BACKGROUND AND AIMS: The relationship between the hepatitis B virus (HBV) and pancreatic cancer remains unclear. Because HBV has been isolated from pancreatic tissue, we hypothesized that HBV may play a role in the development of pancreatic carcinoma. METHODS: This cohort was recruited between 1991 and 1992. Serum samples obtained at enrolment were tested for HBsAg and HBeAg by radioimmunoassay. Pancreatic cancer diagnosis was ascertained through data linkage with profiles of the National Cancer Registry and Death Certification System in Taiwan from 1 January 1991 to 31 December 2007. Multivariate-adjusted hazards ratios (HR(adj)) with 95% confidence intervals (CI) were derived using Cox proportional hazards models. RESULTS: In total 22 471 subjects were followed up for 342 186 person-years and 48 had pancreatic cancer. Chronic carriers of HBsAg had a significantly increased risk of pancreatic cancer showing an HR(adj) (95% CI) of 1.95 (1.01-3.78). This association was most striking in females, individuals < or =50 years, non-smokers and non-drinkers. The HR(adj) (95% CI) of developing pancreatic cancer was 5.73 (1.73-19.05) for HBeAg-seropositive carriers and 1.64 (0.79-3.42) for HBeAg-seronegative carriers compared with HBsAg-seronegative non-carriers. An increased risk of pancreatic cancer was observed for HBsAg-seropositives with HBV DNA > or =300 copies/ml (HR(adj), 2.44; 95% CI, 1.20-4.95), but not for HBsAg-seropositives with HBV DNA <300 copies/ml (HR(adj), 0.64; 95% CI, 0.09-4.67). CONCLUSIONS: In addition to the well-established risk of hepatocellular carcinoma, chronic HBV infection may be associated with an increased risk of pancreatic cancer.
BACKGROUND AND AIMS: The relationship between the hepatitis B virus (HBV) and pancreatic cancer remains unclear. Because HBV has been isolated from pancreatic tissue, we hypothesized that HBV may play a role in the development of pancreatic carcinoma. METHODS: This cohort was recruited between 1991 and 1992. Serum samples obtained at enrolment were tested for HBsAg and HBeAg by radioimmunoassay. Pancreatic cancer diagnosis was ascertained through data linkage with profiles of the National Cancer Registry and Death Certification System in Taiwan from 1 January 1991 to 31 December 2007. Multivariate-adjusted hazards ratios (HR(adj)) with 95% confidence intervals (CI) were derived using Cox proportional hazards models. RESULTS: In total 22 471 subjects were followed up for 342 186 person-years and 48 had pancreatic cancer. Chronic carriers of HBsAg had a significantly increased risk of pancreatic cancer showing an HR(adj) (95% CI) of 1.95 (1.01-3.78). This association was most striking in females, individuals < or =50 years, non-smokers and non-drinkers. The HR(adj) (95% CI) of developing pancreatic cancer was 5.73 (1.73-19.05) for HBeAg-seropositive carriers and 1.64 (0.79-3.42) for HBeAg-seronegative carriers compared with HBsAg-seronegative non-carriers. An increased risk of pancreatic cancer was observed for HBsAg-seropositives with HBV DNA > or =300 copies/ml (HR(adj), 2.44; 95% CI, 1.20-4.95), but not for HBsAg-seropositives with HBV DNA <300 copies/ml (HR(adj), 0.64; 95% CI, 0.09-4.67). CONCLUSIONS: In addition to the well-established risk of hepatocellular carcinoma, chronic HBV infection may be associated with an increased risk of pancreatic cancer.