Fujita Y, Shibata A, Ogimoto I, Kurozawa Y, Nose T, Yoshimura T, et al. 2006. The effect of interaction between hepatitis C virus and cigarette smoking on the risk of hepatocellular carcinoma

Department of Public Health, Kurume University School of Medicine, Kurume 830-0011, Japan.
British Journal of Cancer (Impact Factor: 4.84). 04/2006; 94(5):737-9. DOI: 10.1038/sj.bjc.6602981
Source: PubMed


We evaluated the interaction between hepatitis C virus (HCV) and cigarette smoking on death from hepatocellular cancer in The Japan Collaborative Cohort Study. The odds ratio of death from HCC for smoking was 9.60 (1.50-61.35) and 1.71(0.58-5.08) among anti-HCV positive and negative individuals, respectively.

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    • "There is convincing evidence that alcohol drinking and tobacco smoking increase the risk of primary HCC [34-36] and synergistic effects between hepatitis infection and tobacco smoking or alcohol drinking in the development of HCC has been recently suggested [37-41]. Heavy alcohol drinking significantly elevated HCC risk after adjustment in this study. "
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    ABSTRACT: Background There has been limited study on the effect of infection with different hepatitis C virus (HCV) genotypes on the risk of hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) endemic regions of Asia. Methods Hazard ratios of HCC development were estimated for HBV and HCV co-infected subjects among a community-based prospective cohort. HCV genotype was determined in HCV RNA-positive samples. Incident HCC cases were identified through linkage to the cancer registry. Results HCC incidence was 79 per 100,000 person-years in the study population (50 incident cases among 6,694 individuals within 63,170 person-years with an average of 9.4 years of follow-up); seroprevalence of HBsAg and anti-HCV was 5.2% and 5.6%. Adjusted hazard ratios of HCC by HBsAg positivity and anti-HCV positivity were 13.3 (CI: 7.3-24.4) and 6.7 (CI: 3.6-12.6). HRs of HBV and HCV monoinfection, and HBV/HCV coinfection were 17.1 (CI: 8.4-34.8), 10.4 (CI: 4.9-22.1) and 115.0 (CI: 32.5-407.3). Multiplicative synergistic effect of HBV/HCV coinfection on HCC risk was also observed (synergy index: 4.5, CI: 1.3-15.5). Infection with HCV genotype 1 (HR: 29.7, CI: 13.6-46.8) and mixed infection with genotype 1 and 2 (HR: 68.7, CI: 16.4-288.4) significantly elevated HCC risk, much higher than HBV infection. Conclusions The effect of differences in HCV genotype and the multiplicative synergistic effect of HBV/HCV coinfection on HCC risk shown in the present study underline the need for comprehensive identification of hepatitis infection status in order to prevent and control HCC in this HBV endemic area.
    Full-text · Article · Oct 2012 · BMC Cancer
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    • "Also, patients should avoid drinking alcohol because there is no safe minimum limit of consumption, and alcohol is one of the major risk factors for liver disease and exacerbates the negative effects of hepatitis C [3,15,16]. Additionally, hepatitis C patients are advised not to smoke because smoking may contribute to the progression of the disease and increase the likelihood of developing hepatocellular carcinoma [9,17]. "
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    ABSTRACT: Hepatitis C virus (HCV) is endemic worldwide, and it causes cirrhosis and other complications that often lead to death; nevertheless, our knowledge of the disease and its mechanisms is limited. HCV is most common in underdeveloped nations, including many in Africa and Asia. The virus is usually transmitted by parenteral routes, but sexual, perinatal, and other types of transfer have been known to occur. Approximately 80% of individuals who contract hepatitis C develop a chronic infection, and very few are able to spontaneously clear the virus. Because hepatitis C is asymptomatic in the majority of patients, the presence of HCV RNA in the serum is the best diagnostic tool. Although serious complications from hepatitis C may not occur for 20 years, 1/5 of chronic patients eventually develop life - threatening cirrhosis. More research is needed on the different therapy options for the disease, and many factors, most importantly the genotype of the virus, must be taken into account before beginning any treatment. As there is no vaccine against HCV at present, the most effective and recommended therapy is pegylated-interferon-α-2a plus ribavirin. While interferon is marginally effective as a monotherapy, both adding the moiety and combining it with ribavirin have been shown to dramatically increase its potency. While there are numerous alternative and complementary medicines available for patients with hepatitis C, their efficacy is questionable. Currently, research is being done to investigate other possible treatments for hepatitis C, and progress is being made to develop a vaccine against HCV, despite the many challenges the virus presents. Until such a vaccination is available, prevention and control methods are important in containing and impeding the spread of the virus and mitigating its deleterious effects on the health of people and communities worldwide.
    Full-text · Article · Mar 2012 · Virology Journal
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    • "In contrast, in patients with chronic hepatitis C, the impact of tobacco use on fibrosis progression remains controversial [7] [8] and available data would suggest that cigarette smoking may aggravate necroinflammation, thereby contributing to accelerated fibrogenesis [7] [8] [9] [10]. Finally, in line with the carcinogenic properties of tobacco in several organs, a number of studies indicate that cigarette smoking is associated with an increased incidence of hepatocellular carcinoma in cirrhotic patients [11] [12] [13] [14]. "

    Preview · Article · Jul 2009 · Journal of Hepatology
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