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dc.contributor.authorLópez-Mejías R
dc.contributor.authorGenre F
dc.contributor.authorRemuzgo-Martínez S
dc.contributor.authorRobustillo-Villarino M
dc.contributor.authorGarcía-Bermúdez M
dc.contributor.authorLlorca J
dc.contributor.authorCorrales A
dc.contributor.authorGonzález Juanatey, Carlos 
dc.contributor.authorUbilla B
dc.contributor.authorMiranda Filloy, José Alberto 
dc.contributor.authorMijares V
dc.contributor.authorPina T
dc.contributor.authorBlanco R
dc.contributor.authorAlegre-Sancho JJ
dc.contributor.authorRamírez Huaranga MA
dc.contributor.authorMínguez Sánchez MD
dc.contributor.authorTejera Segura B
dc.contributor.authorFerraz-Amaro I
dc.contributor.authorVicente E
dc.contributor.authorCarmona FD
dc.contributor.authorCastañeda S
dc.contributor.authorMartín J
dc.contributor.authorGonzález-Gay Mantecón, Miguel Ángel 
dc.date.accessioned2017-06-07T07:34:17Z
dc.date.available2017-06-07T07:34:17Z
dc.date.issued2015
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/20.500.11940/8076
dc.description.abstractOBJECTIVES: To determine whether the interleukin-33 (IL-33)-interleukin-1 receptor like 1 (IL-1RL1) signaling pathway is implicated in the risk of subclinical atherosclerosis in patients with rheumatoid arthritis (RA). METHODS: A total of 576 Spanish RA patients from Northern Spain were genotyped for 6 well-known IL33-IL1RL1 polymorphisms (IL33 rs3939286, IL33 rs7025417, IL33 rs7044343, IL1RL1 rs2058660, IL1RL1 rs2310173 and IL1RL1 rs13015714) by TaqMan genotyping assay. The presence of subclinical atherosclerosis was determined by the assessment of carotid intima-media thickness (cIMT) by carotid ultrasound (US). RESULTS: RA patients carrying the TT genotype of the IL33 rs3939286 polymorphism had lower cIMT values than those homozygous for the CC genotype (mean +/- standard deviation (SD): 0.71 +/- 0.14 mm versus 0.76 +/- 0.16 mm, respectively) while patients carrying the CT genotype had intermediate cIMT values (mean +/- SD: 0.73 +/- 0.17 mm). Moreover, RA patients carrying the mutant allele T of the IL33 rs3939286 polymorphism exhibited significantly lower cIMT values than those carrying the wild allele C (mean +/- SD: 0.72 +/- 0.16 mm versus 0.75 +/- 0.18 mm respectively; p = 0.04). The association of both genotype and allele frequencies of IL33 rs3939286 and cIMT levels remained statistically significant after adjustment for sex, age at the time of US study, follow-up and center (p = 0.006 and p = 0.0023, respectively), evidencing that the potential effect conferred by IL33 rs3939286 may be independent of confounder factors. No association with other IL33-IL1RL1 genetic variants was observed. CONCLUSIONS: In conclusion, our results may suggest a potential protective effect of the IL33 rs3939286 allele T in the risk of subclinical atherosclerosis in patients with RA.
dc.description.sponsorshipEuropean Union FEDER
dc.description.sponsorshipInstituto de Salud Carlos III (ISCIII)/Fondo de Investigación Sanitaria
dc.description.sponsorshipEuropean Commission
dc.description.sponsorshipRECTIS Programs del Instituto de Salud Carlos III (ISCIII)
dc.description.sponsorshipEuropean IMI BTCure Program
dc.description.sponsorshipRECTIS Program (RIER)
dc.language.isoeng
dc.rightsAtribución 4.0 Internacional
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAlleles
dc.subject.meshArthritis, Rheumatoid
dc.subject.meshAtherosclerosis
dc.subject.meshCarotid Arteries
dc.subject.meshFemale
dc.subject.meshFollow-Up Studies
dc.subject.meshGene Frequency
dc.subject.meshGenotype
dc.subject.meshHumans
dc.subject.meshInterleukin-33
dc.subject.meshLinkage Disequilibrium
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshPolymorphism, Single Nucleotide
dc.subject.meshReceptors, Interleukin-1 Type I
dc.subject.meshRisk
dc.subject.meshUltrasonography
dc.titleProtective Role of the Interleukin 33 rs3939286 Gene Polymorphism in the Development of Subclinical Atherosclerosis in Rheumatoid Arthritis Patients
dc.typeArtigoes
dc.authorsophosLópez-Mejías R
dc.authorsophosGenre F
dc.authorsophosRemuzgo-Martínez S
dc.authorsophosRobustillo-Villarino M
dc.authorsophosGarcía-Bermúdez M
dc.authorsophosLlorca J
dc.authorsophosCorrales A
dc.authorsophosGonzález-Juanatey C
dc.authorsophosUbilla B
dc.authorsophosMiranda-Filloy JA
dc.authorsophosMijares V
dc.authorsophosPina T
dc.authorsophosBlanco R
dc.authorsophosAlegre-Sancho JJ
dc.authorsophosRamírez Huaranga MA
dc.authorsophosMínguez Sánchez MD
dc.authorsophosTejera Segura B
dc.authorsophosFerraz-Amaro I
dc.authorsophosVicente E
dc.authorsophosCarmona FD
dc.authorsophosCastañeda S
dc.authorsophosMartín J
dc.authorsophosGonzález-Gay MA
dc.identifier.doi10.1371/journal.pone.0143153
dc.identifier.pmid26571131
dc.identifier.sophos19425
dc.issue.number11
dc.journal.titlePLoS One
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Santiago - Complexo Hospitalario Universitario de Santiago::Reumatoloxía
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Lugo - Hospital Universitario Lucus Augusti::Cardioloxía
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Lugo - Hospital Universitario Lucus Augusti::Reumatoloxía
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Santiago::IDIS.- Instituto de investigaciones sanitarias de Santiago
dc.relation.projectIDISCIII/PI06/0024
dc.relation.projectIDISCIII/PS09/00748
dc.relation.projectIDISCIII/PI12/00060
dc.relation.projectIDRETICS/RD12/0009 (RIER)
dc.relation.projectIDISCIII/CD12/00425
dc.relation.projectIDRIER/RD12/0009/0013
dc.rights.accessRightsopenAccess
dc.typesophosArtículo Original
dc.volume.number10


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Atribución 4.0 Internacional
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