Is alcohol a risk factor for liver cirrhosis in HBsAg and anti-HCV negative subjects?

Corrao, Giovanni; Aricò, S; Zambon, Antonella; Torchio, Pierfederico; Lepore, Alberto; Busellu, Giampiero; Orio, Ferdinando di

doi:10.1016/s0168-8278(97)80350-9

Cited by 24 publications

(12 citation statements)

References 39 publications

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“…Other case-control studies carried out in South Europe have demonstrated a dose-effect relationship of increased risk for both cirrhosis and HCC with increasing alcohol intake, when also adjusting for HBV and HCV infection (Corrao et al, 1993(Corrao et al, , 1997Bellentani et al, 1994;Corrao and Arico`, 1998;Kuper et al, 2000a). On the same line, two meta-analyses conducted by Corrao et al (1998aCorrao et al ( , 2004 on the risk of cirrhosis and of various neoplasms, including liver cancer, show a continuous curve of increasing risk of disease with increasing alcohol intake.…”

Section: Dose-effect Relationship and Threshold Of Safe Intakementioning

confidence: 86%

Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence

et al. 2006

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Hepatitis B virus (HBV), hepatitis C virus (HCV) and alcohol consumption are major causes of hepatocellular carcinoma (HCC) worldwide. We performed a systematic review of epidemiologic studies carried out on HCC aetiology in Southern Europe, an area with an intermediatehigh prevalence of these agents as well as of putative risk factors such as tobacco smoking, diabetes and obesity. To retrieve the articles, we performed a Medline search for titles and abstracts of articles. After the Medline search, we reviewed the papers and reference lists to identify additional articles. A synergism between HCV infection and HBV infection, overt (hepatitis B virus antigen (HbsAg) positivity) or occult (HBsAg negativity with presence of HBV DNA in liver or serum), is suggested by the results of some studies. The pattern of the risk for HCC due to alcohol intake shows a continuous dose-effect curve without a definite threshold, although most studies found that HCC risk increased only for alcohol consumption above 40-60 g of ethanol per day. Some evidence supports a positive interaction of alcohol intake probably with HCV infection and possibly with HBV infection. A few studies found that coffee has a protective effect on HCC risk due to various risk factors. Some data also support a role of tobacco smoking, diabetes and obesity as single agents or preferably cofactors in causing HCC. In countries with a relatively high alcohol consumption and intermediate levels of HCV and HBV infections (1-3% of population infected by each virus), such as Mediterranean countries, the three main risk factors together account for about 85% of the total HCC cases, leaving little space to other known risk factors, such as haemochromatosis, and to new, still unrecognised, factors as independent causes of HCC.

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Section: Dose-effect Relationship and Threshold Of Safe Intakementioning

confidence: 86%

Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence

et al. 2006

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“…The findings in this study are compatible with the hypothesis, previously suggested in a study by Sørensen et al [9], that alcohol may have a permissive rather than a dose-dependent effect on alcoholic cirrhosis mortality in men. From other crosssectional, case control and prospective cohort studies a threshold, above which an increased risk of alcoholic liver disease is observed has been estimated to 20-40 g/day [15], 30 g/day [16], 12 -24 g/day (women) and 24-36 g per day (men) [1], 40 g/day [17,18], 40 -80 g/day (fatty liver and alcoholic hepatitis) and 80-160 g/day (fibrosis and cirrhosis) [19], , 50 g/day [20,21]. In the meta-analysis by even low levels resulted in a significantly increased risk of liver disease [22].…”

Section: Discussionmentioning

confidence: 99%

Alcohol and cirrhosis: dose–response or threshold effect?

Kamper-Jørgensen

Grønbæk

Tolstrup

et al. 2004

Journal of Hepatology

137

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“…Although ethanol is a potential carcinogenic promoter [13], the incidence of HCC in which heavy habitual consumption of alcohol alone may have caused the liver disease is low in Japanese [14]. However, it should be emphasized that habitual consumption of alcohol is a well known risk factor for liver cirrhosis [15,16], and HCC often develops in patients with liver cirrhosis. Therefore, alcoholic liver disease by itself could be a carcinogenic condition promoting HCC.…”

Section: Discussionmentioning

confidence: 99%