    • Hageman factor (coagulation factor XII) initiates the intrinsic pathway of blood coagulation.
    • Factor XII deficiency is typically associated with no bleeding complications.
    • The multifaceted roles of factor XII in hemostasis and inflammation are under investigation.

    Observation:

    • A rare case of severe Hageman factor deficiency is presented.
    • The patient experienced arterial thrombosis with embolization to a lower extremity.
    • This contrasts with the usual absence of hemorrhagic issues in factor XII deficiency.

    Findings:

    • Despite severe factor XII deficiency, the patient developed a thrombus.
    • This clinical presentation suggests a potential role for factor XII in preventing pathological clot formation or promoting clot lysis.

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  • The intrinsic pathway's role in thrombosis, rather than just bleeding, is underscored.

    • Implications:

    • Factor XII may play a significant role in clot dissolution (fibrinolysis).
    • Understanding factor XII's function could reveal new therapeutic targets for thrombotic disorders.
    • This case challenges the traditional view of factor XII solely as a pro-coagulant initiator.