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Ammonia mediates cortical hemichannel dysfunction in rodent models of chronic liver disease.氨在慢性肝病啮齿动物模型中介导皮质半通道功能障碍。
Hepatology. 2017 Apr;65(4):1306-1318. doi: 10.1002/hep.29031. Epub 2017 Mar 7.
2
Covert Hepatic Encephalopathy: Can My Patient Drive?隐匿性肝性脑病:我的患者可以开车吗?
J Clin Gastroenterol. 2017 Feb;51(2):118-126. doi: 10.1097/MCG.0000000000000764.
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Hepatic Encephalopathy.肝性脑病
N Engl J Med. 2016 Oct 27;375(17):1660-1670. doi: 10.1056/NEJMra1600561.
4
Neurosteroids in hepatic encephalopathy: Novel insights and new therapeutic opportunities.肝性脑病中的神经甾体:新见解与新治疗机遇
J Steroid Biochem Mol Biol. 2016 Jun;160:94-7. doi: 10.1016/j.jsbmb.2015.11.006. Epub 2015 Nov 14.
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Rifaximin vs. lactulose in treatment of minimal hepatic encephalopathy.利福昔明与乳果糖治疗轻微肝性脑病的对比研究
Liver Int. 2016 Mar;36(3):378-85. doi: 10.1111/liv.12921. Epub 2015 Aug 17.
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Encephalopathy in Wilson disease: copper toxicity or liver failure?威尔逊病中的脑病:铜中毒还是肝功能衰竭?
J Clin Exp Hepatol. 2015 Mar;5(Suppl 1):S88-95. doi: 10.1016/j.jceh.2014.09.002. Epub 2014 Sep 22.
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Pathogenesis of hepatic encephalopathy: role of ammonia and systemic inflammation.肝性脑病的发病机制:氨与全身炎症的作用
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Salivary microbiota reflects changes in gut microbiota in cirrhosis with hepatic encephalopathy.唾液微生物群反映了肝硬化合并肝性脑病患者肠道微生物群的变化。
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Probiotic VSL#3 reduces liver disease severity and hospitalization in patients with cirrhosis: a randomized, controlled trial.益生菌 VSL#3 可降低肝硬化患者的肝脏疾病严重程度和住院率:一项随机对照试验。
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Liver: the gut is a key target of therapy in hepatic encephalopathy.肝脏:肠道是肝性脑病治疗的一个关键靶点。
Nat Rev Gastroenterol Hepatol. 2015 Jan;12(1):7-8. doi: 10.1038/nrgastro.2014.185. Epub 2014 Oct 28.

肝性脑病

Hepatic encephalopathy.

作者信息

Ferenci Peter

机构信息

Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.

出版信息

Gastroenterol Rep (Oxf). 2017 May;5(2):138-147. doi: 10.1093/gastro/gox013. Epub 2017 Apr 18.

DOI:10.1093/gastro/gox013
PMID:28533911
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5421503/
Abstract

Hepatic encephalopathy (HE) is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases. The precise pathophysiology of HE is still under discussion; the leading hypothesis focus on the role of neurotoxins, impaired neurotransmission due to metabolic changes in liver failure, changes in brain energy metabolism, systemic inflammatory response and alterations of the blood brain barrier. HE produces a wide spectrum of nonspecific neurological and psychiatric manifestations. Minimal HE is diagnosed by abnormal psychometric tests. Clinically overt HE includes personality changes, alterations in consciousness progressive disorientation in time and space, somnolence, stupor and, finally, coma. Except for clinical studies, no specific tests are required for diagnosis. HE is classified according to the underlying disease, the severity of manifestations, its time course and the existence of precipitating factors. Treatment of overt HE includes supportive therapies, treatment of precipitating factors, lactulose and/or rifaximin. Routine treatment for minimal HE is only recommended for selected patients.

摘要

肝性脑病(HE)是一种发生于晚期肝病患者的可逆性脑功能受损综合征。HE的确切病理生理学仍在探讨中;主要假说是关注神经毒素的作用、肝功能衰竭代谢变化导致的神经递质传递受损、脑能量代谢改变、全身炎症反应以及血脑屏障的改变。HE会产生广泛的非特异性神经和精神表现。轻微肝性脑病通过异常心理测试来诊断。临床显性肝性脑病包括人格改变、意识改变、在时间和空间上进行性定向障碍、嗜睡、昏睡,最终昏迷。除临床研究外,诊断无需特殊检查。肝性脑病根据基础疾病、表现的严重程度、病程以及诱发因素的存在与否进行分类。显性肝性脑病的治疗包括支持治疗、诱发因素的治疗、乳果糖和/或利福昔明。仅建议对选定患者进行轻微肝性脑病的常规治疗。