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dc.contributor.authorJimenez-Sousa, Maria Angeles 
dc.contributor.authorGómez-Moreno, Ana Zaida
dc.contributor.authorPineda-Tenor, Daniel 
dc.contributor.authorMedrano, Luz Maria 
dc.contributor.authorSánchez-Ruano, Juan José
dc.contributor.authorFernandez-Rodriguez, Amanda 
dc.contributor.authorArtaza-Varasa, Tomas
dc.contributor.authorSaura-Montalbán, José
dc.contributor.authorVazquez-Moron, Sonia 
dc.contributor.authorRyan, Pablo
dc.contributor.authorResino, Salvador 
dc.date.accessioned2019-03-05T15:39:21Z
dc.date.available2019-03-05T15:39:21Z
dc.date.issued2017-12
dc.identifier.citationClin Transl Med. 2017;6(1):26es_ES
dc.identifier.issn2001-1326es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7282
dc.description.abstractBACKGROUND AND AIMS: CXCL9-11 polymorphisms are related to various infectious diseases, including hepatitis C virus (HCV) infection. In this study, we analyzed the association between CXCL9-11 polymorphisms and liver fibrosis in HCV-infected patients. METHODS: We performed a cross-sectional study in 389 patients who were genotyped for CXCL9-11 polymorphisms (CXCL9 rs10336, CXCL10 rs3921, and CXCL11 rs4619915) using the Sequenom's MassARRAY platform. The primary outcome variable was the liver stiffness measurement (LSM). We established three cut-offs of LSM: LSM ≥ 7.1 kPa (F ≥ 2-significant fibrosis), LSM ≥ 9.5 kPa (F ≥ 3-advanced fibrosis), and LSM ≥ 12.5 kPa (F4-cirrhosis). RESULTS: Recessive, overdominant and codominant models of inheritance showed significant values, but the overdominant model was the best fitting our data. In this case, CXCL9 rs10336 AG, CXCL10 rs3921 CG and CXCL11 rs4619915 AG were mainly associated with lower values of LSM [(adjusted GMR (aGMR) = 0.85 (p = 0.005), aGMR = 0.84 (p = 0.003), and aGMR = 0.84 (p = 0.003), respectively]. Patients with CXCL9 rs10336 AG genotype had lower odds of significant fibrosis (LSM ≥ 7.1 kPa) [adjusted OR (aOR) = 0.59 (p = 0.016)], advanced fibrosis (LSM ≥ 9.5 kPa) [aOR = 0.54 (p = 0.010)], and cirrhosis (LSM ≥ 12.5 kPa) [aOR = 0.56 (p = 0.043)]. Patients with CXCL10 rs3921 CG or CXCL11 rs4619915 AG genotypes had lower odds of significant fibrosis (LSM ≥ 7.1 kPa) [adjusted OR (aOR) = 0.56 (p = 0.008)], advanced fibrosis (LSM ≥ 9.5 kPa) [aOR = 0.55 (p = 0.013)], and cirrhosis (LSM ≥ 12.5 kPa) [aOR = 0.57 (p = 0.051)]. Additionally, CXCL9-11 polymorphisms were related to lower liver stiffness under a codominant model of inheritance, being the heterozygous genotypes also protective against hepatic fibrosis. In the recessive inheritance model, the CXCL9 rs10336 AA, CXCL10 rs3921 CC and CXCL11 rs4619915 AA were associated with higher LSM values [(adjusted GMR (aGMR) = 1.19 (p = 0.030), aGMR = 1.21 (p = 0.023), and aGMR = 1.21 (p = 0.023), respectively]. Moreover, patients with CXCL9 rs10336 AA genotype had higher odds of significant fibrosis (LSM ≥ 7.1 kPa) [adjusted OR (aOR) = 1.83 (p = 0.044)] and advanced fibrosis (LSM ≥ 9.5 kPa) [aOR = 1.85 (p = 0.045)]. Furthermore, patients with CXCL10 rs3921 CC or CXCL11 rs4619915 AA genotypes had higher odds of advanced fibrosis (LSM ≥ 9.5 kPa) [aOR = 1.89 (p = 0.038)]. CONCLUSIONS: CXCL9-11 polymorphisms were related to likelihood of having liver fibrosis in HCV-infected patients. Our data suggest that CXCL9-11 polymorphisms may play a significant role against the progression of CHC and could help prioritize antiviral therapy.es_ES
dc.description.sponsorshipThis work has been supported by grants given by Fondo de Investigación de Sanidad en España (FIS) [Spanish Health Founds for Research] [Grant Numbers PI14CIII/00011]. MAJS, LMM and AFR are supported by “Instituto de Salud Carlos III” [Grant Numbers CD13/00013, CD14/00002, and CP14CIII/00010, respectively].es_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectCXCL9-11es_ES
dc.subjectChronic hepatitis Ces_ES
dc.subjectCirrhosises_ES
dc.subjectLiver fibrosises_ES
dc.subjectLiver stiffnesses_ES
dc.subjectSNPses_ES
dc.titleCXCL9-11 polymorphisms are associated with liver fibrosis in patients with chronic hepatitis C: a cross-sectional studyes_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID28755163es_ES
dc.format.volume6es_ES
dc.format.number1es_ES
dc.format.page26es_ES
dc.identifier.doi10.1186/s40169-017-0156-3es_ES
dc.contributor.funderFondo de Investigaciones Sanitariases_ES
dc.contributor.funderInstituto de Salud Carlos III-ISCIIIes_ES
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1186/s40169-017-0156-3.es_ES
dc.identifier.journalClinical and translational medicinees_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI14CIII/00011es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CD13/00013es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CD14/00002es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CP14CIII/00010es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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