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Complement components, complement activation, and acute phase response in systemic lupus erythematosus.

G Sturfelt, A G Sjöholm

    International Archives of Allergy and Applied Immunology
    |January 1, 1984
    PubMed
    Summary
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    Systemic lupus erythematosus (SLE) exacerbations involve distinct inflammatory responses. Extrarenal SLE shows high C-reactive protein (CRP) and complement activation, while renal SLE has less CRP but significant complement involvement and hypocomplementemia.

    Area of Science:

    • Immunology
    • Rheumatology
    • Clinical Chemistry

    Background:

    • Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by diverse clinical manifestations.
    • Understanding the inflammatory and complement system's role during SLE exacerbations is crucial for diagnosis and management.

    Purpose of the Study:

    • To investigate the plasma protein response and complement activation patterns in patients with varying severity of SLE, including extrarenal and renal involvement.
    • To differentiate inflammatory markers and complement consumption in different SLE phenotypes during disease flares.

    Main Methods:

    • Analysis of plasma concentrations of acute-phase reactants like C-reactive protein (CRP) and other proteins.
    • Measurement of complement activation products (C1r-C1s-C1 inactivator complexes, C2a, C3d) and complement components (C1, C2, C3, factors B, D, properdin).

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  • Solid-phase assay to quantify C1q-binding immune complexes and assess complement pathway activation.

    • Main Results:

    • Patients with extrarenal SLE exhibited pronounced acute-phase protein responses (CRP, alpha 1-antichymotrypsin, alpha 1-antitrypsin, orosomucoid) during exacerbations.
    • Complement classical pathway activation was observed in all SLE patients during flares, indicated by elevated C1r-C1s-C1 inactivator complexes and C2a fragments.
    • Hypocomplementemia was typically associated with glomerulonephritis, while complement component participation counteracted hypocomplementemia in extrarenal SLE. Factor D was elevated in renal SLE due to impaired filtration.

    Conclusions:

    • SLE exacerbations involve distinct inflammatory profiles, with prominent CRP elevation in extrarenal disease and significant complement activation across all SLE types.
    • Complement activation, particularly the classical pathway, is a hallmark of SLE flares, with consumption patterns varying based on renal or extrarenal involvement.
    • Elevated factor D in renal SLE suggests its utility as a marker for reduced glomerular filtration in these patients.