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Diffuse intravascular coagulation in liver disease?

P W Straub

    Seminars in Thrombosis and Hemostasis
    |January 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    This review critically examines intravascular coagulation in liver disease, proposing alternative mechanisms for low fibrinogen and elevated fibrin degradation products (FDPs) beyond disseminated intravascular coagulation (DIC). Therapeutic strategies are discussed based on current pathophysiology.

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    Area of Science:

    • Hematology
    • Hepatology
    • Coagulation Disorders

    Background:

    • Liver diseases are associated with complex coagulation abnormalities.
    • Intravascular coagulation has been implicated as a cause of these defects.
    • Existing evidence requires critical re-evaluation.

    Purpose of the Study:

    • To critically review the evidence for intravascular coagulation in liver diseases.
    • To propose alternative pathophysiological mechanisms for hypofibrinogenemia and elevated serum FDPs.
    • To discuss therapeutic approaches based on updated pathophysiology.

    Main Methods:

    • Critical review of existing literature on coagulation in liver disease.
    • Analysis of proposed alternative mechanisms for hypofibrinogenemia.

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  • Evaluation of potential non-DIC pathways for elevated FDPs.

    • Main Results:

    • Evidence for widespread intravascular coagulation in liver disease is not conclusive.
    • Extravascular fibrinogen consumption (e.g., in ascites, necrosis) may explain hypofibrinogenemia.
    • Extravascular proteolysis of fibrinogen could lead to elevated serum FDPs, independent of DIC.

    Conclusions:

    • Alternative mechanisms to DIC should be considered for coagulation defects in liver disease.
    • Understanding these alternative pathways is crucial for effective therapeutic strategies.
    • Further research is needed to elucidate the precise mechanisms of coagulation abnormalities in hepatic conditions.