No contribution of lifestyle and environmental exposures to gender discrepancy of liver disease severity in chronic hepatitis b infection: Observations from the Haimen City cohort.

• Main Authors: Jing Sun, Lucy Robinson, Nora L Lee, Seth Welles, Alison A Evans
• Format: Article
• Language: English
• Published: Public Library of Science (PLoS) 2017-01-01
• Series: PLoS ONE
• Online Access: http://europepmc.org/articles/PMC5409078?pdf=render

BACKGROUND:Previous studies have noted significant gender difference in the risk of liver cancer among hepatitis B chronic infection patients. Some indicated that it might be due to lifestyle-related differences. This paper tests whether or not such a gender discrepancy among the chronic hepatitis B population is confounded by lifestyle and environment related exposures. METHODS:We retrieved a sample of 1863 participants from a prospective cohort in Haimen City, China in 2003. Liver disease severity was categorized as "normal", "mild", "moderate", and "severe" based on a clinical diagnosis. Lifestyle and environmental exposures were measured by questionnaires. We used factor analysis and individual variables to represent lifestyle and environmental exposures. We applied the cumulative logit models to estimate the effect of gender on liver disease severity and how it was impacted by lifestyle and environmental exposures. RESULTS:Gender and HBeAg positivity were independent risk factors for more severe liver disease. Compared to females, males were 2.08 times as likely to develop more severe liver disease (95% CI: 1.66-2.61). Participants who were HBeAg positivite were 2.19 times (95% CI: 1.61-2.96) as likely to develop more severe liver disease compared to those who were negative. Controlling for lifestyle and environmental exposures did not change these estimations. CONCLUSIONS:Males in the HBV infected population have an increased risk of severe liver disease. This gender effect is independent of the lifestyle and environmental exposures addressed in this study. Our findings support the hypothesis that gender discrepancies in HCC risk are attributable to intrinsic differences between males and females.