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dc.contributor.authorPuente, Angela
dc.contributor.authorFortea, Jose Ignacio
dc.contributor.authorPozo, Carmen Del
dc.contributor.authorHuelin, Patricia
dc.contributor.authorCagigal Cobo, María Luisa
dc.contributor.authorSerrano, Marina
dc.contributor.authorCabezas González, Joaquín
dc.contributor.authorArias Loste, María Teresa 
dc.contributor.authorIruzubieta, Paula
dc.contributor.authorCuadrado, Antonio
dc.contributor.authorLlerena, Susana
dc.contributor.authorLopez, Carlos
dc.contributor.authorFábrega García, Emilio 
dc.contributor.authorCrespo García, Javier 
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2020-07-24T08:23:25Z
dc.date.available2020-07-24T08:23:25Z
dc.date.issued2019
dc.identifier.issn2073-4409
dc.identifier.urihttp://hdl.handle.net/10902/18953
dc.description.abstractPortal sinusoidal vascular disease is a presinusoidal cause of portal hypertension (PHT) of unknown etiology, characterized by typical manifestations of PHT (esophageal varices, ascites, portosystemic collaterals), plaquetopenia and splenomegaly with a gradient of portal pressure slightly increased, according to the presinusoidal nature of the PHT. A few cases in the literature have shown a relationship between oxaliplatin and the development of presinusoidal portal hypertension, years after the chemotherapy for colorectal cancer (therefore, different to sinusoidal obstruction syndrome). There are three mechanisms through which oxaliplatin can cause sinusoidal damage: 1) damage at the level of endothelial cells and stimulates the release of free radicals and depletion of glutathione transferase, with altering the integrity of the sinusoidal cells. The damage in the endothelial sinusoidal cells allows to erythrocytes to across into the Dissé space and formation of perisinusoidal fibrosis, 2) the appearance of nodular regenerative hyperplasia is favored by the chronic hypoxia of the centrilobular areas and, finally, 3) oxaliplatin can generate an obliteration of the blood capillaries and zones of parenchymal extinction. These three facts can develop, in a minority of cases, the appearance of a presinusoidal increase of portal pressure, which typically appears years after the completion of chemotherapy and sometimes is underdiagnosed until variceal bleeding, ascites or encephalopathy appear. The knowledge of this pathology is essential to be able to perform an early diagnostic and consult to the hepatologist.es_ES
dc.description.sponsorshipFunding: This research received an external funding of CI18/67/02 Acuerdo de cooperación en el programa de becas de investigación científica de IDIVAL de JANSSEN-CILAG, S.A.es_ES
dc.format.extent10 p.es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rights© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license.es_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.sourceCells . 2019 Nov 24;8(12):1506es_ES
dc.subject.otherOxaliplatines_ES
dc.subject.otherNon-Cirrhotic Portal Hypertensiones_ES
dc.subject.otherPorto Sinusoidal Vascular Diseasees_ES
dc.titlePorto-Sinusoidal Vascular Disease Associated to Oxaliplatin: An Entity to Think about Ites_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherVersionhttps://www.doi.org/10.3390/cells8121506es_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.3390/cells8121506
dc.type.versionpublishedVersiones_ES


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© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license.Excepto si se señala otra cosa, la licencia del ítem se describe como © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license.