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Related Experiment Videos

Susceptibility to thyroid disorders in hepatitis C.

Luigi Muratori1, Dimitrios P Bogdanos, Paolo Muratori

  • 1Department of Internal Medicine, Cardioangiology, Hepatology, Alma Mater Studiorum University of Bologna, Bologna, Italy. luigi.muratori@unibo.it

Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association
|June 14, 2005
PubMed
Summary

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Hepatitis C patients positive for liver/kidney microsomal antibody type 1 (LKM1) who receive interferon treatment are susceptible to autoimmune thyroid disorders (AITDs). This susceptibility is linked to molecular mimicry mechanisms.

Area of Science:

  • Hepatology
  • Immunology
  • Endocrinology

Background:

  • Chronic hepatitis C (HCV) infection is associated with autoimmune thyroid disorders (AITDs), particularly during interferon treatment.
  • Non-organ-specific autoantibodies (NOSAs) are common in HCV patients, raising questions about their role in AITD susceptibility.

Purpose of the Study:

  • To investigate the association between NOSA seropositivity and the susceptibility to developing AITDs in patients with chronic HCV infection.
  • To determine if LKM1 positivity predicts AITD development, especially during interferon therapy.

Main Methods:

  • Evaluated thyroid function and autoantibodies in 348 Italian chronic HCV patients, with 196 receiving interferon therapy.
  • Assessed baseline and interferon-induced thyroid disorders and autoantibody status, including LKM1 antibodies.

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Main Results:

  • Baseline thyroid disorders were more frequent in LKM1-positive patients (29% vs 9%).
  • De novo AITD markers or symptomatic thyroid disorders occurred more often in LKM1-positive patients during interferon therapy (50% vs 3%).
  • LKM1 positivity was a significant predictor of AITD, with cross-reactivity detected in 86% of LKM1-positive HCV patients with thyroid disorders.

Conclusions:

  • HCV patients positive for LKM1 are susceptible to developing AITDs during interferon therapy.
  • Molecular mimicry and epitope spreading are proposed as potential pathogenic mechanisms for AITD development in this context.