Powell E E, Cooksley W G, Hanson R, Searle J, Halliday J W, Powell L W
Department of Medicine, University of Queensland, Australia.
Hepatology. 1990 Jan;11(1):74-80. doi: 10.1002/hep.1840110114.
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 obese; 35 of 42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Initial 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 fibrosis with disturbed 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 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 ultimately result in cirrhosis. Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of "cryptogenic cirrhosis."
42例非酒精性脂肪性肝炎患者接受了中位时间为4.5年（范围为1.5至21.5年）的随访。除2例脂肪代谢障碍患者外，其余均为肥胖者；42例中有35例为女性，32例中有26例血脂异常，15例血糖升高。上腹部疼痛是最常见的就诊原因。初始肝活检标本显示存在大泡性脂肪浸润、小叶（腺泡）炎症、凋亡、马洛里小体（4例）和纤维化（18例）。1例患者在初始诊断时即有肝硬化，另外2例患者肝活检显示有明显纤维化且结构紊乱。系列肝活检标本显示，大多数患者病情进展极小或无明显进展，与其良性临床病程相符。然而，1例患者在5年观察期内从纤维化进展为肝硬化，在广泛纤维化患者中，肝病从活动性炎症演变为无脂肪或炎症的非活动性肝硬化。肝硬化患者后来死于肝细胞癌。肝脏改变的严重程度或类型与肥胖、高脂血症或高血糖程度无关。然而，在个别患者中，糖尿病控制不佳和体重快速下降先于脂肪性肝炎发作。我们得出结论，非酒精性脂肪性肝炎是一种肝脏炎症的病因，其组织学表现类似于酒精性肝病，但通常进展缓慢且严重程度较低。然而，该疾病最终可能导致肝硬化。非酒精性脂肪性肝炎应与酒精性脂肪性肝炎相鉴别，并被视为“隐源性肝硬化”的另一个病因。
