title: The inflammatory bases of hepatic encephalopathy.
abstract: A hypothesis about the inflammatory etiopathogeny mediated by astroglia of hepatic encephalopathy is being proposed. Three evolutive phases are considered in chronic hepatic encephalopathy: an immediate or nervous phase with ischemia-reperfusion, which is associated with reperfusion injury, edema and oxidative stress; an intermediate or immune phase with microglia hyperactivity, which produces cytotoxic cytokines and chemokines and is involved in enzyme hyperproduction and phagocytosis; and a late or endocrine phase, in which neuroglial remodeling, with an alteration of angiogenesis and neurogenesis, stands out. The increasingly complex trophic meaning that the metabolic alterations have in the successive phases making up this chronic inflammation could explain the metabolic regression produced in acute and acute-on-chronic hepatic encephalopathy. In these two types of hepatic encephalopathy, characterized by edema, neuronal nutrition by diffusion would guarantee an appropriate support of substrates, in accordance with the reduced metabolic needs of the cerebral tissue.
authors.affiliation: Psychobiology Laboratory, School of Psychology, University of Oviedo, Asturias, Spain.
authors.forename: Jorge-Luis
authors.initials: JL
authors.lastname: Arias
authors.forename: Maria-Angeles
authors.initials: MA
authors.lastname: Aller
authors.forename: Fernando
authors.initials: F
authors.lastname: Sánchez-Patan
authors.forename: Jaime
authors.initials: J
authors.lastname: Arias
mesh_terms: D000208:Acute Disease; D001253:Astrocytes / Q000473:pathology / Q000502:physiology; D002908:Chronic Disease; D004679:Encephalomyelitis / Q000209:etiology*; D006501:Hepatic Encephalopathy / Q000150:complications* / Q000276:immunology / Q000473:pathology; D006801:Humans; D018384:Oxidative Stress; D016176:T-Lymphocyte Subsets / Q000276:immunology