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非酒精性脂肪性肝病:诊断、发病机制及管理

Nonalcoholic fatty liver disease: diagnosis, pathogenesis, and management.

作者信息

Başaranoğlu Metin, Örmeci Necati

机构信息

Department of Gastroenterology, Türkiye Yüksek İhtisas Hospital, Ankara, Turkey.

出版信息

Turk J Gastroenterol. 2014 Apr;25(2):127-32. doi: 10.5152/tjg.2014.7675.

DOI:10.5152/tjg.2014.7675
PMID:25003670
Abstract

Nonalcoholic fatty liver disease (NAFLD) is an umbrella term that covers both a relatively benign condition, which is simple steatosis, and nonalcoholic steatohepatitis (NASH). NASH is characterized by a chronic and progressive liver pathology that may progress to cirrhosis, end-stage liver disease, hepatocellular carcinoma, and liver transplantation. Despite the growing body of evidence, one of the important and unresolved problems is the pathogenesis of NASH. It might be a metabolic disturbance as a primary abnormality in NAFLD. Insulin resistance is at the center of these metabolic abnormalities. Then, hepatocyte injury might be induced by oxidative stress. This ongoing process progresses to NASH, even to cirrhosis in some patients. In addition to oxidative stress, possibilities for the next hit are lipid peroxidation, reactive metabolites, adipose tissue products, transforming growth factor-β₁, Fas ligand, mitochondrial dysfunction, respiratory chain deficiency, and intestinal microbiota. Currently, there is no well-established and approved therapy. Recommendations are to improve existing co-morbidities, such as obesity, hyperlipidemia, or type 2 diabetes, and lifestyle modification with weight loss and exercise.

摘要

非酒精性脂肪性肝病(NAFLD)是一个统称,涵盖了一种相对良性的状况,即单纯性脂肪变性,以及非酒精性脂肪性肝炎(NASH)。NASH的特征是一种慢性进行性肝脏病变,可能进展为肝硬化、终末期肝病、肝细胞癌以及肝移植。尽管证据越来越多,但一个重要且未解决的问题是NASH的发病机制。它可能是一种代谢紊乱,作为NAFLD的主要异常情况。胰岛素抵抗是这些代谢异常的核心。然后,氧化应激可能会诱导肝细胞损伤。这个持续的过程会进展为NASH,甚至在一些患者中进展为肝硬化。除了氧化应激外,下一个打击因素还可能是脂质过氧化、反应性代谢产物、脂肪组织产物、转化生长因子-β₁、Fas配体、线粒体功能障碍、呼吸链缺陷以及肠道微生物群。目前,尚无成熟且获批的治疗方法。建议改善现有的合并症,如肥胖、高脂血症或2型糖尿病,并通过减肥和运动来改变生活方式。

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