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dc.contributor.authorUstun, N.
dc.contributor.authorTok, F.
dc.contributor.authorKalyoncu, U.
dc.contributor.authorMotor, S.
dc.contributor.authorYuksel, R.
dc.contributor.authorYagiz, A. E.
dc.contributor.authorGuler, H.
dc.contributor.authorTurhanoglu, A. D.
dc.date.accessioned2019-12-10T11:20:24Z
dc.date.available2019-12-10T11:20:24Z
dc.date.issued2014
dc.identifier.issn0303-464X
dc.identifier.urihttps://doi.org/
dc.identifier.urihttp://hdl.handle.net/11655/15329
dc.description.abstractObjective: To determine the serum Dickkopf-related protein 1 (Dkk-1) and sclerostin levels, and their relationship to structural damage and disease activity in patients with ankylosing spondylitis (AS), as well as to compare the serum Dldc-1 and sclerostin levels in patients receiving and not receiving anti-TNF-alpha treatment. Materials and Methods: This cross-sectional study included 44 AS patients and 41 healthy age- and gender-matched controls. Demographic data, disease activity parameters, and Bath AnIcylosing Spondylitis Radiologic Index (BASRI) scores were recorded. Serum Dkk-1 and sclerostin levels were measured using commercially available ELISA. Results: Serum Dkk-1 levels were lower (P > 0.05) and sclerostin levels were significantly lower (P < 0.05) in the AS patients than in the controls. Dkk-1 and sclerostin levels were similar in the patients that did and didn't receive anti-TNF-alpha treatment, and in the patients with active and inactive disease (P > 0.05). There wasn't a correlation between serum Dkk-1 or sclerostin levels, and disease activity indices (P > 0.05). BASRI scores did not correlate with serum Dkk-1 or sclerostin levels (P > 0.05). Discussion: Sclerostin expression is impaired in AS, but this is not the case for Dkk-1. The lack of an association between Dkk-1 or sclerostin levels, and anti-TNF-alpha treatment, disease activity indices, and radiological damage might indicate that neither the Dkk-1 nor sclerostin level induce inflammation and radiological damage in AS patients. Pathologic bone formation in AS might be due to molecular dysfunction of sclerostin and Dkk-1 at the cellular level.
dc.language.isoen
dc.publisherPublisaude-Edicoes Medicas Lda
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectRheumatology
dc.titleSclerostin And Dkk-1 In Patients With Ankylosing Spondylitis
dc.typeinfo:eu-repo/semantics/article
dc.relation.journalActa Reumatologica Portuguesa
dc.contributor.departmentİç Hastalıkları
dc.identifier.volume39
dc.identifier.issue2
dc.identifier.startpage146
dc.identifier.endpage151
dc.description.indexWoS


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