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Fibrinogen and dysfibrinogenemia

E E Morse

    Annals of Clinical and Laboratory Science
    |July 1, 1980
    PubMed
    Summary
    This summary is machine-generated.

    Acquired dysfibrinogenemia, often seen in liver disease or DIC, results from fibrinogen molecule structural changes. These alterations impair fibrin formation, mimicking congenital fibrinogen defects.

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    Area of Science:

    • Biochemistry
    • Hematology

    Background:

    • Fibrinogen structure and function are increasingly understood through amino acid sequencing.
    • Abnormal fibrinogens provide insights into fibrinogen's functional structure.

    Observation:

    • Acquired dysfibrinogenemia is more prevalent than previously recognized.
    • It is associated with conditions such as liver disease, cancer, fibrinolysis, and disseminated intravascular coagulation (DIC).

    Findings:

    • Recent studies indicate that slow fibrin formation in these conditions stems from structural changes within the fibrinogen molecule itself.
    • These subtle structural alterations lead to functional dysfibrinogenemia, resembling congenital fibrinogenopathies.
    • A case study highlights dysfibrinogenemia in a patient with liver cirrhosis and DIC.

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    Implications:

    • This research reframes the understanding of acquired dysfibrinogenemia, emphasizing intrinsic fibrinogen defects over extrinsic inhibitors.
    • It suggests a need to re-evaluate diagnostic approaches for patients presenting with coagulation abnormalities.
    • The findings underscore the clinical relevance of acquired fibrinogen structural changes in various pathological states.