Sclerostin and Dkk-1 in patients with ankylosing spondylitis

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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.date.accessioned2024-09-18T19:54:24Z
dc.date.available2024-09-18T19:54:24Z
dc.date.issued2014
dc.departmentHatay Mustafa Kemal Üniversitesien_US
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.en_US
dc.identifier.endpage151en_US
dc.identifier.issn0303-464X
dc.identifier.issue2en_US
dc.identifier.pmid25111416en_US
dc.identifier.scopus2-s2.0-84908381844en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage146en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7719
dc.identifier.volume39en_US
dc.identifier.wosWOS:000343366800007en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherPublisaude-Edicoes Medicas Ldaen_US
dc.relation.ispartofActa Reumatologica Portuguesaen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAnkylosing spondylitisen_US
dc.subjectStructural damageen_US
dc.subjectAnti-TNF-alphaen_US
dc.subjectDkk-1en_US
dc.subjectSclerostinen_US
dc.titleSclerostin and Dkk-1 in patients with ankylosing spondylitisen_US
dc.typeArticleen_US

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