Elevated cerebral lactate : implications in the pathogenesis of hepatic encephalopathy
dc.contributor.author | Bosoi, Cristina R. | |
dc.contributor.author | Rose, Christopher | |
dc.date.accessioned | 2020-11-11T14:26:22Z | |
dc.date.available | NO_RESTRICTION | fr |
dc.date.available | 2020-11-11T14:26:22Z | |
dc.date.issued | 2014-06-11 | |
dc.identifier.uri | http://hdl.handle.net/1866/24040 | |
dc.publisher | Springer | fr |
dc.subject | Hepatic encephalopathy | fr |
dc.subject | Lactate | fr |
dc.subject | Brain edema | fr |
dc.subject | Ammonia | fr |
dc.title | Elevated cerebral lactate : implications in the pathogenesis of hepatic encephalopathy | fr |
dc.type | Article | fr |
dc.contributor.affiliation | Université de Montréal. Faculté de médecine. Département de médecine | fr |
dc.identifier.doi | 10.1007/s11011-014-9573-9 | |
dcterms.abstract | Hepatic encephalopathy (HE), a complex neuropsychiatric syndrome, is a frequent complication of liver failure/disease. Increased concentrations of lactate are commonly observed in HE patients, in the systemic circulation, but also in the brain. Traditionally, increased cerebral lactate is considered a marker of energy failure/impairment however alterations in lactate homeostasis may also lead to a rise in brain lactate and result in neuronal dysfunction. The latter may involve the development of brain edema. This review will target the significance of increased cerebral lactate in the pathogenesis of HE. | fr |
dcterms.isPartOf | urn:ISSN:0885-7490 | fr |
dcterms.isPartOf | urn:ISSN:1573-7365 | fr |
dcterms.language | eng | fr |
UdeM.ReferenceFournieParDeposant | http://dx.doi.org/10.1007/s11011-014-9573-9 | fr |
UdeM.VersionRioxx | Version acceptée / Accepted Manuscript | fr |
oaire.citationTitle | Metabolic brain disease | fr |
oaire.citationVolume | 29 | fr |
oaire.citationStartPage | 919 | fr |
oaire.citationEndPage | 925 | fr |
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