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Review
. 2014 Nov 21;20(43):15943-54.
doi: 10.3748/wjg.v20.i43.15943.

Alcohol and hepatocellular carcinoma: a review and a point of view

Affiliations
Review

Alcohol and hepatocellular carcinoma: a review and a point of view

Gianni Testino et al. World J Gastroenterol. .

Abstract

It is well recognized that one cause of chronic liver disease and hepatocellular carcinoma (HCC) is alcohol consumption. Research in Italy and the United States concludes that the most common cause of HCC (responsible for 32% to 45% of HCC) is alcohol. It has recently been shown that a significant relationship between alcohol intake, metabolic changes, and hepatitis virus infection does exist. Alcohol may be a factor in the development of HCC via direct (genotoxic) and indirect mechanisms (cirrhosis). There is only one way of diagnosing HCC, which is early identification through surveillance, when curative treatments become possible. After stopping alcohol intake the risk of liver cancer decreases by 6% to 7% a year, and an estimated time period of 23 years is also needed. Therefore, surveillance is also important in former drinkers and, in our opinion, independently from the presence of compensated cirrhosis. In cases of very early stage (VES) and early stage with portal hypertension, liver transplantation is the optimal option; and in cases of associated disease, percutaneous ethanol injections, radiofrequency and microwave ablation are the ideal treatments. Despite the possibility of detecting microvascular invasion with HR, several studies and some randomized controlled trials revealed that overall survival and DSF rates in patients with VES HCC are much the same after ablation and HR. Therefore, ablation can be regarded as a first-line choice for patients with VES HCC. It is important to emphasize that the choice of treatment should be weighed carefully in the context of a multidisciplinary cancer team.

Keywords: Alcohol; Alcoholic liver disease; Hepatocellular carcinoma; Percutaneous ablation.

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Figures

Figure 1
Figure 1
Alcohol ANS carcinogenesis. ADH: Alcohol dehydrogenase; CYP2E1: Cytochrome P4502E1; ALDH: Aldehyde dehydrogenase; ROS: Reactive oxygen species.

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