Hepatitis B and C virus infection, alcohol drinking, and hepatocellular carcinoma: a case-control study in Italy. Brescia HCC Study

Cattedra di Igiene dell'Università di Brescia, Italy.
Hepatology (Impact Factor: 11.19). 09/1997; 26(3):579-84. DOI: 10.1002/hep.510260308
Source: PubMed

ABSTRACT We performed a case-control study to assess the association of hepatocellular carcinoma (HCC) with hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and alcohol drinking. We recruited as cases 172 subjects with an initial diagnosis of HCC, who were admitted to the two major hospitals in the province of Brescia, northern Italy, and 332 subjects, sex-, age-, and hospital-matched, who were admitted to the Departments of Ophthalmology, Dermatology, Urology, Cardiology, and Internal Medicine, as controls. Of the HCC cases, 23.8% were positive for HBsAg and 37.8% for HCV RNA; among the controls, 5.4% were positive for HBsAg and 4.8% for HCV RNA. History of heavy alcohol intake (>80 g of ethanol per day for at least 5 years) was found among 58.1% of the cases and among 36.4% of the controls. The relative risks (RRs) for HBsAg, HCV RNA positivity, and heavy alcohol intake were, respectively: 11.4 (95% confidence interval: 5.7-22.8), 23.2 (95% confidence interval: 11.8-45.7), and 4.6 (95% confidence interval: 2.7-7.8). Positive interactions (synergisms) between both HBsAg positivity and HCV RNA positivity and heavy alcohol intake were found, suggesting more than additive effects of viral infections and alcohol drinking on the risk of HCC. Infection with HCV genotype 1b showed a higher risk than type 2 (RR = 2.9; 95% confidence interval: 0.9-10), suggesting a major role for the former type in causing HCC. On the basis of population attributable risks (AR), heavy alcohol intake seems to be the single most relevant cause of HCC in this area (AR: 45%), followed by HCV (AR: 36%), and HBV (AR: 22%) infection.

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    • "In developing countries, the major concern in HCC frequently belongs to HCV long lasting infection. Chronic HCV infection mostly leads to hepatic cirrhosis before developing HCC (Donato et al., 1997). Additionally, occult HCV was also reported in patients with chronic un-explained hepatitis (Lerat et al., 2004). "
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    ABSTRACT: Hepatocellular carcinoma (HCC) became a prevalent disease in many populations worldwide. It initiates many economic problems in management modalities and leads to increasing mortality rates. Many trials are made all over the world to implement specific early markers for detection and prediction of the disease, hoping to set a more precise strategy for liver cancer prevention. Unfortunately, many economic, cultural and disciplinary levels contribute to confounding preventive strategies. Many risk factors seem to predispose HCC, which either present individually or collectively depending on the environmental situations. Previous articles discussed many risk factors participating in hepatocellular carcinogenesis, although most of them did not handle collectively the current up to date causes. In this article, the pathogenesis and most of risk factors of HCC are briefly discussed. Most of the intermediating steps of HCC pass through molecular and transcriptional events leading eventually to hepatocyte malignant transformation. These steps are mainly triggered by hepatitis B, C or transfusion-transmitted virus, either alone, or with other factors. Diabetes seems to be greatly a leading disease. Schistosomiasis, a blood infestation, mostly disturbs Nile habitants leading also to bladder, renal and hepatic cancers. Alcoholism, food and water pollutants and some other drugs can lead to HCC. Additionally, some hereditary diseases, as hemochromatosis, -1-antitrypsin deficiency and tyrosinaemia are known to develop to HCC, if not discovered.
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    • "There is epidemiological evidence that chronic coinfection with HBV and HCV may lead to a more severe prognosis. While some studies failed to demonstrate such a synergism (Donato et al., 1997), other studies clearly demonstrate a greater than additive risk of HCC in patients coinfected with HBV and HCV (Kew et al., 1997; Tsai et al., 1996). A meta-analysis of 32 studies involving a total of 4560 cases of HCC and 6988 controls revealed that the odds ratio (OR) of HCC for people coinfected with HBV and HCV (OR = 135; 95% confidence 79.7–242) was greater than additive of the independent risks of chronic infection with either HBV (OR = 20.4; "
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    ABSTRACT: Transgenic mice expressing the full-length HCV coding sequence were crossed with mice that express the HBV X gene-encoded regulatory protein HBx (ATX mice) to test the hypothesis that HBx expression accelerates HCV-induced liver pathogenesis. At 16 months (mo) of age, hepatocellular carcinoma was identified in 21% of HCV/ATX mice, but in none of the single transgenic animals. Analysis of 8-mo animals revealed that, relative to HCV/WT mice, HCV/ATX mice had more severe steatosis, greater liver-to-body weight ratios, and a significant increase in the percentage of hepatocytes staining for proliferating cell nuclear antigen. Furthermore, primary hepatocytes from HCV, ATX, and HCV/ATX transgenic mice were more resistant to fas-mediated apoptosis than hepatocytes from nontransgenic littermates. These results indicate that HBx expression contributes to increased liver pathogenesis in HCV transgenic mice by a mechanism that involves an imbalance in hepatocyte death and regeneration within the context of severe steatosis.
    Virology 05/2006; 347(2):466-75. DOI:10.1016/j.virol.2005.11.050 · 3.28 Impact Factor
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    • "The corresponding figures for patients with decompensated cirrhosis are substantially lower, 0 and 28%, respectively. Factors associated with an increased risk of hepatic decompensation include active viral replication, regular alcohol consumption, and coinfection with HIV or HCV [20] [21]. A study of 161 European patients (28% HBeAgpositive ) with compensated HBV-cirrhosis followed for a median of 6.6 years found that those with HBeAg and detectable HBV DNA by hybridization assay had a higher cumulative probability of decompensation (18%), compared to HBeAg-negative/HBV DNA-positive patients (13%) and HBeAg-negative/HBV DNA-negative patients (4%) (PZ 0.04) [19]. "
    Journal of Hepatology 02/2005; 42 Suppl(1):S54-64. DOI:10.1016/j.jhep.2004.11.014 · 10.40 Impact Factor
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