Coffee Reduces Risk for Hepatocellular Carcinoma: An Updated Meta-Analysis.

University of Milan, Milano, Lombardy, Italy
Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association (Impact Factor: 7.9). 05/2013; 11(11). DOI: 10.1016/j.cgh.2013.04.039
Source: PubMed


BACKGROUND: & Aims: Coffee consumption has been proposed to reduce risk for hepatocellular carcinoma (HCC). We performed a meta-analysis of articles published through 2012 to provide updated information on how coffee drinking affects risk for HCC. METHODS: We performed a PubMed/MEDLINE search of the papers published from 1966 through September 2012 for original articles, in English, on case-control or cohort studies that associated coffee consumption with liver cancer or HCC. We calculated the summary relative risk (RR) for any, low, and high consumption of coffee vs no consumption. The cut-off point for low vs high consumption was set to 3 cups per day in 9 studies and 1 cup per day in 5 studies. RESULTS: : The summary RR for any coffee consumption vs no consumption was 0.60 from 16 studies, comprising a total of 3153 HCC cases (95% confidence interval [CI], 0.50-0.71); the RRs were 0.56 from 8 case-control studies (95% CI, 0.42-0.75) and 0.64 from 8 cohort studies (95% CI, 0.52-0.78). Compared with no coffee consumption, the summary RR was 0.72 (95% CI, 0.61-0.84) for low consumption and 0.44 (95% CI, 0.39-0.50) for high consumption. The summary RR was 0.80 (95% CI, 0.77-0.84) for an increment of 1 cup of coffee per day. The inverse relationship between coffee and HCC risk was consistent regardless of subjects' sex, alcohol drinking, or history of hepatitis or liver disease. CONCLUSION: : Based on a meta-analysis of 16 studies, the RR for any coffee consumption vs no consumption is 0.60. The association might partly or largely exist because patients with liver and digestive diseases reduce their coffee intake. However, coffee has been shown to affect liver enzymes and development of cirrhosis, and could therefore protect against liver carcinogenesis.

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    • "Risk factors for HCC include infection with hepatitis B (HBV) and hepatitis C viruses (HCV), history of diabetes mellitus, nonalcoholic fatty liver disease and cirrhosis, heavy alcohol consumption, and cigarette smoking [3] [4] [5]. Coffee consumption appears to have a favorable effect [6]. Further, genetic factors appear to modulate the individual susceptibility as the siblings of HCC "
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    ABSTRACT: Aim. The aim of our study was to assess whether selected single nucleotide polymorphisms of CYP1A1 and 2E1, GSTM1, GSTT1, and SULT1A1 influence susceptibility towards HCC, considering their interaction with cigarette smoking. Methods. We recruited HCC cases and controls among patients admitted to the hospital “Agostino Gemelli,” from January 2005 until July 2010. Odds ratios (OR) of HCC were derived from unconditional multiple logistic regression. Gene-gene and gene-smoking interaction were quantified by computing the attributable proportion (AP) due to biological interaction. Results. The presence of any CYP2E15B variant allele (OR: 0.23; 95% CI: 0.06-0.71) and CYP2E16 variant allele (OR: 0.08; 95% CI: 0.01–0.33) was inversely related to HCC. There was a borderline increased risk among carriers of combined CYP1A12A and SULT1A1 variant alleles (OR: 1.67; 95% CI: 0.97–3.24). A significant biological interaction was observed between GSTT1 and smoking (AP = 0.48; 95% CI: 0.001–0.815), with an OR of 3.13 (95% CI: 1.69–5.82), and borderline significant interaction was observed for SULT1A1 and smoking (AP = 0.36; 95% CI: −0.021–0.747), with an OR of 3.05 (95% CI: 1.73–5.40). Conclusion. CYP2E15B and CYP2E16 polymorphisms have a favourable effect on the development of HCC, while polymorphisms of GSTT1 and SULT1A1 might play role in increasing the susceptibility among smokers.
    BioMed Research International 06/2014; 2015. DOI:10.1155/2015/179867 · 2.71 Impact Factor
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    ABSTRACT: Description: The Centers for Disease Control and Prevention (CDC) and a group of governmental and private sector partners developed these evidence-based recommendations to increase the proportion of hepatitis C virus (HCV)-infected persons who know their status and are linked to appropriate care and treatment. The recommendations also address brief alcohol screening, as alcohol accelerates progression of liver disease among HCV-infected individuals. These recommendations augment CDC's 1998 and 1999 recommendations based on risk and medical indications and are not meant to replace those recommendations. Methods: These recommendations are based on systematic reviews of evidence published from 1995 through February 2012 in MEDLINE, EMBASE, CINAHL, the Cochrane Central Register of Controlled Trials, Sociological Abstracts, and Database of Abstracts of Reviews of Effects. Selected studies included cross-sectional and cohort studies that addressed either prevalence of hepatitis C in the United States or clinical outcomes (for example, hepatocellular carcinoma and serious adverse events) among treated patients and systematic reviews of trials that assessed effectiveness of brief screening interventions for alcohol consumption. The Grading of Recommendations Assessment, Development, and Evaluation framework was used to assess quality of the evidence. RECOMMENDATION 1: Adults born during 1945-1965 should receive 1-time testing for HCV without prior ascertainment of HCV risk. (Grade: strong recommendation; moderate-quality evidence). RECOMMENDATION 2: All persons with identified HCV infection should receive a brief alcohol screening and intervention as clinically indicated, followed by referral to appropriate care and treatment services for HCV infection and related conditions (Grade: strong recommendation; moderate-quality evidence).
    Annals of internal medicine 08/2012; 157(11). DOI:10.7326/0003-4819-157-9-201211060-00529 · 17.81 Impact Factor

  • Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 06/2013; 11(11). DOI:10.1016/j.cgh.2013.05.042 · 7.90 Impact Factor
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