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Complement activation in chronic liver disease

L E Munoz, D De Villiers, D Markham

    Clinical and Experimental Immunology
    |March 1, 1982
    PubMed
    Summary
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    Chronic active liver disease (CALD) and primary biliary cirrhosis (PBC) show complement activation, unlike alcohol-induced liver disease (ALD). Diminished liver function, not complement activation, affects ALD patients.

    Area of Science:

    • Immunology
    • Hepatology
    • Complement System

    Background:

    • Chronic active liver disease (CALD), primary biliary cirrhosis (PBC), and alcohol-induced liver disease (ALD) are distinct liver conditions.
    • The complement system plays a role in immune responses and inflammation.
    • Previous research suggests complement activation may be involved in certain liver diseases.

    Purpose of the Study:

    • To investigate complement system activation in different types of chronic liver disease.
    • To differentiate between complement-mediated liver damage and damage due to impaired liver function.

    Main Methods:

    • Serum concentrations of complement components (e.g., C3d) and regulatory proteins were measured.
    • Patients were categorized into groups: HBsAg positive CALD, PBC, HBsAg negative CALD, and ALD.

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  • Analysis focused on identifying patterns of complement activation and correlation with liver synthetic function.

    • Main Results:

    • HBsAg positive CALD and PBC patients showed increased C3d concentrations, indicating classical and alternative complement pathway activation.
    • Regulatory protein levels (C3bINA, beta IH globulin) were normal in these patients.
    • HBsAg negative CALD and ALD patients did not show evidence of increased complement activation; reduced complement levels correlated with diminished hepatic synthetic function.
    • Specifically, C4 synthesis may be reduced in autoimmune CALD.

    Conclusions:

    • Complement activation is implicated in HBsAg positive CALD and PBC.
    • In HBsAg negative CALD and ALD, reduced complement levels are likely due to impaired liver synthesis rather than activation.
    • Autoimmune CALD may involve specific reductions in C4 synthesis.