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Polymorphonuclear leucocyte function during acute viral hepatitis.

A Lazzarin, M Galli, F Caredda

    Bollettino Dell'Istituto Sieroterapico Milanese
    |January 1, 1984
    PubMed
    Summary
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    Hepatitis impairs polymorphonuclear (PMN) phagocytosis, with recovery seen in non-addicts. However, parenteral drug-addicts show persistent phagocytic deficits, suggesting a serum factor may inhibit neutrophil activity.

    Area of Science:

    • Immunology
    • Hepatology
    • Infectious Diseases

    Background:

    • Hepatitis A, B, and non-A, non-B infections can impact immune function.
    • Polymorphonuclear (PMN) cells play a crucial role in the innate immune response through phagocytosis.
    • Parenteral drug-addicts (P.D.A.) represent a population with unique health challenges and potential immune dysregulation.

    Purpose of the Study:

    • To investigate the phagocytic activity of PMNs in patients with acute viral hepatitis (A, B, non-A, non-B).
    • To compare PMN phagocytosis between non-addicts and parenteral drug-addicts with hepatitis.
    • To explore the potential role of serum factors and immune complexes in modulating PMN function during hepatitis.

    Main Methods:

    • Phagocytosis assays were performed on PMNs from patients with different types of hepatitis and controls.

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  • Patient groups included non-addicts and parenteral drug-addicts (P.D.A.).
  • Phagocytic activity was assessed at admission, discharge, and three months post-episode, with additional tests using normal human serum.

    • Main Results:

    • A significant reduction in PMN phagocytosis was observed in non-addicts during acute hepatitis, with recovery for hepatitis A by discharge and for B and non-A, non-B by three months.
    • Parenteral drug-addicts (P.D.A.) showed similar initial phagocytic impairment as non-addicts but exhibited a persistent deficit three months post-episode.
    • Incubation with normal serum enhanced phagocytosis in patients, and circulating immune complexes were detected in sera, suggesting an inhibitory role.

    Conclusions:

    • Acute hepatitis temporarily impairs PMN phagocytosis, with varying recovery rates depending on hepatitis type and patient group.
    • Parenteral drug-addicts (P.D.A.) experience a more prolonged deficit in phagocytic activity following hepatitis.
    • A serum factor, potentially involving circulating immune complexes, likely contributes to the inhibition of neutrophil phagocytosis in acute hepatitis.