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酒精摄入对肝脂肪变性进展的协同和有害影响。

Synergistic and Detrimental Effects of Alcohol Intake on Progression of Liver Steatosis.

机构信息

Clinica Medica "Augusto Murri", Department of Biomedical Sciences and Human Oncology, University of Bari Medical School-Piazza Giulio Cesare 11, 70124 Bari, Italy.

Department of Medicine II Saarland University Medical Center, Saarland University, 66424 Homburg, Germany.

出版信息

Int J Mol Sci. 2022 Feb 27;23(5):2636. doi: 10.3390/ijms23052636.

DOI:10.3390/ijms23052636
PMID:35269779
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8910376/
Abstract

Nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are the most common liver disorders worldwide and the major causes of non-viral liver cirrhosis in the general population. In NAFLD, metabolic abnormalities, obesity, and metabolic syndrome are the driving factors for liver damage with no or minimal alcohol consumption. ALD refers to liver damage caused by excess alcohol intake in individuals drinking more than 5 to 10 daily units for years. Although NAFLD and ALD are nosologically considered two distinct entities, they show a continuum and exert synergistic effects on the progression toward liver cirrhosis. The current view is that low alcohol use might also increase the risk of advanced clinical liver disease in NAFLD, whereas metabolic factors increase the risk of cirrhosis among alcohol risk drinkers. Therefore, special interest is now addressed to individuals with metabolic abnormalities who consume small amounts of alcohol or who binge drink, for the role of light-to-moderate alcohol use in fibrosis progression and clinical severity of the liver disease. Evidence shows that in the presence of NAFLD, there is no liver-safe limit of alcohol intake. We discuss the epidemiological and clinical features of NAFLD/ALD, aspects of alcohol metabolism, and mechanisms of damage concerning steatosis, fibrosis, cumulative effects, and deleterious consequences which include hepatocellular carcinoma.

摘要

非酒精性脂肪性肝病(NAFLD)和酒精性肝病(ALD)是全球最常见的肝脏疾病,也是普通人群中非病毒性肝硬化的主要原因。在 NAFLD 中,代谢异常、肥胖和代谢综合征是导致肝脏损伤的驱动因素,这些因素与酒精摄入无关或摄入极少。ALD 是指个体饮酒过量(每年超过 5 至 10 个日常单位)导致的肝脏损伤。尽管 NAFLD 和 ALD 在病学上被认为是两个不同的实体,但它们在向肝硬化进展方面表现出连续性,并具有协同作用。目前的观点是,低水平的酒精摄入也可能增加 NAFLD 患者发生晚期临床肝病的风险,而代谢因素则会增加酒精高危饮酒者发生肝硬化的风险。因此,现在特别关注代谢异常的个体,这些个体即使少量饮酒或 binge drink,也会导致肝纤维化进展和肝脏疾病临床严重程度的风险增加。有证据表明,在存在 NAFLD 的情况下,酒精摄入没有安全限量。我们讨论了 NAFLD/ALD 的流行病学和临床特征、酒精代谢的各个方面,以及脂肪变性、纤维化、累积效应和有害后果(包括肝细胞癌)的损伤机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/434c/8910376/6d491d07cc2f/ijms-23-02636-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/434c/8910376/5bb6a7c6e49d/ijms-23-02636-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/434c/8910376/6d491d07cc2f/ijms-23-02636-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/434c/8910376/5bb6a7c6e49d/ijms-23-02636-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/434c/8910376/6d491d07cc2f/ijms-23-02636-g002.jpg

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