Serum Heparanase Level Is Decreased in Stable Coronary Artery Disease

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dc.contributor.authorGurbuz, Ahmet Seyfeddin
dc.contributor.authorOzturk, Semi
dc.contributor.authorEfe, Suleyman Cagan
dc.contributor.authorYilmaz, Mehmet Fatih
dc.contributor.authorYanik, Raziye Ecem
dc.contributor.authorYaman, Ali
dc.contributor.authorKirma, Cevat
dc.date.accessioned2024-02-23T14:26:40Z
dc.date.available2024-02-23T14:26:40Z
dc.date.issued2019
dc.departmentNEÜen_US
dc.description.abstractObjective: Heparanase (HPA), mammalian endo-beta-D-glu-cu-ronidase, separates heparan sulfate chains of proteoglycans and changes the structure of the extracellular matrix. We investigated whether serum levels of HPA differ in patients with stable coronary artery disease (SCAD) and subjects with normal coronary arteries. Methods: This study enrolled 92 patients with SCAD and 34 controls with normal coronary arteries. Levels of HPA were measured by a commercially available human HPA enzyme-linked immunosorbent assay kit. Results: Serum HPA levels were significantly lower in the SCAD group (137.5 [104.1-178.9] vs. 198.8 [178.2-244.9] pg/mL; p < 0.001). Serum HPA levels were significantly higher in subjects with diabetes mellitus (DM) compared to those without DM (p = 0.008). Levels of HPA were lower in the SCAD group, both in the diabetic and nondiabetic subgroups, as compared to controls (p < 0.001 for both subgroups). Levels of HPA positively correlated with fasting blood glucose (FBG) (r: 0.42; p < 0.001). In multiple logistic regression analysis, serum HPA level (odds ratio [OR]: 0.975; 95% confidence interval [CI]: 0.966, 0.985; p < 0.001) and FBG (OR: 1.028; 95% CI: 1.010, 1.047; p = 0.002) were independently associated with SCAD. The receiver operating characteristic curve showed that HPA levels less than 160.6 pg/mL predicted SCAD with 65% sensitivity and 97% specificity (AUC: 0.80; 95% CI: 0.728, 0.878; p < 0.001). Conclusion: Diabetes and FBG levels were closely associated with serum levels of HPA. Low serum levels of HPA may predict SCAD in both diabetic and nondiabetic populations.en_US
dc.identifier.doi10.1159/000503085
dc.identifier.endpage580en_US
dc.identifier.issn1011-7571
dc.identifier.issn1423-0151
dc.identifier.issue6en_US
dc.identifier.pmid31480068en_US
dc.identifier.scopus2-s2.0-85075813094en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage573en_US
dc.identifier.urihttps://doi.org/10.1159/000503085
dc.identifier.urihttps://hdl.handle.net/20.500.12452/14284
dc.identifier.volume28en_US
dc.identifier.wosWOS:000507400600011en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofMedical Principles And Practiceen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAtherosclerosisen_US
dc.subjectDiabetes Mellitusen_US
dc.subjectHeparanaseen_US
dc.titleSerum Heparanase Level Is Decreased in Stable Coronary Artery Diseaseen_US
dc.typeArticleen_US

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