Three histological distinct lesions occur in the evaluation of alcohol-induced liver disease. The most common, occurring in 90% of heavy drinkers, is fatty liver (hepatic steatosis); 10-35% of heavy drinkers acquire alcoholic hepatitis, and 10-20% acquire alcohol cirrhosis (fibrosis, nodules, loss of normal structure).

Alcohol leads to liver damage by several mechanisms: the production of acetaldehyde, free radicals, and cytokines as alcohol is metabolized; the passage of bacterial endotoxins through the intestinal wall is enhanced by the presence of alcohol; and alcohol-induced cell death and inflammation, which lead to scarring (Lieber, 1998).

Hepatic steatosis is a common, reversible condition that may progress to cirrhosis in about 7% of cases (Gish, 1996). Signs and symptoms of alcoholic steatosis include nausea, vomiting, hepatomegaly, right-upper-quadrant pain, and tenderness. Ascites and jaundice are uncommon. Laboratory data may reveal mild elevation of transaminases, alkaline phosphatase, or bilirubin. Clinically, fatty liver may mimic or coexist with alcoholic hepatitis. Symptoms of alcoholic fatty liver, as well as alcoholic hepatitis, should resolve with abstinence.

Alcoholic hepatitis frequently coexists with fatty liver and cirrhosis. Symptoms include anorexia, nausea, vomiting, fever, chills, and abdominal pain. Hepatomegaly and right-upper-quadrant tenderness are common.

Transaminase levels rarely exceed 500 international units (IU), with a typical ratio of aspartate aminotransferase to alanine aminotransferase of 2:1 to 5:1. Liver biopsy can be helpful in distinguishing fatty liver from hepatitis and from cirrhosis. Ascites, encephalopathy, high bilirubin levels, and prolongation of the prothrombin time are poor prognostic indicators that portend an increased mortality. Treatment consists of abstinence and nutritional support. Treatment with steroids, propylthiouracil, and colchicines has yielded mixed results. There is a relative-risk increase of 14-20 for individuals who drink more than five drinks per day, although wine drinkers are at a lower risk than beer or liquor drinkers (Becker, Gronbaek, Johansen, & Sorensen, 2002). Women have a higher incidence of alcoholic hepatitis and cirrhosis than men, although the mechanisms underlying these gender differences is not known. Alcoholic cirrhosis develops as a result of prolonged hepatocyte damage, leading to centrilobular inflammation and fibrosis. The latter pathology causes portal hypertension and the development of varices. Esophageal varices may bleed spontaneously, or bleeding may be precipitated by respiratory tract infections, nonsteroidal anti-inflammatory drugs, and alcohol. Cirrhosis also leads to ascites, clotting deficiencies, secondary malnutrition, and hepatic encephalopa-thy (Sutton & Shields, 1995).

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