RISK-FACTORS FOR CIRRHOSIS IN PATIENTS WITH CHRONIC HEPATITIS-C VIRUS-INFECTION - RESULTS OF A CASE-CONTROL STUDY

The role of the viral genotype, especially genotype 1b, in the severit y 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. Host genetic or environmental factors such as heterozygous MZ alpha(1)-antitrypsin deficiency or alcoholism, coul d also be potential risk factors for the development of cirrhosis. The aim of this study was to compare the prevalence of genotypes, alpha(1 )-antitrypsin phenotype, past hepatitis D virus infection, and alcohol consumption in cirrhotic and noncirrhotic patients with chronic hepat itis C. We conducted a case-control study comparing 84 consecutive cir rhotic patients with chronic hepatitis C (cases) with 84 noncirrhotic patients with chronic hepatitis C (controls) selected from a cohort of 464 patients hospitalized during the same period. Controls were paire d with cases according to age, sex, risk factors, and date of infectio n, HCV genotypes were determined using the InnoLiPA technique (Innogen etics, Zwijnaarde, Belgium) and classified according to the method of Simmonds, Patients were divided in three groups according to alcohol c onsumption: <30 g/d (light), 30 to 80 g/d (moderate), and >80 g/d (hea vy). Cirrhotic and noncirrhotic patients were not significantly differ ent in terms of genotype distribution (1a/1b/2a/3a/others/ undetermine d: 10/48/7/17/0/2 versus 11/43/10/10/5/5), alpha(1)-antitrypsin phenot ype distribution (MM/MS/MZ: 84%/14%/2% vs. 87%/11%/2%, respectively), and prevalence of antibody to hepatitis B core antigen positivity (29% vs. 23%). Alcohol consumption was significantly different between cas es and controls (L/M/H: 58%/27%/16% vs. 76%/15%/9%, respectively; P < .05). Two conclusions regarding patients with chronic hepatitis C viru s infection can be drawn from this study: 1) viral genotype, especiall y 1b, past hepatitis B virus infection, and heterozygous MZ alpha(1)-a ntitrypsin deficiency are not risk factors for cirrhosis; and 2) alcoh ol consumption, even moderate, is a risk factor for cirrhosis.