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Cited 28 time in webofscience Cited 34 time in scopus
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The association between interleukin-6 polymorphisms and rheumatoid arthritis: a meta-analysis

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dc.contributor.authorLee, Young Ho-
dc.contributor.authorBae, Sang-Cheol-
dc.contributor.authorChoi, Sung Jae-
dc.contributor.authorJi, Jong Dae-
dc.contributor.authorSong, Gwan Gyu-
dc.date.accessioned2021-08-02T19:28:17Z-
dc.date.available2021-08-02T19:28:17Z-
dc.date.issued2012-07-
dc.identifier.issn1023-3830-
dc.identifier.issn1420-908X-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/27507-
dc.description.abstractThe aim of this study was to determine whether the functional interleukin-6 (IL-6) promoter -174 G/C and -572 G/C polymorphisms confer susceptibility to rheumatoid arthritis (RA) in ethnically different populations. Meta-analysis was conducted on the associations between these IL-6 polymorphisms and RA. A total of nine studies involving 3,851 subjects (RA 2,053 and controls 1,798) were considered in this study and ethnicity-specific meta-analysis was performed on European subjects. In all study subjects, meta-analysis revealed a trend toward to an association between RA and the IL-6 -174 G allele (odds ratio [OR] = 0.699, 95 % confidence interval [CI] = 0.463-1.054, p = 0.088). Stratification by ethnicity indicated a significant association between RA and the IL-6 -174 G/C polymorphism in Europeans using the dominant (OR = 0.329, 95 % CI = 0.155-0.699, p = 0.004) and recessive (OR = 0.823, 95 % CI = 0.679-0.997, p = 0.047) models. Meta-analysis of the IL-6 -572 G/C polymorphism showed no association between RA and the IL-6 -572 G allele in all study subjects (OR = 1.641, 95 % CI = 0.613-4.397, p = 0.324). This meta-analysis shows that the IL-6 -174 G/C polymorphism may confer susceptibility to RA in Europeans.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherBirkhauser Verlag-
dc.titleThe association between interleukin-6 polymorphisms and rheumatoid arthritis: a meta-analysis-
dc.typeArticle-
dc.publisher.location스위스-
dc.identifier.doi10.1007/s00011-012-0459-1-
dc.identifier.scopusid2-s2.0-84865145810-
dc.identifier.wosid000305228500002-
dc.identifier.bibliographicCitationInflammation Research, v.61, no.7, pp 665 - 671-
dc.citation.titleInflammation Research-
dc.citation.volume61-
dc.citation.number7-
dc.citation.startPage665-
dc.citation.endPage671-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.subject.keywordPlusSYSTEMIC-LUPUS-ERYTHEMATOSUS-
dc.subject.keywordPlusPROMOTER POLYMORPHISM-
dc.subject.keywordPlusIL-6 GENE-
dc.subject.keywordPlusTNF-ALPHA-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordPlusPLASMA-
dc.subject.keywordAuthorInterleukin-6-
dc.subject.keywordAuthorPolymorphism-
dc.subject.keywordAuthorRheumatoid arthritis-
dc.subject.keywordAuthorMeta-analysis-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs00011-012-0459-1-
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