Contents

Disclaimer

Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Show Summary Details
Page of

Alcoholic liver disease 

Alcoholic liver disease
Chapter:
Alcoholic liver disease
Author(s):

Ewan Forrest

DOI:
10.1093/med/9780198746690.003.0327
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2021. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 05 March 2021

The incidence of alcoholic liver disease (ALD) follows the trend of per capita alcohol consumption, with hepatic injury which extends from fatty liver to alcoholic hepatitis and cirrhosis. It is unclear how alcohol causes liver disease, but postulated mechanisms include (1) oxidative stress and acetaldehyde generated by the metabolism of ethanol, and (2) innate and adaptive immune responses. Factors determining the susceptibility to liver disease in heavy drinkers are believed to include a variety of host and environmental factors, with genetic factors increasingly recognized. Clinical manifestations are extremely variable, and some patients remain relatively well while others suffer the effects of severe hepatic failure. Although patients can come to light with a life-threatening complication, most often they develop symptoms which are not immediately related to the liver, such as nonspecific digestive symptoms or psychiatric complaints. The key to the early recognition of alcohol-related disease is having a high index of suspicion, with confirmation by (1) direct questioning for alcohol history and alcohol-related symptoms; (2) clinical examination for signs of chronic liver disease; (3) supportive investigations, including aspartate aminotransferase, which is less than 500 IU/litre and greater than the alanine aminotransferase level; and (4) liver biopsy, which may be required in some cases of diagnostic uncertainty and to confirm the stage of the disease, revealing alcoholic fatty liver, alcoholic hepatitis, or cirrhosis. Management is governed by the stage and severity of the liver disease, but always includes abstinence and adequate nutritional support. In selected patients with severe acute alcoholic hepatitis, corticosteroids can reduce short-term mortality. Transplantation remains the only effective treatment for advanced alcoholic cirrhosis, although this remains controversial, mainly because of concerns about post-transplant recidivism.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.