Non-alcoholic fatty liver disease, has recently become increasingly recognized and may progress to end-stage liver disease. It is histologically indistinguishable from the liver damage that is secondary to alcohol abuse, but occurs in people with no history of alcohol excess. Non-alcoholic fatty liver disease has a wide spectrum of liver damage ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. The combination of steatosis, infiltration by mononuclear or polymorphonuclear cells (or both), and hepatocyte ballooning and spotty necrosis is known as nonalcoholic steatohepatitis (NASH). Non-alcoholic fatty liver disease is the most common cause of abnormal liver blood results among adults in the USA. It is particularly common in those with combined diabetes and obesity: in a group of severely obese patients with diabetes, 100% were found to have mild steatosis, 50% had NASH and 19% had cirrhosis. Insulin resistance seems to be the most reproducible causative factor in the development of non-alcoholic fatty liver disease and NASH, and this condition is increasingly viewed as part of the spectrum of the metabolic syndrome.
Malaise and a sensation of fullness or discomfort in the right hypochondrium are recognized symptoms when symptoms exist and hepatomegaly is the only consistent physical sign. Mild to moderate elevation of liver enzymes is often the only laboratory abnormality and fatty infiltration of the liver produces a diffuse increase in echogenicity on ultrasonography as compared with the kidneys. Liver biopsy provides an ultimate diagnosis. No satisfactory drug therapy is available for this condition, but encouraging results have been obtained with gemfibrozil, metformin, ursodeoxycholic acid and glitazones.
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