title: [Molecular aspects of hepatic encephalopathy].
abstract: BACKGROUND
  Liver fibrosis and its end stage, cirrhosis, is an enormous worldwide health problem. Hepatic encephalopathy (HE) or portal-systemic encephalopathy continues to be a major clinical problem of long-term cirrhosis. In this review we emphasise the molecular basis of HE and the involvement of oxidative stress in the development of this disease.
  
  
  BACKGROUND
  Several studies suggest that the pathogenesis of HE could be multifactorial and have implicated different factors, such as alterations in blood brain barrier, substances; such as ammonia and manganese, neurotransmission disorders such as dopamine, glutamate and GABA.
  
  
  METHODS
  HE is a severe complication of both acute and chronic liver failure. Neuropathologically, it is characterized by astrocyte changes known as Alzheimer type II astrocytosis. In addition, astrocytes manifest altered expression of astrocyte-specific proteins, such as, glial fibrillary acidic protein, glutamine synthetase, monoamine oxidase and peripheral type benzodiazepine receptors.
  
  
  CONCLUSIONS
  HE is a complex neuropsychiatric syndrome associated with liver failure. These alterations are products of increases in oxidative stress in brain due to neurotoxin activity. The main strategy for HE treatment is directed at ammonia reduction, which can be achieved either by decreasing its absorption/production or increasing its removal.
authors.affiliation: Unidad de Biotecnología Médica y Farmacéutica, Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco, CIATEJ, Guadalajara, México.
authors.forename: A L
authors.initials: AL
authors.lastname: Márquez-Aguirre
authors.forename: A A
authors.initials: AA
authors.lastname: Canales-Aguirre
authors.forename: U
authors.initials: U
authors.lastname: Gómez-Pinedo
authors.forename: F J
authors.initials: FJ
authors.lastname: Gálvez-Gastélum
mesh_terms: D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D004298:Dopamine / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006501:Hepatic Encephalopathy / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009498:Neurotoxins / Q000378:metabolism; D018384:Oxidative Stress; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D009498:Neurotoxins; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D004298:Dopamine