even moderate, is a risk factor for cirrhosis. (HEPATOLOGY The role of the viral genotype, especially genotype 1b, in 1997;26:776-779.) the severity of liver injury induced by chronic hepatitis C virus (HCV) infection is unclear, probably because of confounding factors such as the date and mode of contamination.
Cirrhosis occurs after 10 to 20 years in approximately Host genetic or environmental factors such as heterozygous 20% of patients with chronic hepatitis C. [1][2][3] The duration of MZ a 1 -antitrypsin deficiency or alcoholism, could also be poinfection is the only risk factor clearly identified for the onset tential risk factors for the development of cirrhosis. The aim of cirrhosis in this population. 1 Identification of other risk of this study was to compare the prevalence of genotypes, factors, which determine why some patients are more suscepa 1 -antitrypsin phenotype, past hepatitis B virus infection, and tible to liver damage than others, is crucial. It is likely that alcohol consumption in cirrhotic and noncirrhotic patients many interrelated variables are involved, including virologiwith chronic hepatitis C. We conducted a case-control study cal, host, and environmental factors. The role of the viral comparing 84 consecutive cirrhotic patients with chronic hepgenotype, especially genotype 1b, in the severity of liver inatitis C (cases) with 84 noncirrhotic patients with chronic jury induced by chronic hepatitis C virus (HCV) infection hepatitis C (controls) selected from a cohort of 464 patients is controversial. [4][5][6][7][8][9][10][11] Recent studies have shown that the prevahospitalized during the same period. Controls were paired lence of the different HCV genotypes is related to the date with cases according to age, sex, risk factors, and date of and mode of contamination. 12,13 As a result, the relationship infection. HCV genotypes were determined using the Innobetween genotype 1b and cirrhosis could be a result of con-LiPA technique (Innogenetics, Zwijnaarde, Belgium) and clasfounding factors. The aim of this case-control study was to sified according to the method of Simmonds. Patients were assess the role of viral genotype in the onset of cirrhosis by divided in three groups according to alcohol consumption: determining the prevalence of HCV genotypes in patients รต30 g/d (light), 30 to 80 g/d (moderate), and รบ80 g/d (heavy). with and without cirrhosis who were paired for age, sex, and Cirrhotic and noncirrhotic patients were not significantly difmode and date of infection. Other potential risk factors such ferent in terms of genotype distribution (1a/1b/2a/3a/others/ as heterozygous MZ a 1 -antitrypsin deficiency, alcohol conundetermined: 10/48/7/17/0/2 versus 11/43/10/10/5/5), a 1sumption, and past hepatitis B virus (HBV) infection were antitrypsin phenotype distribution (MM/MS/MZ: 84%/14%/ also analyzed. 2% vs. 87%/11%/2%, respectively), and prevalence of antibody PATIENTS AND METHODS to hepatitis B core antigen positivity (29% vs. 23%). Alcohol consumption was significantly different between cases and Study Population controls (L/M/H: 58%/27%/16% vs. 76%/15%/9%, respec-Cases. Between 1989 and 1993, 84 consecutive patients with cirtively; P รต .05). Two conclusions regarding patients with rhotic chronic hepatitis C were admitted to our unit. Chronic HCV chronic hepatitis C virus infection can be drawn from this infection was diagnosed by using an antibody to hepatitis C virus study: 1) viral genotype, especially 1b, past hepatitis B virus (anti-HCV) enzyme-linked immunosorbent assay 2 (ELISA 2) infection, and heterozygous MZ a 1 -antitrypsin deficiency are method and confirmed by recombinant immunoblot assay 2 (RIBA 2) testing. The diagnosis of cirrhosis was confirmed histologically not risk factors for cirrhosis; and 2) alcohol consumption, in 65 patients by the presence of fibrosis and regenerative nodules. The other 19 patients had evidence of decompensated cirrhosis (hyperbilirubinemia, esophageal varices, ascites, or encephalopa-Abbreviations: HCV, hepatitis C virus; HBV, hepatitis B virus; anti-Hcv, antibody thy).
to hepatitis C virus; ELISA, enzyme-linked immunosorbent assay; RIBA, recombinant Controls. During the same period, 464 consecutive patients with immunoblot assay; ALT, alanine transaminase; IV, intravenous; HBsAg, hepatitis B noncirrhotic chronic hepatitis C were admitted. Chronic hepatitis C surface antigen; HIV, human immunodeficiency; RT-PCR, reverse-transcription polywas defined as follows: elevated alanine transaminase (ALT) serum merase chain reaction.
From the 1 Unite ยดd'He ยดpatologie, 2 Service de Bacte ยดriologie-Virologie, and 3 Service de activity for more than 6 months, anti-HCV ELISA 2 positivity, RIBA