THE NATURAL-HISTORY OF NONALCOHOLIC STEATOHEPATITIS - A FOLLOW-UP-STUDY OF 42 PATIENTS FOR UP TO 21 YEARS
THE NATURAL-HISTORY OF NONALCOHOLIC STEATOHEPATITIS - A FOLLOW-UP-STUDY OF 42 PATIENTS FOR UP TO 21 YEARS
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DOI：
10.1002/hep.1840110114
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发表时间：
1990-01-01
期刊：
影响因子：
13.5
通讯作者：
POWELL, LW
中科院分区：
文献类型：
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作者：
POWELL, EE;COOKSLEY, WGE;POWELL, LW
42例非酒精性脂肪性肝炎患者随访时间中位数为4.5年（范围为1.5至21.5年）。除2例脂肪营养不良外，其余均为肥胖；42名患者中有35名是女性，其中26名是高脂血症患者，15名是高血糖症患者。上腹部疼痛是最常见的原因。初步肝活检标本显示存在大泡性脂肪浸润、小叶（腺泡）炎症、细胞凋亡、Mallory小体（4例）和纤维化（18例）。一名受试者的初始诊断为肝硬化，另外两名受试者的肝活检显示明显的纤维化，结构紊乱。连续肝活检标本显示，大多数患者的疾病进展很小或没有明显进展，符合其良性临床病程。然而，在5年的观察期间，有1例患者表现出从纤维化到肝硬化的进展，在广泛纤维化的患者中，肝脏疾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、高脂血症或高血糖的程度无关。然而，个别患者，糖尿病控制不佳和体重迅速减轻先于脂肪性肝炎发病。我们得出结论，非酒精性脂肪性肝炎是肝脏炎症的原因，组织学上类似于酒精性肝病，但通常进展缓慢，严重程度较低。然而，这种紊乱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区分开来，并被认为是“隐源性肝硬化”的进一步病因。
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, 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.".