Xing Liu1,2, Aileen Baecker1, Ming Wu3, Jin-Yi Zhou3, Jie Yang3, Ren-Qiang Han3, Pei-Hua Wang3, Zi-Yi Jin2, Ai-Min Liu4, Xiaoping Gu4, Xiao-Feng Zhang5, Xu-Shan Wang5, Ming Su6, Xu Hu6, Zheng Sun7, Gang Li7, Alan Fu1, Su Yon Jung8,9, Lina Mu10, Na He2, Liming Li11, Jin-Kou Zhao3, Zuo-Feng Zhang1,8,12. 1. Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California. 2. Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China. 3. Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China. 4. Dafeng Center for Disease Control and Prevention, Dafeng, Jiangsu, China. 5. Ganyu Center for Disease Control and Prevention, Ganyu, Jiangsu, China. 6. Chuzhou County Center for Disease Control and Prevention, Chuzhou, Jiangsu, China. 7. Tongshan County Center for Disease control and Prevention, Tongshan, Jiangsu, China. 8. Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, California. 9. School of Nursing, UCLA, Los Angeles, California. 10. Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, The State University of New York, Buffalo, New York. 11. Department of Epidemiology, School of Public Health, Peking University, Beijing, China. 12. Center for Human Nutrition, David Geffen School of Medicine, UCLA, Los Angeles, California.
Abstract
BACKGROUND & AIMS: The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined. METHODS: We conducted a population-based case-control study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero-markers were assayed using blood samples. Semi-Bayes (SB) adjustments were applied to provide posterior estimates. RESULTS: Both family history of liver cancer (adjusted odds ratios [OR]: 4.32, 95% confidence intervals [CI]: 3.25-5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33-11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16-13.82) for HBsAg- and HBcAb-positive; 7.57 (95% CI: 4.87-11.77) for HBsAg-, HBeAg- and HBcAb-positive; and 3.62 (95% CI: 2.47-5.31) for HBsAg-, HBeAb- and HBcAb-positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03-1.32). The SB-adjusted OR of HBV-positive individuals with family history of liver cancer was 41.34 (95% posterior interval [PI]: 23.69-72.12) compared with those HBV-negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41-5.75). CONCLUSIONS: Super-additive and super-multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer.
BACKGROUND & AIMS: The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined. METHODS: We conducted a population-based case-control study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero-markers were assayed using blood samples. Semi-Bayes (SB) adjustments were applied to provide posterior estimates. RESULTS: Both family history of liver cancer (adjusted odds ratios [OR]: 4.32, 95% confidence intervals [CI]: 3.25-5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33-11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16-13.82) for HBsAg- and HBcAb-positive; 7.57 (95% CI: 4.87-11.77) for HBsAg-, HBeAg- and HBcAb-positive; and 3.62 (95% CI: 2.47-5.31) for HBsAg-, HBeAb- and HBcAb-positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03-1.32). The SB-adjusted OR of HBV-positive individuals with family history of liver cancer was 41.34 (95% posterior interval [PI]: 23.69-72.12) compared with those HBV-negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41-5.75). CONCLUSIONS: Super-additive and super-multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer.
Authors: Tomas Andersson; Lars Alfredsson; Henrik Källberg; Slobodan Zdravkovic; Anders Ahlbom Journal: Eur J Epidemiol Date: 2005 Impact factor: 8.082
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