Nonalcoholic fatty liver disease (NAFLD) is characterized by fatty infiltration of hepatocytes (hepatic steatosis) in a person who habitually consumes less than 20 g of ethanol per day for females and less than 30 g per day for males. NAFLD is distinguished from alcoholic liver disease, which can have a similar histological presentation. In some people with NAFLD, hepatic steatosis is accompanied by hepatic inflammation, in which case the condition is called nonalcoholic steatohepatitis (NASH). Risk factors for NAFLD include obesity, type 2 diabetes, and hypertriglyceridemia. Insulin resistance, mitochondrial dysfunction, and oxidative stress appear to be involved in the pathogenesis of the condition.1 Some investigators have suggested that NAFLD is a feature of the metabolic syndrome.
NASH may progress to hepatic fibrosis, cirrhosis, or hepatocellular carcinoma. In contrast, hepatic steatosis without an inflammatory component does not typically progress to more severe liver disease. However, hepatic steatosis appears to be an independent risk factor for cardiovascular disease and is associated with increased all-cause mortality. In addition, the presence of hepatic steatosis may increase the progression rate of other liver diseases, such as hepatitis C.
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