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肝性脑病的发病机制。

Pathogenesis of hepatic encephalopathy.

机构信息

Department of Gastroenterology, Hepatology and Infectious Diseases, Jagiellonian University Medical College, Sniadeckich Street 5, 31-531 Krakow, Poland.

出版信息

Gastroenterol Res Pract. 2012;2012:642108. doi: 10.1155/2012/642108. Epub 2012 Dec 17.

DOI:10.1155/2012/642108
PMID:23316223
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3534214/
Abstract

Hepatic encephalopathy can be a serious complication of acute liver failure and chronic liver diseases, predominantly liver cirrhosis. Hyperammonemia plays the most important role in the pathogenesis of hepatic encephalopathy. The brain-blood barrier disturbances, changes in neurotransmission, neuroinflammation, oxidative stress, GABA-ergic or benzodiazepine pathway abnormalities, manganese neurotoxicity, brain energetic disturbances, and brain blood flow abnormalities are considered to be involved in the development of hepatic encephalopathy. The influence of small intestine bacterial overgrowth (SIBO) on the induction of minimal hepatic encephalopathy is recently emphasized. The aim of this paper is to present the current views on the pathogenesis of hepatic encephalopathy.

摘要

肝性脑病是急性肝衰竭和慢性肝病(主要是肝硬化)的严重并发症。血氨升高在肝性脑病的发病机制中起着最重要的作用。血脑屏障障碍、神经递质传递变化、神经炎症、氧化应激、GABA 能或苯二氮䓬途径异常、锰神经毒性、脑能量代谢紊乱和脑血流异常被认为与肝性脑病的发展有关。最近强调了小肠细菌过度生长(SIBO)对轻微肝性脑病的诱导作用。本文旨在介绍肝性脑病发病机制的最新观点。

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本文引用的文献

1
Persistent hyperammonemia is associated with complications and poor outcomes in patients with acute liver failure.持续性高血氨与急性肝衰竭患者的并发症和不良预后有关。
Clin Gastroenterol Hepatol. 2012 Aug;10(8):925-31. doi: 10.1016/j.cgh.2012.04.011. Epub 2012 Apr 17.
2
Reduced brain levels of DHEAS in hepatic coma patients: significance for increased GABAergic tone in hepatic encephalopathy.肝昏迷患者大脑中 DHEAS 水平降低:肝性脑病中 GABA 能紧张度增加的意义。
Neurochem Int. 2012 Jul;61(1):48-53. doi: 10.1016/j.neuint.2012.03.020. Epub 2012 Apr 3.
3
Pathogenesis of hepatic encephalopathy and brain edema in acute liver failure: role of glutamine redefined.急性肝衰竭肝性脑病和脑水肿的发病机制:谷氨酰胺作用的重新定义。
Neurochem Int. 2012 Jun;60(7):690-6. doi: 10.1016/j.neuint.2012.02.001. Epub 2012 Feb 21.
4
Contribution of hyperammonemia and inflammatory factors to cognitive impairment in minimal hepatic encephalopathy.高血氨和炎症因子对轻微型肝性脑病认知障碍的影响。
Metab Brain Dis. 2012 Mar;27(1):51-8. doi: 10.1007/s11011-011-9269-3. Epub 2011 Nov 10.
5
Dynamic susceptibility contrast-enhanced first-pass perfusion MR imaging in patients with subclinical hepatic encephalopathy.无症状性肝性脑病患者的动态磁敏感对比增强首过灌注磁共振成像。
J Neuroradiol. 2012 Dec;39(5):290-4. doi: 10.1016/j.neurad.2011.09.002. Epub 2011 Nov 1.
6
Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy.急性和慢性肝性脑病中的脑能量代谢和线粒体功能障碍。
Neurochem Int. 2012 Jun;60(7):697-706. doi: 10.1016/j.neuint.2011.09.007. Epub 2011 Oct 1.
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Alterations of blood brain barrier function in hyperammonemia: an overview.高血氨症中血脑屏障功能的改变:概述。
Neurotox Res. 2012 Feb;21(2):236-44. doi: 10.1007/s12640-011-9269-4. Epub 2011 Aug 27.
8
Interaction between cytokines and ammonia in the mitochondrial permeability transition in cultured astrocytes.细胞因子与氨在培养星形胶质细胞中线粒体通透性转换中的相互作用。
J Neurosci Res. 2011 Dec;89(12):2028-40. doi: 10.1002/jnr.22708. Epub 2011 Jul 11.
9
Validation of the psychometric hepatic encephalopathy score (PHES) for identifying patients with minimal hepatic encephalopathy.验证心理性肝性脑病评分(PHES)用于识别轻微肝性脑病患者的有效性。
Dig Dis Sci. 2011 Oct;56(10):3014-23. doi: 10.1007/s10620-011-1684-0. Epub 2011 Apr 3.
10
Pro-inflammatory cytokines are raised in extrahepatic portal venous obstruction, with minimal hepatic encephalopathy.在肝外门静脉阻塞伴轻微肝性脑病患者中,促炎细胞因子升高。
J Gastroenterol Hepatol. 2011 Jun;26(6):979-86. doi: 10.1111/j.1440-1746.2011.06706.x.