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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Onur I. 1, Oz F. 1, Yildiz S. 2, Kuplay H. 3, Yucel C. 3, Sigirci S. 2, Elitok A. 1, Pilten S. 4, Kasali K. 5, Yasar Cizgici A. 1, Erentug V. 3, Dinckal H. M. 2
1 Department of Cardiology, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey;
2 Cardiology Clinic, Bagcilar Education and Research Hospital, Istanbul, Turkey;
3 Cardiovascular Surgery Clinic, Bagcilar Education and Research Hospital, Istanbul, Turkey;
4 Department of Biochemistry, Bagcilar Education and Research Hospital, Istanbul, Turkey;
5 Department of Biostatistics, Istanbul School of medicine, Istanbul University, Istanbul, Turkey
AIM: Recent evidence suggests that omentin-1, a visceral adipose-derived cytokine, may play a role in atherosclerosis The aim of this study was to evaluate whether serum omentin-1 levels are associated with peripheral artery disease (PAD) and its severity.
METHODS: The present study was cross-sectional and observational. We enrolled 123 patients with PAD and 50 age-matched subjects without PAD. The cardiovascular risk factors, ankle-brachial index (ABI), and serum omentin-1 levels were assessed in all participants.
RESULTS: Patients with PAD had significantly lower omentin-1 levels than those without PAD (206. ±48.4 vs. 345. ±80 ng/mL, respectively; 0.001). A correlation analysis revealed positive correlations between the omentin-1 level and the ABI ( 0.52, P=0.008). After adjusting for cardiovascular risk factors, a decreased omentin-1 level was found to be an independent predictor of both PAD and its severity as measured by ABI in multivariate logistic regression analysis.
CONCLUSION: The current study suggests a strong association between decreased serum omentin-1 levels and PAD and its severity. Thus, omentin-1 may be a novel biomarker for PAD.