Does α1-antitrypsin phenotype PiMZ increase the risk of fibrosis in liver disease due to hepatitis C virus infection?

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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 α1-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 α1-antitrypsin phenotype was determined by isoelectric focusing.


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).


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

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