Does alpha1-antitrypsin phenotype PiMZ increase the risk of fibrosis in liver disease due to hepatitis C virus infection?

Eur J Gastroenterol Hepatol. 2006 May;18(5):521-3. doi: 10.1097/00042737-200605000-00011.

Abstract

Background: The factors influencing the development of hepatic fibrosis, a key factor in determining outcome, are incompletely understood in hepatitis C. It has been suggested that the heterozygous Z mutation of the alpha1-antitrypsin gene (PiMZ) predisposes to more severe liver damage when infected by the hepatitis C virus. This retrospective cross-sectional study was designed to compare the prevalence of PiMZ in hepatitis C patients with different degrees of fibrosis.

Patients and methods: One hundred and forty-one patients from the Trent Hepatitis C Study Group's database were selected for study. Forty-six had no fibrosis on liver biopsy, 53 had cirrhosis and 42 had intermediate fibrosis. The alpha1-antitrypsin phenotype was determined by isoelectric focusing.

Results: There was no significant difference between the prevalence of PiMZ in the three groups--there was just one patient in each group. Comparing those with no fibrosis with those with cirrhosis, the odds ratio was 0.87 (95% confidence interval, 0.05-14).

Conclusion: Our results do not support the hypothesis that the presence of the PiMZ phenotype predisposes to more severe fibrosis in patients with hepatitis C.

MeSH terms

  • Adult
  • Cross-Sectional Studies
  • Female
  • Genetic Predisposition to Disease / genetics
  • Hepatitis C, Chronic / complications*
  • Heterozygote
  • Humans
  • Liver Cirrhosis / genetics*
  • Male
  • Middle Aged
  • Mutation
  • Phenotype
  • Retrospective Studies
  • Risk Factors
  • alpha 1-Antitrypsin / genetics*

Substances

  • alpha 1-Antitrypsin