Incidence and Cofactors of Hepatitis C Virus-related Hepatocellular Carcinoma: A Prospective Study of 12,008 Men in Taiwan

Sun, Chien‐An; Wu, Der-Min; Lin, Chia-Chin; Lu, Sheng–Nan; You, San–Lin; Wang, Li-Yu; Wu, Mei-Hsuan; Chen, Chien‐Jen

doi:10.1093/aje/kwg041

Cited by 222 publications

(125 citation statements)

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“…Sun et al (2003) suggest that the adjusted relative risk of HCC development was 3.9 for smokers who were positive for anti-HCV in comparison with that for nonsmokers who were negative for anti-HCV. Yu et al (1991) reported that there were significantly synergistic effects of anti-HCV with cigarette smoking.…”

Section: Discussionmentioning

confidence: 93%

“…The odds ratio of death from HCC for smoking was 9.60 (1. 50 -61.35) Many studies have reported that chronic hepatitis C virus (HCV) infection is a risk factor for hepatocellular carcinoma (HCC) (Mori et al, 2000;El-Serag, 2002;Sun et al, 2003;Ayoola and Gadour, 2004), HCV appearing to be more hepatocarcinogenic than hepatitis B virus (HBV) (Pang et al, 2005). While alcohol is a well established risk factor for HCC, there is evidence that cigarette smoking is also a risk factor (Mukaiya et al, 1998;Mizoue et al, 2000;Chen et al, 2003), though some studies reported no or an insignificant association (La Vecchia et al, 1988;Evans et al, 2002).…”

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confidence: 99%

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The effect of interaction between hepatitis C virus and cigarette smoking on the risk of hepatocellular carcinoma

et al. 2006

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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) Many studies have reported that chronic hepatitis C virus (HCV) infection is a risk factor for hepatocellular carcinoma (HCC) (Mori et al, 2000;El-Serag, 2002;Sun et al, 2003;Ayoola and Gadour, 2004), HCV appearing to be more hepatocarcinogenic than hepatitis B virus (HBV) (Pang et al, 2005). While alcohol is a well established risk factor for HCC, there is evidence that cigarette smoking is also a risk factor (Mukaiya et al, 1998;Mizoue et al, 2000;Chen et al, 2003), though some studies reported no or an insignificant association (La Vecchia et al, 1988;Evans et al, 2002). Recently, an association between diabetes mellitus and HCC (or HCV) has been reported (Caronia et al, 1999;Toyoda et al, 2001). We evaluated the interaction between HCV infection and cigarette smoking by means of a nested case -control study from a large cohort. MATERIALS AND METHODSThe Japan Collaborative Cohort Study (JACC Study) for Evaluation of Cancer Risk sponsored by the Ministry of Education, Science, Sports and Culture of Japan (Monbusho) is a large prospective cohort study, which was mounted from 1988 to 1990 in 45 areas in Japan. The number of subjects is 110 792 (46 465 males and 64 327 females) who were 40 -79 years of age at the time of the baseline survey. Individual informed consent to participate in the study was obtained in 36 out of 45 areas . The subjects were asked to complete a self-administered questionnaire about past medical history, various life style factors and marital status as baseline information. The detailed design of the JACC study has been described previously (Ohno and Tamakoshi, 2001;Watanabe et al, 2005). During the approximately 10 years of follow-up through December 31, 1999, there were 550 deaths from liver cancer that were coded as C22 in the International Classification of Diseases and Related Health Problems, 10th Revision. Those survey participants who underwent healthscreening checks sponsored by municipalities were asked to donate blood samples during the same period as the questionnaire survey. Eventually, 39 242 subjects provided blood samples . Baseline serum samples had been collected 120 of the 550 subjects who died of liver cancer. As the control group, sera of 11 543 subjects from the same geographical areas as the 120 deaths also were screened for anti-HCV. Deaths (nine) coded as C22.9 (liver cancer not otherwise specified) were excluded from this analysis, while deaths (five) coded as C22.1 (intrahepatic cholangiocarcinoma and cholangiohepatoma; included among non-HCC deaths), leaving 106 deaths from HCC that were regarded as the end point of this analysis. The total subjects were 11 654 but as the sera of 34 cases and controls could not be screened because of insufficient serum volume, the sera of 11 620 subjects were screened for antibody to HCV (anti-HCV) an...

