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Teschke. Hepatoma Res 2019;5:40 Hepatoma Research
DOI: 10.20517/2394-5079.2019.0017

Review Open Access

Hepatocellular carcinoma in alcoholic liver disease:
mechanistic considerations and clinical facts

Rolf Teschke

Department of Internal Medicine II, Division of Gastroenterology and Hepatology, Klinikum Hanau, Hanau, Academic Teaching
Hospital of the Medical Faculty, Goethe University Frankfurt/Main, Frankfurt/Main, Germany.
Correspondence to: Prof. Rolf Teschke, Department of Internal Medicine II, Klinikum Hanau, Teaching Hospital of the Goethe
University of Frankfurt/Main, Leimenstrasse 20, D-63450 Hanau, Germany. E-mail: rolf.teschke@gmx.de

How to cite this article: Teschke R. Hepatocellular carcinoma in alcoholic liver disease: mechanistic considerations and clinical
facts. Hepatoma Res 2019;5:40. http://dx.doi.org/10.20517/2394-5079.2019.0017

Received: 12 Oct 2019 First Decision: 30 Oct 2019 Revised: 6 Nov 2019 Accepted: 6 Nov 2019 Published: 15 Nov 2019

Science Editor: Darrell Crawford Copy Editor: Jing-Wen Zhang Production Editor: Jing Yu

Abstract

Received: First Decision: Revised: Accepted: Published: Alcoholic hepatocellular carcinoma (AHCC) represents a lethal stage, emerging in the course of severe injurious
stages of alcoholic liver disease including cirrhosis. AHCC only affects a few alcohol consumers, certainly not all
Science Editor: Copy Editor: Production Editor: Jing Yu individuals who consume large amounts of alcohol over a long period of time, suggesting a role of yet unknown
genetic risk or protection factors. Most likely, hepatic DNA is ultimately involved, attacked by intermediate products
derived from reactive oxygen species (ROS) generated from cytochrome P450 2E1 of the NADPH and oxygen
dependent microsomal ethanol-oxidizing system whereby ethanol is metabolized. Ethanol and acetaldehyde are
activated to procarcinogens, to be promoted to ultimate carcinogens by ROS and causatives for AHCC instead
of any other putative chemical contained in alcoholic beverages. Prevention of HCC associated with cirrhosis is
best accomplished by early recognition of alcohol abuse at the stage of alcoholic fatty liver rather than alcoholic
hepatitis (AH) or alcoholic steatohepatitis (ASH), leading to the advice of consequent abstinence from alcohol.
Abstinence early started effectively prevents AHCC development, as opposed to late begin of abstinence that lacks
risk reduction. Although drug therapy may partially be effective in AH or ASH, no established drug options are
available for a realistic therapy of AHCC. Liver transplantation is controversially discussed and can be considered,
but may be an option for only a few patients on a case by case base. In conclusion, AHCC results from a ROS
dependent conversion of ethanol and acetaldehyde to procarcinogens as promoters of AHCC.

Keywords: Alcohol, alcoholic liver disease, alcoholic cirrhosis, alcoholic hepatocellular carcinoma, microsomal
ethanol-oxidizing system, cytochrome P450 2E1, reactive oxygen species, carcinogens

© The Author(s) 2019. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
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