© 2005 by the American Diabetes Association, Inc.
Associations Between Liver Histology and Severity of the Metabolic Syndrome in Subjects With Nonalcoholic Fatty Liver Disease
1 Department of Gastroenterology, St. Vincents Hospital, Fitzroy, Australia Address correspondence and reprint requests to Dr. Marno C. Ryan, Department of Medicine, 4th Floor Clinical Sciences Building, St. Vincents Hospital, 41 Victoria Parade, Fitzroy 3065 Victoria, Australia. E-mail: marno.ryan@svhm.org.au
Abbreviations: ATP, Adult Treatment Panel DEXA, dual-energy X-ray absorptiometry HOMA, homeostasis model assessment NAFLD, nonalcoholic fatty liver disease NASH, nonalcoholic steatohepatitis
Nonalcoholic fatty liver disease (NAFLD) is associated with a histopathological picture resembling alcohol-induced liver injury occurring in subjects who consume insignificant amounts of alcohol. In NAFLD, steatosis alone is associated with good prognosis, whereas nonalcoholic steatohepatitis (NASH) can progress to fibrosis and cirrhosis in up to 30% of cases, potentially leading to liver failure and hepatocellular carcinoma. The prevalence of NAFLD and NASH in the U.S. is estimated at 1020 and 23%, respectively (1,2,3). The metabolic syndrome, as defined by Adult Treatment Panel (ATP) III criteria, incorporates features known to predict cardiovascular disease and type 2 diabetes (4). NAFLD has been demonstrated to be associated with features of the metabolic syndrome, including hyperglycemia (5,6), dyslipidemia (5,6), hypertension (7), and central obesity (7,8). In addition, insulin resistance, even without these other features, is almost universal in subjects with NAFLD (6). However, the factors specifically associated with hepatic inflammation, fibrosis, and thus liver disease progression are still being elucidated. In this study of human subjects with NAFLD, we explored specific relationships between hepatic histology and markers of the metabolic syndrome.
Forty-six subjects with NAFLD were recruited from clinics. The diagnosis was based on the histological presence of macrovesicular steatosis, with or without lobular inflammation, hepatocellular degeneration, or
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