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The necessity of the liver being the organ responsible for metabolism of alcohol exposes it to many untoward toxic side effects. In the first instance of hepatic steatosis, fibrosis may occur indolently over years, slowly converting a greasy, steatotic liver into a cirrhotic liver. In the case of alcoholic hepatitis, brisk sinusoidal fibrosis may lead to more rapid development of cirrhosis, with the liver extensively subdivided by sublobular fibrous septa developing in the midst of extensive ongoing inflammation and hepatocellular destruction. Continued destruction of the parenchyma after cirrhosis has developed may produce a densely fibrotic organ with little remaining parenchyma., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most prevalent chronic liver disease. Nonalcoholic steatohepatitis (NASH), the more severe form of NAFLD, has an increased risk for progression to cirrhosis. The available data suggest increased morbidity and mortality among those patients with advanced histologic severity such as NASH and fibrosis. Despite the lack of a universally accepted histologic definition of NAFLD and inconsistency among pathologists regarding histologic findings essential to the diagnosis of NASH, a few studies have identified specific histologic findings (particularly fibrosis regardless of stage) that are able to predict NAFLD-related mortality as being most important., (Copyright © 2012 Elsevier Inc. All rights reserved.)