Forty‐two patients with nonalcoholic steatohepatitis were followed for a median of 4.5 yr (range = 1.5 to 21.5 yr). Except for two patients with lipodystrophy, all were obeser; 35 o f42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Inital liver biopsy specimens showed the presence of macrovesicular fatty infiltration, lobular (acinar) inflammation, apoptosis, Mallory bodies (in four cases) and fibrosis (in 18 cases). Cirrhosis was present at initial diagnosis in one subject and in another two subjects liver biopsy showed marked and in another two subjects liver biopsy showed marked fibrosis with distured architecture. Serial liver biopsy specimens revealed minimal or no apparent progression of the disorder in most of the patients, in keeping with their benign clinical course. However, one patient showed progression from fibrosis to cirrhosis during the 5‐yr observation period, and in the patients with extensive fibrosis the the liver disease evolved from one of active inflammation to one of inactive cirrhosis without fat or inflammation. The patient with cirrhosis later died of hepatocellular carcinoma. The severity or type of hepatic change did not correlate with the degree of obesity, hyperlipidemia or hyperglycemia. However, in individual patients, poorly controlled diabetes and rapid weight loss preceded the onset of steatohepatitis.

We conclude that nonalcoholic steatohepatitis is a cause of hepatic inflammation histologically resembling that of alcohol‐induced liver disease but usually slowly progressive and of low‐grade severity. However, the disorder may ultimatley result in cirrhosis, Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of “cryptogenic cirrhosis.” (HEPATOLOGY 1990; 11: 74–80.)