Nonalcoholic steatohepatitis may cause severe fibrosis, cirrhosis, and hepatocellular carcinoma, but supporting evidence is based on indirect data. Few publications have examined the results of repeat liver biopsies to evaluate progression of fibrosis. The aims of this study were to assess rate of fibrosis progression in untreated patients with nonalcoholic steatohepatitis and to identify associated variables. Among 106 patients, a second liver biopsy was proposed to those who had undergone their first liver biopsy at least 3 years before. None of them had been given pharmacological therapy. Liver biopsy samples were evaluated blindly. Variables were compared between patients with (group I?) and without (group NP) fibrosis progression, using a Wdcoxon rank-sum test for numerical variables and a difference of two binomial proportions for categorical ones. Twenty-two patients (median age, 45 years; age range, 20-69 years; 13 women; diabetes in 8 patients, obesity in 10 patients) underwent a second liver biopsy 4.3 years (range, 3.0-14.3 years) after the first. Fibrosis progression was found in 7 patients in group P (31.8%), no progression was found in 15 patients in group NP. There were no differences between both groups regarding age, gender, diabetes, hyperlipidemia, ALT levels, AST-to-ALT ratio levels, albumin levels, prothrombin activity, steatosis, or inflammation. Obesity was significantly more prevalent in group P (86%) than in group NP (27%; P = .01). Basal body mass index was higher in group P (median, 33.2; range, 29.1-38.2) than in group NP (median, 29.0; range, 24.0-38.1; P = .024). Time between biopsies w a s not different between groups. In conclusion, progression of liver fibrosis was found in a third of nonalcoholic steatohepatitis patients 4.3 years after the first liver biopsy, and obesity and body mass index were the only associated factors with such progression. (HEPATOLOGY 2004;40: 820 -826.) N onalcoholic fatty liver disease is probably the main cause of chronic liver disease in the West.' The histological spectrum of nonalcoholic fatty liver disease includes simple steatosis (type I), steatosis plus lobular inflammation (type 2), steatosis plus ballooning degeneration (type 3), and steatosis plus ballooning degeneration plus Mallory bodies or fibrosis (type 4).2
This classification is clinically important. Whereas simple steatosis seems to be a benign and nonprogressive condition,3,* nonalcoholic steatohepatitis (NASH) that includes the types 3 and 4 of nonalcoholic fatty liver disease