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Section: Discussionmentioning

confidence: 93%

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confidence: 99%

The effect of interaction between hepatitis C virus and cigarette smoking on the risk of hepatocellular carcinoma

et al. 2006

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“…Most HCC patients have a chronic liver disease in the background liver, among which chronic viral hepatitis due to hepatitis C virus (HCV) or hepatitis B virus (HBV) is very common [5][6][7]. Surveillance for HCC is now a part of standard clinical practice for patients with chronic viral hepatitis [8].…”

Section: Introductionmentioning

confidence: 99%

Ultrasound surveillance for early detection of hepatocellular carcinoma among patients with chronic hepatitis C

et al. 2009

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Background and aims Ultrasonography is the most frequently used modality in surveillance for HCC among patients with chronic hepatitis C. However, the optimal surveillance interval is still controversial and the usefulness of supplementary tumor marker determination has not been confirmed. Methods A total of 243 cases of naive HCC were detected among 1,431 patients with chronic hepatitis C under outpatient-based surveillance. The mode of HCC detection, including ultrasound surveillance interval, was retrospectively examined and the relation between the interval and detected tumor size was analyzed. Tumor volume doubling time was estimated from exponential increase in serum tumor marker levels when applicable. Results HCC was first detected by ultrasonography in 221 patients. Ultrasound surveillance interval, ranging between 2 and 8 months, was not correlated with the size of tumor at detection. Patients with cirrhosis were likely to be surveyed at shorter intervals. The size of tumor exceeded 30 mm only in three (1.4%) cases. They were all positive for a biomarker and the estimated tumor doubling time was short. In 14 cases, HCC was first detected by CT indicated by abnormal rise in tumor marker levels despite negative ultrasound findings. In the remaining eight cases, ultrasonography had been replaced by CT as surveillance modality because of excessive obesity or coarseness of liver parenchyma.Conclusions Ultrasound surveillance at 6-month intervals was appropriate in general for the detection of HCC at a size smaller than 30 mm. However, in patient with established cirrhosis, more frequent screening would be needed to detect tumors of the same size.

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“…Taiwan, with high prevalence rates of both cirrhosis and liver cancer, has an increasing rate of betel (Areca catechu) chewing; the nuts are chopped and, with Piper betle vine flower heads, used as betel-chews by a tenth of the 23 million inhabitants currently (2) . This habit is recognized to be carcinogenic in man (2) and has been reported to be associated with LC and with HCC in Taiwan (3)(4)(5)(6) .…”

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Impact of chewing betel-nut (Areca catechu) on liver cirrhosis and hepatocellular carcinoma: a population-based study from an area with a high prevalence of hepatitis B and C infections

Boucher²,

Chiu

et al. 2009

Public Health Nutr.

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Background: Chewing betel-nuts (Areca catechu) is carcinogenic but the risk for hepatocellular carcinoma (HCC) and liver cirrhosis (LC) is little considered. Worldwide 600 million people chew betel, including emigrants from palmgrowing countries. Objective: We aimed to assess the relationships and dose-response effects of betel chewing on LC and HCC risks, since habit cessation could reduce the increased risks of HCC and LC found in such communities. Subjects: Screening 60 326 subjects aged 30-79 years in a population-based study in Taiwan identified LC in 588 and HCC in 131 subjects. Demographic features, hepatitis B/C infections, other risk factors and betel chewing were noted. Multiple Cox regression models were used to assess independent relationships, interactions and synergisms between age, betel chewing and hepatitis B/C. Results: Betel chewing increased LC and HCC risk 4?25-fold (95 % CI 2?9, 6?2) in current chewers and 1?89-fold (95 % CI 1?13, 3?16) in ex-chewers v. neverchewers, with dose effects for quantity, duration and cumulative exposure in chewers. Subjects without hepatitis B/C infections had 5?0-fold (95 % CI 2?87, 9?03) increased risk of LC/HCC v. never-chewers, and betel chewing had an additive synergistic effect on hepatitis B/C-related risks. Risk reduction with betel habit cessation could exceed that expected from immunization programmes for hepatitis B and C. Conclusion: Increased risks of cirrhosis and hepatocellular cancer were found in betel chewers free of hepatitis B/C infection, and these risks were synergistically additive to those of hepatitis B/C infections. Estimated risk reduction from effective anti-betel chewing programmes would be sizeable.

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Incidence and Cofactors of Hepatitis C Virus-related Hepatocellular Carcinoma: A Prospective Study of 12,008 Men in Taiwan

Cited by 222 publications

References 44 publications

The effect of interaction between hepatitis C virus and cigarette smoking on the risk of hepatocellular carcinoma

The effect of interaction between hepatitis C virus and cigarette smoking on the risk of hepatocellular carcinoma

Ultrasound surveillance for early detection of hepatocellular carcinoma among patients with chronic hepatitis C

Impact of chewing betel-nut (Areca catechu) on liver cirrhosis and hepatocellular carcinoma: a population-based study from an area with a high prevalence of hepatitis B and C infections

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