Article ID Journal Published Year Pages File Type
3808121 Medicine 2007 4 Pages PDF
Abstract

Alcoholic liver disease (ALD) is a significant burden on the healthcare systems in the developed world and deaths from ALD continue to rise in the UK. The first stage of ALD – fatty liver – is present in most heavy drinkers and is due to a combination of reduced fat oxidation and export from the liver and increased fatty acid synthesis. Alcoholic hepatitis, characterized by liver inflammation and cell death, is due to a combination of oxidative and endoplasmic reticulum-mediated cell stress and the intrahepatic release of pro-inflammatory cytokines as a result of portal endotoxaemia. Fibrosis and subsequent cirrhosis result from the expected healing response to liver injury, although a direct fibrogenic effect of acetaldehyde and oxidation products may also be important. The risk of developing advanced ALD is increased in proportion to cumulative alcohol dose, and in females and patients who are overweight or glucose intolerant. Presentation at all stages of ALD ranges from an incidental finding of abnormal liver function tests to acute liver failure and encephalopathy or decompensated cirrhosis with portal hypertension. Reduction in alcohol intake is the cornerstone of management. Patients with alcoholic hepatitis who are free of infection benefit from corticosteroids, and pentoxifylline may also be of benefit. There are no specific therapies for patients with cirrhosis. Liver transplantation should be considered for abstinent patients with evidence of decompensation or small hepatocellular carcinomas.

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