Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Oct 28;20(40):14652-9.
doi: 10.3748/wjg.v20.i40.14652.

Alcoholic disease: liver and beyond

Alba Rocco  1 , Debora Compare  1 , Debora Angrisani  1 , Marco Sanduzzi Zamparelli  1 , Gerardo Nardone  1
Affiliations
Review

Alcoholic disease: liver and beyond

Alba Rocco et al. World J Gastroenterol. .

Abstract

The harmful use of alcohol is a worldwide problem. It has been estimated that alcohol abuse represents the world's third largest risk factor for disease and disability; it is a causal factor of 60 types of diseases and injuries and a concurrent cause of at least 200 others. Liver is the main organ responsible for metabolizing ethanol, thus it has been considered for long time the major victim of the harmful use of alcohol. Ethanol and its bioactive products, acetaldehyde-acetate, fatty acid ethanol esters, ethanol-protein adducts, have been regarded as hepatotoxins that directly and indirectly exert their toxic effect on the liver. A similar mechanism has been postulated for the alcohol-related pancreatic damage. Alcohol and its metabolites directly injure acinar cells and elicit stellate cells to produce and deposit extracellular matrix thus triggering the "necrosis-fibrosis" sequence that finally leads to atrophy and fibrosis, morphological hallmarks of alcoholic chronic pancreatitis. Even if less attention has been paid to the upper and lower gastrointestinal tract, ethanol produces harmful effects by inducing: (1) direct damaging of the mucosa of the esophagus and stomach; (2) modification of the sphincterial pressure and impairment of motility; and (3) alteration of gastric acid output. In the intestine, ethanol can damage the intestinal mucosa directly or indirectly by altering the resident microflora and impairing the mucosal immune system. Notably, disruption of the intestinal mucosal barrier of the small and large intestine contribute to liver damage. This review summarizes the most clinically relevant alcohol-related diseases of the digestive tract focusing on the pathogenic mechanisms by which ethanol damages liver, pancreas and gastrointestinal tract.

Keywords: Alcohol and gastrointestinal tract; Alcoholic liver disease; Alcoholic pancreatitis.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Main steps of alcohol metabolism in the liver. ADH: Alcohol dehydrogenase; ALDH: Acetaldehyde dehydrogenase.
See this image and copyright information in PMC

References

    1. World Health Organization. Global Status Report on Alcohol and Health 2011. Available from: http://www.who.int/substance_abuse/publications/global_alcohol_report/ms....
    1. Singal AK, Anand BS. Recent trends in the epidemiology of alcoholic liver disease. Clin Liv Dis. 2013;2:53–56. - PMC - PubMed
    1. Mann RE, Smart RG, Govoni R. The epidemiology of alcoholic liver disease. Alcohol Res Health. 2003;27:209–219. - PMC - PubMed
    1. Mendenhall CL. Anabolic steroid therapy as an adjunct to diet in alcoholic hepatic steatosis. Am J Dig Dis. 1968;13:783–791. - PubMed
    1. Mandayam S, Jamal MM, Morgan TR. Epidemiology of alcoholic liver disease. Semin Liver Dis. 2004;24:217–232. - PubMed

MeSH terms