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dc.contributor.authorMedrano, Luz Maria 
dc.contributor.authorGarcia-Broncano, Pilar 
dc.contributor.authorBerenguer, Juan
dc.contributor.authorGonzález-García, Juan
dc.contributor.authorJimenez-Sousa, Maria Angeles 
dc.contributor.authorGuardiola, Josep M
dc.contributor.authorCrespo, Manuel
dc.contributor.authorQuereda, Carmen
dc.contributor.authorSanz, José
dc.contributor.authorCanorea, Isabel 
dc.contributor.authorCarrero, Ana
dc.contributor.authorHontañón, Victor
dc.contributor.authorMuñoz-Fernández, Ma Ángeles
dc.contributor.authorResino, Salvador 
dc.date.accessioned2020-05-12T08:46:28Z
dc.date.available2020-05-12T08:46:28Z
dc.date.issued2018
dc.identifier.citationAIDS. 2018 Jun 1;32(9):1095-1105es_ES
dc.identifier.issn0269-9370es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/10051
dc.description.abstractOBJECTIVES: Immune dysregulation is a hallmark of HIV and hepatitis C virus (HCV) infections. We aimed to evaluate the relationship between liver stiffness measurement (LSM) and biomarkers of T-cell activation, bacterial translocation, inflammation, endothelial dysfunction, and coagulopathy in HIV/HCV-coinfected patients. DESIGN: Cross-sectional study. METHODS: We studied 238 HIV/HCV-coinfected patients, 32 healthy controls, and 39 HIV-monoinfected patients. Patients were stratified according to LSM into four groups: less than 12.5, 12.5-25, 25-40, and more than 40 kPa. T-cell subsets were measured using flow cytometry and plasma biomarkers using immunoassays. RESULTS: HIV/HCV-coinfected patients had higher biomarker levels of immune activation in peripheral blood [T-cell activation (CD4CD38 and CD8CD38), bacterial translocation (soluble CD14), inflammation [IL-1b, IL-6, IL-8, IL-18, IFN-γ-inducible protein 10 (IP-10)] endothelial dysfunction [soluble vascular cell adhesion molecule 1 (sVCAM1), soluble intercellular cell adhesion molecule 1 (sICAM1), and soluble tumor necrosis factor receptor 1 (sTNFR1)], and coagulopathy (plasminogen activator inhibitor-1)] than healthy controls and HIV-monoinfected patients. Moreover, in HIV/HCV-coinfected patients, a direct relationship between LSM and immune activation [T-cell activation (CD8CD38 bacterial translocation (lipopolysaccharide), inflammation (IL-8, IP-10), endothelial dysfunction (sVCAM1, sICAM1, and sTNFR1), and coagulopathy (D-dimer)] was found. Subsequently, patients were stratified into different fibrosis stages, finding that patients with cirrhosis who had LSM at least 40 kPa showed higher biomarker values of immune activation [T-cell activation (CD4CD38 and CD8CD38), bacterial translocation (lipopolysaccharide), inflammation (IL-8, IL-6, IP-10), endothelial dysfunction (sVCAM1, sICAM1, and sTNFR1), and coagulopathy (D-dimer)] than patients from the other three groups (<12.5, 12.5-25, and 25-40 kPa). CONCLUSION: T-cell activation, bacterial translocation, inflammation, endothelial dysfunction, and coagulopathy increased with the severity of liver fibrosis in HIV/HCV-coinfected patients, particularly in patients who had LSM at least 40 kPa.es_ES
dc.description.sponsorshipWe want to particularly acknowledge the patients in this study for their participation and to the Spanish HIV HGM BioBank integrated in the Spanish AIDS Research Network (RIS) and collaborating Centers for the generous gifts of clinical samples used in this work. The HIV BioBank, integrated in the Spanish AIDS Research Network, is supported by the Institute of Health Carlos III, ISCIII, Spanish Health Ministry (grant no. RD06/0006/0035 and RD12/0017/0037) as part of the State Plan for Scientific and Technical Research and Innovation and cofinanced by ISCIII-Sub-Directorate General for Research Assessment and Promotion and European Regional Development Fund (ERDF) and Foundation for Research and Prevention of AIDS in Spain (FIPSE). This study would not have been possible without the collaboration of all the patients, medical and nursing staff and data managers who have taken part in the project [The GESIDA 3603b Cohort Study Group (Supporting document), which show all collaborators]. The RIS Cohort (CoRIS) is funded by the ISCIII through the Spanish AIDS Research Network (RIS C03/173 and RD12/0017/0018) as part of the State Plan for Scientific and Technical Research and Innovation and cofinanced by ISCIII-Sub-Directorate General for Research Assessment and Promotion and European Regional Development Fund (ERDF). The current study was supported by grants from Instituto de Salud Carlos III (ISCII; grant numbers PI14/01094 and PI14CIII/00011) and Ministerio de Sanidad, Servicios Sociales. e Igualdad (grant number EC11–241). The study was also funded by the RD16CIII/0002/0002 and RD16/0025/0017 projects as part of the Plan Nacional R + D + I and cofunded by ISCIII-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER). J.B. is an investigator from the Programa de Intensificación de la Actividad Investigadora en el Sistema Nacional de Salud (I3SNS), Refs INT15/00079 and INT16/00100.es_ES
dc.language.isoenges_ES
dc.publisherLippincott Williams & Wilkins (LWW) es_ES
dc.type.hasVersionAMes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshBacterial Translocation es_ES
dc.subject.meshBiomarkers es_ES
dc.subject.meshCoinfection es_ES
dc.subject.meshCross-Sectional Studies es_ES
dc.subject.meshFemale es_ES
dc.subject.meshFlow Cytometry es_ES
dc.subject.meshHIV Infections es_ES
dc.subject.meshHepatitis C, Chronic es_ES
dc.subject.meshHumans es_ES
dc.subject.meshInflammation es_ES
dc.subject.meshLiver es_ES
dc.subject.meshMale es_ES
dc.subject.meshMiddle Aged es_ES
dc.subject.meshSeverity of Illness Index es_ES
dc.subject.meshLymphocyte Activation es_ES
dc.titleElevated liver stiffness is linked to increased biomarkers of inflammation and immune activation in HIV/hepatitis C virus-coinfected patientses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID29438197es_ES
dc.format.volume32es_ES
dc.format.number9es_ES
dc.format.page1095-1105es_ES
dc.identifier.doi10.1097/QAD.0000000000001787es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.contributor.funderFundación para la Investigación y la Prevención del Sida en España 
dc.identifier.e-issn1473-5571es_ES
dc.relation.publisherversionhttps://doi.org/10.1097/QAD.0000000000001787es_ES
dc.identifier.journalAIDS (London, England)es_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RD06/0006/0035es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RD12/0017/0037es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RIS C03/173es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RD12/0017/0018es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/PI14/01094es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/PI14CIII/00011es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RD16CIII/0002/0002es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/RD16/0025/0017es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/INT15/00079es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/INT16/00100es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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