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Influence of HFE gene polymorphism on the progression and treatment of chronic hepatitis C

P Lebray1, H Zylberberg, S Hue

  • 1Unité d'Hépatologie, CHU Necker, Paris, France.

Journal of Viral Hepatitis
|March 5, 2004
PubMed

Insights

In chronic hepatitis C patients, elevated iron levels weakly correlated with liver disease severity. However, the HFE H63D mutation positively predicted response to interferon therapy, suggesting an immunogenetic role.

Area of Science:

  • Hepatology
  • Immunogenetics
  • Viral Hepatitis

Background:

  • Chronic hepatitis C (CHC) is a significant cause of liver disease.
  • Iron metabolism and HFE gene mutations are implicated in liver disease progression.
  • Interferon-alpha based therapy is a standard treatment for CHC.

Purpose of the Study:

  • To investigate the association between iron parameters, HFE mutations, and liver histology in CHC patients.
  • To evaluate the impact of iron status and HFE mutations on virological response to interferon-alpha therapy.

Main Methods:

  • Analysis of liver histology, serum iron parameters, and HFE gene mutations (C282Y, H63D) in 273 CHC patients.
  • Assessment of virological response to interferon-alpha therapy in 146 patients.
  • Correlation analysis between iron load, HFE status, histological activity, and treatment response.

Main Results:

  • HFE C282Y and H63D heterozygotes showed higher serum iron parameters; H63D patients had higher intrahepatic iron.
  • No significant association was found between HFE mutations and histological activity.
  • Elevated ferritinaemia predicted a poor response to therapy, while the H63D mutation was a positive predictor for sustained virological response.

Conclusions:

  • Serum and intrahepatic iron levels are weakly correlated with histological activity in CHC.
  • HFE mutations are not directly linked to histological activity but influence treatment response.
  • The HFE H63D mutation may be an immunogenetic factor improving interferon therapy outcomes in CHC.

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