Evaluating the Predictive Value of Endocan in Peripheral Arterial Disease
DOI:
https://doi.org/10.58600/eurjther2976Keywords:
Endocan, endothelial dysfunction, Inflammation, peripheral arterial diseaseAbstract
Objective: Endothelial dysfunction in the pathogenesis of peripheral arterial disease (PAD), one of the diseases driven by atherosclerosis, is increasingly being studied. This study aims to evaluate the potential of endocan levels to predict PAD.
Methods: A total of 76 patients were enrolled in this research. Of these, 46 were patients whose PAD was confirmed by imaging methods, while the control cohort comprised 30 individuals who were shown not to have PAD by imaging methods. Laboratory data, serum endocan levels were measured, and inflammatory indices (neutrophil-lymphocyte ratio and systemic immune-inflammation index) were calculated. Logistic regression and ROC analytical methods were applied to evaluate the effects of endocan and inflammatory indices on PAD.
Results: Significantly increased endocan levels were observed in the PAD group compared to the control group (1.34 ± 0.11 vs. 0.94 ± 0.23 ng/mL; p < 0.001). Inflammation index values were also higher in the PAD group versus the control cohort. Logistic regression demonstrated that diabetes mellitus and LDL cholesterol were the strongest traditional risk factors for PAD development. Endocan was also recognized as a standalone risk factor in the logistic regression analysis (OR: 1.862; 95% CI: 1.315–2.636). ROC analysis showed that the threshold value for endocan in PAD was 1.27 ng/mL (69.6% sensitivity and 62.3% specificity, AUC = 0.674).
Conclusion: Our study found that, in addition to conventional risk factors, endocan levels were also elevated in PAD patients. Furthermore, we established a threshold value of 1.27 ng/mL in imaging-confirmed PAD patients. This study highlights the role of endothelial dysfunction in PAD and suggests that endocan, in conjunction with traditional risk factors and inflammatory markers, may serve as a complementary biomarker for the disease. Our findings represent hypothesis-generating data that warrant validation in larger, prospective studies.
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