Literature DB >> 22489256

Hepatic encephalopathy: An approach to its multiple pathophysiological features.

Juan Carlos Perazzo1, Silvina Tallis, Amalia Delfante, Pablo Andrés Souto, Abraham Lemberg, Francisco Xavier Eizayaga, Salvador Romay.   

Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric complex syndrome, ranging from subtle behavioral abnormalities to deep coma and death. Hepatic encephalopathy emerges as the major complication of acute or chronic liver failure. Multiplicity of factors are involved in its pathophysiology, such as central and neuromuscular neurotransmission disorder, alterations in sleep patterns and cognition, changes in energy metabolism leading to cell injury, an oxidative/nitrosative state and a neuroinflammatory condition. Moreover, in acute HE, a condition of imminent threat of death is present due to a deleterious astrocyte swelling. In chronic HE, changes in calcium signaling, mitochondrial membrane potential and long term potential expression, N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations, and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be observed. The main molecule indicated as responsible for all these changes in HE is ammonia. There is no doubt that ammonia, a neurotoxic molecule, triggers or at least facilitates most of these changes. Ammonia plasma levels are increased two- to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite, glutamine (GLN), lead to hyperammonemic conditions. Removal of hepatic ammonia is a differentiated work that includes the hepatocyte, through the urea cycle, converting ammonia into GLN via glutamine synthetase. Under pathological conditions, such as liver damage or liver blood by-pass, the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be considered. This editorial will focus on issues where, to the best of our knowledge, more research is needed in order to clarify, at least partially, controversial topics.

Entities:  

Keywords:  Ammonia and central nervous system; Hepatic encephalopathy; Hyperammonemia; Liver failure

Year:  2012        PMID: 22489256      PMCID: PMC3321490          DOI: 10.4254/wjh.v4.i3.50

Source DB:  PubMed          Journal:  World J Hepatol


  176 in total

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Journal:  Brain Res       Date:  1995-12-24       Impact factor: 3.252

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Journal:  Exp Brain Res       Date:  1981       Impact factor: 1.972

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  9 in total

Review 1.  Current pathogenetic aspects of hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy.

Authors:  Halina Cichoż-Lach; Agata Michalak
Journal:  World J Gastroenterol       Date:  2013-01-07       Impact factor: 5.742

Review 2.  Elevated cerebral lactate: Implications in the pathogenesis of hepatic encephalopathy.

Authors:  Cristina R Bosoi; Christopher F Rose
Journal:  Metab Brain Dis       Date:  2014-06-11       Impact factor: 3.584

3.  Acetyl-L-carnitine for patients with hepatic encephalopathy.

Authors:  Arturo J Martí-Carvajal; Christian Gluud; Ingrid Arevalo-Rodriguez; Cristina Elena Martí-Amarista
Journal:  Cochrane Database Syst Rev       Date:  2019-01-05

4.  Saline is as effective as nitrogen scavengers for treatment of hyperammonemia.

Authors:  G van Straten; M G M de Sain-van der Velden; I M van Geijlswijk; R P Favier; S J Mesu; N E Holwerda-Loof; M van der Ham; H Fieten; J Rothuizen; B Spee; N M Verhoeven-Duif
Journal:  Sci Rep       Date:  2017-10-13       Impact factor: 4.379

5.  Efficacy of orally administered sodium benzoate and sodium phenylbutyrate in dogs with congenital portosystemic shunts.

Authors:  Giora van Straten; Diewke van Dalen; Sietske J Mesu; Jan Rothuizen; Erik Teske; Bart Spee; Robert P Favier; Ingeborg M van Geijlswijk
Journal:  J Vet Intern Med       Date:  2019-03-27       Impact factor: 3.333

6.  Is NMDA-Receptor-Mediated Oxidative Stress in Mitochondria of Peripheral Tissues the Essential Factor in the Pathogenesis of Hepatic Encephalopathy?

Authors:  Elena Kosenko; Lyudmila Tikhonova; Gubidat Alilova; Carmina Montoliu
Journal:  J Clin Med       Date:  2022-02-04       Impact factor: 4.241

7.  Do Triphasic Waves and Nonconvulsive Status Epilepticus Arise From Similar Mechanisms? A Computational Model.

Authors:  Sophie Ligtenstein; Jiangling Song; Jin Jin; Haoqi Sun; Luis Paixao; Sahar Zafar; M Brandon Westover
Journal:  J Clin Neurophysiol       Date:  2021-09-01       Impact factor: 2.590

8.  Outcome of non-surgical dietary treatment with or without lactulose in dogs with congenital portosystemic shunts.

Authors:  Robert P Favier; Eline de Graaf; Ronald J Corbee; Anne Kummeling
Journal:  Vet Q       Date:  2020-12       Impact factor: 3.320

9.  Resolution of Severe Neurologic Signs Following Intravenous Lipid Emulsion Therapy in a Young Dog With a Portosystemic Shunt: Case Report.

Authors:  Amanda M Spillane; Jenica L Haraschak; Maureen A McMichael
Journal:  Front Vet Sci       Date:  2021-12-08
  9 in total

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