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Cited 19 time in webofscience Cited 22 time in scopus
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Vitamin D receptor FokI, BsmI, and TaqI polymorphisms and susceptibility to rheumatoid arthritis A meta-analysis

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dc.contributor.authorSong, G. G.-
dc.contributor.authorBae, Sang Cheol-
dc.contributor.authorLee, Y. H.-
dc.date.accessioned2021-07-30T05:28:29Z-
dc.date.available2021-07-30T05:28:29Z-
dc.date.issued2016-04-
dc.identifier.issn0340-1855-
dc.identifier.issn1435-1250-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/5069-
dc.description.abstractObjective The aim of this study was to explore whether vitamin D receptor (VDR) polymorphisms are associated with susceptibility to rheumatoid arthritis (RA). Methods Meta-analyses were conducted on the associations between the VDR FokI, BsmI, and TaqI polymorphisms and RA. Results A total of seven studies were considered in the meta-analysis, involving a total of 923 patients and 912 controls. Meta-analysis of the VDR FokI polymorphism showed no association between RA and the F allele in the entire studied cohort (odds ratio, OR = 1.1740, 95 % confidence interval, CI = 0.994–1.387, p = 0.059). However, stratification by ethnicity revealed a significant association between the F allele and RA in Europeans (OR = 1.402, 95 % CI = 1.126–1.746, p = 0.003). Furthermore, an association was found between RA and the VDR FokI polymorphism using both the dominant model and homozygote contrast. Meta-analysis revealed no association between RA and the VDR BsmI B and TaqI T polymorphisms in Europeans (OR for the B allele = 1.065, 95 % CI = 0.911–1.245, p = 0.427; OR for the T allele = 1.065, 95 % CI = 0.834–1.361, p = 0.613). Conclusion This meta-analysis suggests that the VDR FokI polymorphism is associated with susceptibility to RA in European populations.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherDr. Dietrich Steinkopff Verlag-
dc.titleVitamin D receptor FokI, BsmI, and TaqI polymorphisms and susceptibility to rheumatoid arthritis A meta-analysis-
dc.typeArticle-
dc.publisher.location독일-
dc.identifier.doi10.1007/s00393-015-1581-6-
dc.identifier.scopusid2-s2.0-84941336537-
dc.identifier.wosid000373646700014-
dc.identifier.bibliographicCitationZeitschrift für Rheumatologie, v.75, no.3, pp 322 - 329-
dc.citation.titleZeitschrift für Rheumatologie-
dc.citation.volume75-
dc.citation.number3-
dc.citation.startPage322-
dc.citation.endPage329-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaRheumatology-
dc.relation.journalWebOfScienceCategoryRheumatology-
dc.subject.keywordPlusSYSTEMIC-LUPUS-ERYTHEMATOSUS-
dc.subject.keywordPlusGENE POLYMORPHISMS-
dc.subject.keywordPlusASSOCIATION-
dc.subject.keywordPlusOSTEOPOROSIS-
dc.subject.keywordPlusPOPULATION-
dc.subject.keywordPlusGENOTYPES-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordAuthorImmune system-
dc.subject.keywordAuthorAutoimmune diseases-
dc.subject.keywordAuthorHormone receptors, nuclear-
dc.subject.keywordAuthorMEDLINE-
dc.subject.keywordAuthorLinkage disequilibrium-
dc.identifier.urlhttps://link.springer.com/article/10.1007/s00393-015-1581-6-
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