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Tacrolimus treatment increases bone formation in patients with rheumatoid arthritis

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dc.contributor.authorKang, Kwi Young-
dc.contributor.authorJu, Ji Hyeon-
dc.contributor.authorSong, Yeong Wook-
dc.contributor.authorYoo, Dae-Hyun-
dc.contributor.authorKim, Ho-Youn-
dc.contributor.authorPark, Sung-Hwan-
dc.date.accessioned2022-07-16T08:42:19Z-
dc.date.available2022-07-16T08:42:19Z-
dc.date.issued2013-08-
dc.identifier.issn0172-8172-
dc.identifier.issn1437-160X-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/162224-
dc.description.abstractTacrolimus is a calcineurin inhibitor, and it is used for the treatment of rheumatoid arthritis (RA). It works by inhibiting nuclear factor of activated T cells and inducting immunosuppression. This study aims to evaluate the influence of tacrolimus on the bone metabolism of patients with RA. Twenty-eight RA patients in three centers received tacrolimus 3 mg once daily for 24 weeks. Blood samples for evaluating bone metabolism and cytokines were collected at Weeks 0 and 24. We measured the serum C-telopeptide of type I collagen (sCTx-I), osteocalcin and inflammatory cytokines. We analyzed the data using the Kruskal-Wallis test and Spearman's correlation. IL-2 and IL-6 were significantly decreased after the administration of tacrolimus (p = 0.027 and p = 0.024). There was no significant difference in the serum level of sCTx-I before and after treatment. The level of serum osteocalcin at Week 24 was significantly increased compared to the level at Week 0 (p = 0.002). The increase of osteocalcin was correlated with the reductions of IL-2 and IFN-gamma (r = 0.405, p = 0.033 and r = 0.380, p = 0.046, respectively). Tacrolimus treatment increased bone formation markers in RA patients. This suggests that tacrolimus may play a role to inhibit bone erosion by increasing bone formation as well as improving the clinical symptoms of RA.-
dc.format.extent5-
dc.language영어-
dc.language.isoENG-
dc.publisherSpringer Verlag-
dc.titleTacrolimus treatment increases bone formation in patients with rheumatoid arthritis-
dc.typeArticle-
dc.publisher.location독일-
dc.identifier.doi10.1007/s00296-012-2370-z-
dc.identifier.scopusid2-s2.0-84880918198-
dc.identifier.wosid000322120400035-
dc.identifier.bibliographicCitationRheumatology International, v.33, no.8, pp 2159 - 2163-
dc.citation.titleRheumatology International-
dc.citation.volume33-
dc.citation.number8-
dc.citation.startPage2159-
dc.citation.endPage2163-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaRheumatology-
dc.relation.journalWebOfScienceCategoryRheumatology-
dc.subject.keywordPlusCYCLOSPORINE-A-
dc.subject.keywordPlusFK506-
dc.subject.keywordPlusNFAT-
dc.subject.keywordPlusDIFFERENTIATION-
dc.subject.keywordPlusOSTEOBLAST-
dc.subject.keywordPlusRATS-
dc.subject.keywordAuthorTacrolimus-
dc.subject.keywordAuthorCalcineurin-
dc.subject.keywordAuthorOsteoblast-
dc.subject.keywordAuthorNFAT-
dc.subject.keywordAuthorOsteocalcin-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs00296-012-2370-z-
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