Serum salusin-? levels in systemic lupus erythematosus and systemic sclerosis

Basit Öğe Kaydı
dc.authorwosidÜSTÜNDAĞ, BİLAL/V-9780-2018
dc.contributor.authorKoca, Suleyman Serdar
dc.contributor.authorOzgen, Metin
dc.contributor.authorIsik, Bahar
dc.contributor.authorDagli, Mustafa Necati
dc.contributor.authorUstundag, Bilal
dc.contributor.authorIsik, Ahmet
dc.date.accessioned2024-08-04T21:01:08Z
dc.date.available2024-08-04T21:01:08Z
dc.date.issued2014
dc.departmentİnönü Üniversitesien_US
dc.description.abstractObjective: Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc), chronic inflammatory diseases, demonstrate an increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. Salusin-alpha is a novel bioactive peptide that suppresses the formation of macrophage foam cells, and its serum level is significantly lower in patients with angiographically proven coronary artery disease. The aims of the study were to assess serum salusin-alpha level and its potential association with the predictors of atherosclerosis in SLE and SSc. Material and Methods: The study included 20 SLE and 22 SSc patients and 23 healthy controls (HC). All of the participants were female. Tumour necrosis factor-alpha (TNF-alpha), IL-6 and salusin-alpha levels, homeostasis model assessment for insulin resistance (HOMA-IR) index and common carotid intima-media thickness (IMT) were determined. Results: Salusin-alpha levels were lower and the IMTs were higher in the SLE and SSc groups than in the HC group. The salusin-alpha level was correlated with neither the disease activity scores nor cytokine levels and IMT in the SLE and SSc groups, although it was correlated with triglyceride level in the SLE group (r=-0.564, p=0.012), and with HOMA-IR index in the HC group (r=0.485, p=0.019). Conclusion: The present preliminary study may support the idea that SSc leads to subclinical atherosclerosis, as in SLE. Moreover, it can be concluded that the decreased salusin-a levels in SLE and SSc may contribute to subclinical atherosclerosis. However, further studies with larger sample size are needed to demonstrate this contribution in SLE and SSc.en_US
dc.identifier.doi10.5152/eurjrheum.2014.004
dc.identifier.endpage17en_US
dc.identifier.issn2147-9720
dc.identifier.issn2148-4279
dc.identifier.issue1en_US
dc.identifier.pmid27708865en_US
dc.identifier.startpage14en_US
dc.identifier.urihttps://doi.org/10.5152/eurjrheum.2014.004
dc.identifier.urihttps://hdl.handle.net/11616/104115
dc.identifier.volume1en_US
dc.identifier.wosWOS:000218656100005en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAvesen_US
dc.relation.ispartofEuropean Journal of Rheumatologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectSystemic lupus erythematosusen_US
dc.subjectsystemic sclerosisen_US
dc.subjectatherosclerosisen_US
dc.subjectsalusin-alphaen_US
dc.titleSerum salusin-? levels in systemic lupus erythematosus and systemic sclerosisen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu