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In their review article last year, Wilkin and Voss1 made no reference to the potential impact of the metabolic syndrome upon the liver. Non-alcoholic fatty liver disease (NAFLD) should be numbered among the consequences of insulin resistance, hyperinsulinaemia and continued weight gain.2 It encompasses a spectrum of liver injury ranging from uncomplicated macrovesicular steatosis on the one hand, through non-alcoholic steatohepatitis (NASH, i.e. steatosis, ballooning degeneration of hepatocytes, neutrophil infiltration and pericentral pericellular fibrosis) to cirrhosis and liver failure at the opposite extreme. NAFLD is now judged the most likely explanation for non-specific liver test abnormalities among patients referred for evaluation thereof.3 Furthermore, NASH may have been responsible for a substantial proportion of cases of cryptogenic cirrhosis referred for and undergoing orthotopic liver transplantation.4
The diagnosis of NAFLD should be considered in any patient who exhibits one or more components of the metabolic syndrome5 and has abnormal liver tests, demonstrates clinical features of chronic liver disease, or both. As with other complications of the metabolic syndrome the more components that are present, the greater the likelihood that the patient has NAFLD. However, risk factors in and of themselves are not yet reliable predictors of the degree of fibrosis that may be present, and thus the extent of liver dysfunction and/or portal hypertension.2 Therefore, liver biopsy remains an important diagnostic tool among such patients.
In addition to increasing our understanding of the pathophysiology of NAFLD—e.g. which patients with uncomplicated steatosis may develop inflammation and fibrosis—it is vital that the potential impact of NASH and subsequent end-stage liver disease be appreciated and accepted by non-liver physicians. Otherwise, it may yet be the case that the burden of NASH upon liver transplant services will exceed that of chronic hepatitis C virus liver disease.