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Chronic hepatitis C virus infection and risk of hepatocellular carcinoma: a community-based prospective study on 19,565 residents in Taiwan
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Reported by Jules Levin
AASLD, Nov 2-6, 2007, Boston, MA
M. Lee1; H. Yang2; C. Liu3; S. You2; P. Chen3; C. Chen1, 2
1. Institute of Epidemiology, National Taiwan University, Taipei city, Taiwan.
2. Genomics Research Center, Academia Sinica, Taipei city, Taiwan.
3. Department of Internal Medicine, National Taiwan University Hospital, Taipei city, Taiwan.
"HCV infection, elevated serum ALT levels, and cigarette smoking are important HCC risk predictors for HBsAg-seronegatives in Taiwan....
.....Compared with anti-HCV- seronegative participants as the referent group, the HRadj (95% CI) was 8.0 (4.3-14.7) for anti-HCV-seropositives with undetectable HCV RNA, 6.6 (3.9-11.2) for anti-HCV-seropositives with detectable genotype 1 HCV RNA, and 6.2 (3.3-11.7) for anti-HCV-seropositives with detectable genotype non-1 HCV RNA after adjustment for age, gender, cigarette smoking and serum ALT level at study entry. The HRadj (95% CI) was 2.7 (1.7-4.1) and 7.6 (4.4-13.1), respectively, for serum ALT levels of 16-45 and >45 IU/L compared with ALT level <15 IU/L."
Background and aims: Chronic hepatitis C virus (HCV) infection is an important risk predictor of hepatocellular carcinoma (HCC). But the cumulative HCC incidence associated with chronic HCV infection has rarely been examined by community-based long-term follow-up studies. This prospective study aimed to evaluate the impacts of HCV on HCC in Taiwan, where chronic hepatitis B is hyperendemic.
Methods: A total of 19,565 residents who were HBsAg-seronegative and free of liver cirrhosis or HCC at entry were enrolled during 1991 to 1992. There were 1,041 anti-HCV-seropositives and 18,524 anti-HCV-seronegatives. They were followed until December 31, 2004. The newly diagnosed HCC was ascertained through computerized data linkage with the national cancer registry profile. In total, 111 newly developed HCC were identified. Cox's proportional hazards model was used to estimate multivariate-adjusted hazard ratio (HRadj) and its 95% confidence intervals (CI) for each risk factor included in the regression analyses.
Results: During the follow-up of 246,154 person-years, the cumulative HCC incidence per 100,000 person-years was 26 for anti-HCV-seronegative participants, 290 for anti-HCV-seropositives with undetectable HCV RNA, 464 for anti-HCV- seropositives with detectable genotype 1 HCV RNA, and 370 for anti-HCV- seropositives with detectable genotype non-1 HCV RNA.
Compared with anti-HCV- seronegative participants as the referent group, the HRadj (95% CI) was 8.0 (4.3-14.7) for anti-HCV-seropositives with undetectable HCV RNA, 6.6 (3.9-11.2) for anti-HCV-seropositives with detectable genotype 1 HCV RNA, and 6.2 (3.3-11.7) for anti-HCV-seropositives with detectable genotype non-1 HCV RNA after adjustment for age, gender, cigarette smoking and serum ALT level at study entry. The HRadj (95% CI) was 2.7 (1.7-4.1) and 7.6 (4.4-13.1), respectively, for serum ALT levels of 16-45 and >45 IU/L compared with ALT level <15 IU/L. Cigarette smoking was also associated with an increased HCC risk with an HRadj (95% CI) of 1.7 (1.0-2.8).
In the stratification analyses, the age-gender-adjusted HRadj (95% CI) for the anti-HCV- seropositives with undetectable HCV RNA, anti-HCV-seropositives with detectable genotype 1 HCV RNA, and anti-HCV-seropositives with detectable genotype non-1 HCV RNA was 25.7 (7.3-90.9), 10.7 (3.3-34.6) and 11.3 (3.3-39.7), respectively, for those with ALT levels at entry >45 IU/L. The corresponding figures were 5.2 (2.2-12.0), 9.8 (5.3-18.2), and 7.5 (3.2-17.5) for those with ALT levels at entry < 45 IU/L.
Conclusion: HCV infection, elevated serum ALT levels, and cigarette smoking are important HCC risk predictors for HBsAg-seronegatives in Taiwan.
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