Non-alcoholic fatty liver disease (NAFLD) is increasingly diagnosed worldwide and considered to be the commonest liver disorder in Western countries. It comprises a disease spectrum which includes variable degrees of simple steatosis (fatty liver), non-alcoholic steatohepatitis (NASH) and cirrhosis. Simple steatosis is benign, whereas steatohepatitis (NASH) is characterized by hepatocyte injury, inflammation and fibrosis which can lead to cirrhosis, liver failure and hepatocellular carcinoma (HCC).
NAFLD is strongly associated with obesity, insulin resistance, hypertension and dyslipidemia and is now regarded as the liver manifestation of the metabolic syndrome. Rapid spread of the obesity �pandemic� in adults and children, coupled with the realization that the outcomes of obesity-related liver disease are not entirely benign, has led to rapid growth in clinical and basic studies in NAFLD.
NAFLD affects up to a third of individuals in the developed world and is an increasing indication for transplantation. Dietary and genetic factors determine susceptibility to NAFLD and its progression. NAFLD may also be involved in the pathogenesis of cardiovascular disease. Most patients present with incidentally found abnormal liver blood tests. Diagnosis is usually one of exclusion. Liver biopsy is required for disease staging, but new imaging modalities and biomarkers are emerging which may eventually fulfill this role. There is, as yet, no firm evidence-based treatment for NAFLD. Therapy is currently directed at treating components of the metabolic syndrome which may also be beneficial for the liver. The recent elucidation of the mechanisms leading to progressive disease suggest a variety of novel targets worthy of testing in animal models of NAFLD and subsequently in pilot studies in humans.
This review will concentrate on an update of clinical aspects of this increasingly important disease.