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The fibrinogenopathies.

E E Morse

    Annals of Clinical and Laboratory Science
    |May 1, 1978
    PubMed
    Summary
    This summary is machine-generated.

    Abnormal fibrinogens, like fibrinogen Detroit, can result from single amino acid changes, causing severe bleeding or thrombosis. These genetic defects impact fibrinogen

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    Area of Science:

    • Biochemistry
    • Hematology
    • Molecular Biology

    Background:

    • Abnormal fibrinogens are associated with various clinical, functional, and biochemical issues.
    • Fibrinogen Detroit serves as a key example of how molecular alterations impact function.

    Purpose of the Study:

    • To review the clinical, functional, and biochemical abnormalities linked to abnormal fibrinogens.
    • To highlight the impact of single amino acid substitutions on fibrinogen function and clinical outcomes.

    Main Methods:

    • Literature review of reported cases and studies on abnormal fibrinogens.
    • Analysis of functional defects, including fibrinopeptide release, polymerization, and clot stabilization.

    Main Results:

    • A single amino acid substitution in fibrinogen can cause significant functional abnormalities.

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  • Observed functional defects include abnormal fibrinopeptide A/B release, impaired polymerization, and poor clot stabilization.
  • These molecular changes can lead to clinical consequences such as bleeding or thrombosis.

    • Conclusions:

    • Single amino acid substitutions in critical regions of fibrinogen can lead to severe bleeding or thrombotic disorders.
    • Understanding these molecular defects is crucial for diagnosing and managing patients with abnormal fibrinogens.