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Objective: The aim of this study was to investigate the role of alcohol dehydrogenase type 3 (ADH3), glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms in modifying hepatocellular carcinoma (HCC) risk according to alcohol intake., Methods: A hospital-based case-control study was conducted in two areas of North Italy. Two-hundred cases hospitalized for HCC and 400 controls were recruited. Genotypes were determined using PCR and the PCR/restriction fragment length polymorphism-based method., Results: There was no association of the putative risk genotypes ADH3(1-1), GSTM1 null and GSTT1 null with HCC (odds ratio [OR], 0.8; 95% confidence interval [CI], 0.5-1.3; OR, 1.0; 95% CI, 0.6-1.5; OR, 0.8; 95% CI, 0.4-1.4, respectively). A steady increase in HCC risk with increasing alcohol intake, which did not vary according to ADH3 and GSTT1 genotypes, was observed. Nevertheless, the OR for HCC due to an alcohol intake of >100 g of ethanol per day increased in subjects with GSTM1 null genotype (OR, 8.5; 95% CI, 3.9-18.6) compared to GSTM1 non-null genotype (OR, 4.5; 95% CI, 2.0-10.0)., Conclusions: ADH3(1-1) and GSTT1 null genotypes did not modify the risk of HCC due to alcohol intake whereas an influence of GSTM1 null genotype for high ethanol consumption was suggested.

Background/aims: The role of coffee in the development of hepatocellular carcinoma (HCC) is debated. The aim of this study was to investigate the role of coffee in HCC, taking the main risk factors into account., Methods: A hospital-based case-control study was conducted in an area of northern Italy. We recruited 250 HCC cases and 500 controls hospitalized for any reasons other than neoplasms, and liver and alcohol-related diseases. Subjects were interviewed on their lifetime history of coffee consumption using a standardized questionnaire., Results: Coffee consumption in the decade before the interview was associated with a decreasing risk of HCC with a clear dose-effect relation. With respect to non-drinking subjects, the odds ratios (ORs) were: 0.8, (95% CI 0.4-1.3) for 1-2 cups/day, 0.4 (95% CI 0.2-0.8) for 3-4 cups/day and 0.3 (95% CI 0.1-0.7) for 5 or more cups/day. The ORs for HCC decreased for drinking >2, compared to 0-2 cups/day of coffee, for an alcohol intake >80 g/day (OR from 5.7 to 3.3), for presence of hepatitis B virus infection (OR from 16.4 to 7.3) or hepatitis C virus infection (OR from 38.2 to 9.0)., Conclusions: Coffee drinking was inversely associated with HCC regardless of its aetiology.

Objective: We investigated the relation between hepatocellular carcinoma (HCC) etiology and biological and clinical parameters indicative of severity of liver disease and/or tumor characteristics and patient survival., Methods: We prospectively recruited 384 patients (82.3% male) with first diagnosis of HCC from 1995 to 1998 in Brescia, Italy. Etiology was assessed by interviewing patients regarding their history of alcohol intake and by testing sera for hepatitis B surface antigen and anti-hepatitis C virus (HCV) antibodies and HCV RNA., Results: Heavy alcohol intake (>60 g of ethanol per day for at least 1 decade) was found in 33.1% of cases, hepatitis B virus (HBV) infection in 9.4%, HCV in 19.8%, hemochromatosis in 1.3%, alcohol and HBV in 12.0%, alcohol and HCV in 16.1%, HBV and HCV in 3.1%, and no factor in 5.2%. Patients with HBV infection with or without heavy alcohol intake were significantly younger than the others (61.7 vs 64.7 yr, p < 0.001). The proportion of males was significantly higher in patients with heavy alcohol intake alone than in the other patient groups (93.7% vs 77.3%, p < 0.001). Among patients with HCV infection with or without heavy alcohol intake, fewer patients had maximum tumor diameter > 5 cm than the others (12% vs 29.1%, p < 0.001). Eighty patients (20.8%) were alive at the end of follow-up (median survival, 17.7 months), and no differences were observed in survival rates by HCC risk factor., Conclusions: Although some differences were observed in severity of liver disease or tumor characteristics according to etiology, patient survival was not influenced by HCC etiology.