Nonalcoholic fatty liver disease: pathogenesis and histological findings, with emphasis on mitochondrial alterations.

Hepatic steatosis unrelated to alcoholism may occur either by itself or as part of nonalcoholic fatty liver disease. This disease encompasses a wide spectrum of morphologic alterations, ranging from steatosis to a more severe stage, accompanied by fibrosis, which may lead to cirrhosis. Nonalcoholic fatty liver disease is very important in current clinical practice. First, it has a high prevalence rate, affecting from 15% to 25% of the general population and more than 80% of obese and diabetic patients. Second, there is a diversity of related conditions, such as nutritional factors (malnutrition, total parenteral nutrition), hepatitis C, metabolic disease (Wilson’s disease, glycogenosis, lipodystrophy and others) and drug toxicity (valproate, amiodarone, etc.). Histological changes and the natural history of nonalcoholic fatty liver disease probably reflect a complex multifactorial process in which the genetic environment has considerable importance, since it is still unknown why some patients have only steatosis while others develop steatohepatitis, cirrhosis or hepatocellular carcinoma. In order to better understand the pathogenesis of nonalcoholic fatty liver disease, there are several articles correlating fatty liver to mitochondrial changes (increase in mitochondrial size and density, changes in the mitochondrial matrix and cristae as well as the presence of megamitochondria with crystalline inclusions). Early identification of the various forms of steatosis with concomitant mitochondrial changes may have a fundamental importance in the prognosis of the disease. Additionally, microvesicular steatosis, as it relates to these changes, may correspond to early histological damage in NAFLD, with a worse clinical progression of the disease. Indexing terms: Nonalcoholic fatty liver disease. Fatty liver. Mitochondria, liver. Hepatic disease.