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

ArticleinBritish Journal of Cancer 94(5):737-9 · April 2006with18 Reads
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.
    • "In contrast to hepatitis C, the impact of tobacco use in fibrosis progression remains controversial [10] and available materials would suggest that the cigarette smoking may aggravate necro-inflammation, thereby contributing to accelerated fibrogenosis [11]. Also, 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 [12]. Many people believe that they are safe from the risk of second-hand smoke as long as they are not the ones smoking or do not allow smoking in their homes or other areas they frequent whereas considerable evidences indicate that exposure to environmental tobacco (ETS) or " passive smoking " is harmful to the health of non- smokers [13]. "
    [Show abstract] [Hide abstract] ABSTRACT: Aims: This work aims at determining the effect of cigarette smoke on the liver of albino Wistar rats, to evaluate the histological, as well as the biochemical changes in the adult albino rat’s liver and to elucidate the relationship between exposure period and effect. Study Design: An experimental study which lasted for 4 weeks was conducted at the Animal House of The College of Health Sciences, Nnamdi Azikiwe University, Nnewi campus. Methodology: Twenty four (24) adult albino Wistar rats were divided into four groups (A, B, C and D) each consisting of six rats. The average weight of each group was taken. Group A (normal control) had no exposure to cigarette smoke throughout the period of experiment. Groups B, C and D were exposed to cigarette smoke for two, three and four weeks respectively. The duration of exposure for each cigarette is 10±4 minutes and one hour interval was left between burning of each cigarette. After the experiment, blood samples were collected through direct cardiac punctures and delivered into plain test tubes for biochemical assay, and the animals painlessly sacrificed under chloroform anesthesia. The liver was excised, fixed in 10% formal saline for 48 hours and processed using paraffin wax processing techniques. Results: Rats in groups B, C and D showed varying degrees of loss of appetite, moderate irritability and breathing difficulties with significant decrease in body weights after second and third weeks (P=.001). Significant increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities between the control and test groups was observed (P=0.000). Histologicaly, the liver of rats in group C shows marked necrosis and fatty deposition. Conclusion: The study reveals adverse effect of passive cigarette smoke on the liver morphology and biochemistry of the animal model. The need for similar study in humans is advocated.
    Full-text · Article · May 2015 · BMC Cancer
    • "It is believed that obesity in HCV patients plays a crucial role in fibrosis progression [160,161]. Patients should also avoid drinking alcohol and smoking as alcohol is reported as one of the major risk factor for liver diseases [162,163] and smoking may contribute to the development of diseases and increase the possibility of hepatocellular carcinoma progression [164]. Approaches to control spread of HCV infection include primary and second prevention activities. "
    [Show abstract] [Hide abstract] ABSTRACT: Safe blood transfusion where hepatitis is endemic In South-East Asia the prevalence of hepatitis B and C virus infections is high. Accurate – yet low-cost – screening of blood donors is crucial to avoid transfusion-transmitted disease. On (DATE) Le Viet will defend his thesis “Safe Blood Transfusion: Screening for Hepatitis B and Hepatitis C Virus Infections in Potential Blood Donors in Rural Southeast Asia” for the PhD degree at the Faculty of Health Sciences at UiT. The first aim of the thesis is to identify the accuracy of rapid tests for detection of acute hepatitis B, occult hepatitis B, and hepatitis C virus infections in potential blood donor in rural Vietnam and Cambodia. The second aim is to estimate prevalence of these infections among potential rural blood donors in Vietnam, and to examine the accuracy of enzyme immunoassay (EIA) technique in blood donor screening. The final goal is to estimate the risk of transfusion-transmitted hepatitis B in Vietnamese blood donors based on the available prevalence data and estimated prevalence of occult hepatitis B infection. 2,400 blood samples from potential voluntary rural blood donors in a multicentre cross-sectional study in Cambodia and Vietnam were analysed with rapid and EIA tests for detection of HBsAg, anti-HBc and anti-HCV at local laboratories. 640 randomly selected blood samples were blindly validated in a Norwegian accredited micro-laboratory by a chemiluminescent micro particle immunoassay technique (CMIA). Rapid test for donor screening of hepatitis proved to have far lover accuracy than claimed by the manufacturer; especially the false-negative rate was unacceptably high. The study revealed that hepatitis B infection is endemic in rural Vietnam and almost half of Vietnamese population is or has been infected with hepatitis B while hepatitis C infection is rare. The results indicate that the EIA performance in blood donor screening in Vietnam may be sub-optimal. The major risk factors for post- transfusion are HBsAg false-negative results and potential occult hepatitis B infections. Increased test sensitivity and locally validated HBsAg assays are recommended.
    Full-text · Thesis · Nov 2014 · BMC Cancer
    • "and cirrhosis compare to HBV genotype B [33]. There is convincing evidence that alcohol drinking and tobacco smoking increase the risk of primary HCC343536 and synergistic effects between hepatitis infection and tobacco smoking or alcohol drinking in the development of HCC has been recently suggested3738394041. Heavy alcohol drinking significantly elevated HCC risk after adjustment in this study. "
    [Show abstract] [Hide abstract] 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
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