Alcoholic liver disease

Abstract 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.