Is the lymphoma risk reduced in viral hepatitis? A cirrhotic patient with triple malignancies.
Department of Gastroenterology, Goztepe Teaching and Research Hospital, Istanbul, Turkey.The American Journal of Gastroenterology (Impact Factor: 7.55). 09/2011; 106(9):1719-20; author reply 1720. DOI:10.1038/ajg.2011.214
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ABSTRACT: Although hepatitis C virus (HCV) infection has been shown to be associated with development of non-Hodgkin's lymphoma (NHL), few studies have investigated the association between chronic HBV infection and NHL. The purpose of this study was to compare the incidence of NHL between patients with and without chronic hepatitis B virus (HBV) infection. Using automated laboratory result and clinical data from two United States health systems, we identified individuals with chronic HBV infection from January 1, 1995 through December 31, 2001. Using each health system's population-based tumor registry, we identified all cases of NHL diagnosed through December 31, 2002. We excluded any individual with a history of NHL or human immunodeficiency virus (HIV). We fit Cox proportional hazards models to calculate hazard ratios comparing the incidence of NHL between chronic HBV-infected patients (N = 3,888) and patients without HBV (N = 205,203) drawn from the source populations. We identified 8 NHL cases in the chronic HBV infection cohort and 111 cases in the comparison cohort. Patients with chronic HBV infection were 2.8 times more likely to develop NHL than matched comparison patients (adjusted hazard ratio = 2.80, 95% confidence interval = 1.16-6.75), after controlling for age, race, sex, income, Charlson comorbidity index, study site, and HCV infection. CONCLUSION: chronic HBV-infected patients were nearly 3 times more likely to develop NHL than comparison patients.Hepatology 08/2007; 46(1):107-12. · 12.00 Impact Factor
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ABSTRACT: The present meta-analysis was conducted to evaluate the strength and the consistency of the association between hepatitis C virus (HCV) infection and non-Hodgkin lymphoma (NHL) and other lymphoid neoplasms. Only studies with >or=100 cases which were also adjusted for sex and age were included. Fifteen case-control studies and three prospective studies contributed to present analysis, nine of which had not been included in previous meta-analyses. We calculated the pooled relative risks (RR) with corresponding 95% confidence intervals (95% CI), as a weighted average of the estimated RRs by random-effect models. The pooled RR of all NHL among HCV-positive individuals was 2.5 (95% CI, 2.1-3.0), but substantial heterogeneity was found between studies and by study design. Pooled RRs were 2.5 (95% CI, 2.1-3.1) in case-control studies and 2.0 (95% CI, 1.8-2.2) in cohort ones. The strongest source of heterogeneity seemed to be the prevalence of HCV among NHL-free study subjects (RR for NHL among HCV-positive individuals 3.0 and 1.9, respectively, for >or=5% and <5% HCV prevalence). RRs were consistently increased for all major B-NHL subtypes, T-NHL, and primary sites of NHL presentation. Thus, previous suggestions that the RRs for HCV differed by NHL subtype were not confirmed in our meta-analysis. Associations weaker than with NHL were found between HCV infection and Hodgkin's lymphoma (RR, 1.5; 95% CI, 1.0-2.1) and multiple myeloma (RR, 1.6; 95% CI, 0.7-3.6), but they were based on much fewer studies than NHL. The etiologic fraction of NHL attributable to HCV varies greatly by country, and may be upward of 10% in areas where HCV prevalence is high.Cancer Epidemiology Biomarkers & Prevention 12/2006; 15(11):2078-85. · 4.56 Impact Factor
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