Syndecan 1 may slow the progression of subclinical atherosclerosis in patients with ankylosing spondylitis

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dc.contributor.authorYilmaz, Pinar Diydem
dc.contributor.authorKadiyoran, Cengiz
dc.contributor.authorGoktepe, Mevlut Hakan
dc.contributor.authorAkkubak, Yasemin
dc.contributor.authorIcli, Abdullah
dc.contributor.authorKucuk, Adem
dc.date.accessioned2024-02-23T14:20:29Z
dc.date.available2024-02-23T14:20:29Z
dc.date.issued2023
dc.departmentNEÜen_US
dc.description.abstractBackground Subclinical atherosclerosis may be seen at an early age of ankylosing spondylitis (AS). Syndecan 1 (S1) expression is increased in response to proinflammatory cytokine and inflammation. High S1 may reduce carotid atherosclerosis progression. We aimed to investigate the relationship between S1 levels and subclinical atherosclerosis in patients with AS. Methods Fifty-eight patients diagnosed with AS and 58 age-, sex-, and body mass index-matched controls were included in the study. S1 level and carotid intima-media thickness (cIMT) were evaluated using appropriate methods. Results AS patients' cIMT (0.53 +/- 0.1 vs 0.45 +/- 0.1 mm, p = .008), S1 (6.0 [1.7-149.2] vs 5.5 [1.0-29.8] ng/ml, p = .020), CRP (C-reactive protein) (2.1 [0.1-19.7] vs 1.1 [0.3-9.6] mg/dl, p = .012), fibrinogen (330.2 +/- 87.0 vs 278.0 +/- 54.5 mg/dl, p < .001) values were significantly higher than the values of the control group. There was a negative correlation between cIMT and CRP (p = .034), age (p < .001), disease duration (p = .005), BASDAI (p = .048) and fibrinogen (p = .009) in AS patients. There was a negative correlation between cIMT and S1 (p = .029). In multivariate analysis, an independent relationship was found between cIMT and age (beta = 0.611, p < .001) and syndecan (beta = -0.196, p = .046). Conclusion S1 level may rise in AS patients to suppress the inverse effects of proinflammatory cytokines and inflammation. A negative relationship between the cIMT values of AS patients and S1 level may reveal that S1 has a protective effect on the development of atherosclerosis in AS patients, independent of disease activity.en_US
dc.identifier.doi10.1080/10641963.2022.2156529
dc.identifier.issn1064-1963
dc.identifier.issn1525-6006
dc.identifier.issue1en_US
dc.identifier.pmid36524421en_US
dc.identifier.scopus2-s2.0-85144172617en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.urihttps://doi.org/10.1080/10641963.2022.2156529
dc.identifier.urihttps://hdl.handle.net/20.500.12452/13174
dc.identifier.volume45en_US
dc.identifier.wosWOS:000898430700001en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofClinical And Experimental Hypertensionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAnkylosing Spondylitisen_US
dc.subjectSyndecan 1en_US
dc.subjectCarotid Intima-Media Thickness (Cimt)en_US
dc.subjectSubclinical Atherosclerosisen_US
dc.titleSyndecan 1 may slow the progression of subclinical atherosclerosis in patients with ankylosing spondylitisen_US
dc.typeArticleen_US

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