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The association of elevated circulating endocan levels with lung function decline in COPD patients.
Background: Endocan is thought to be a novel inflammatory marker that is associated with a variety of inflammatory diseases. However, its role in the pathogenesis of COPD remains unclear. This study aims to explore the potential role of endocan in COPD.
Methods: In total, 27 healthy volunteers, 55 COPD patients and 36 acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients were included in the study. Basic demographic characteristics, clinical features and blood samples were collected. Magnetic luminex screening assays were used to detect the concentration of endocan, Fas and Fas ligand (Fas-L) in plasma. Differences between groups were compared using an Independent sample t -test, Welch's t -test, chi-squared test and Wilcoxon rank sum test. The correlations of plasma endocan with lung function parameters, Fas and Fas-L were analyzed by Pearson's partial correlation test (adjusted for age, gender, body mass index and smoking history) and multiple linear regression.
Results: Plasma endocan levels in COPD patients were significantly higher than those in healthy volunteers (509.7±18.25 pg/mL vs 434.8±18.98 pg/mL ( P =0.0124)), and AECOPD patients had the highest levels of endocan (524.7±27.18 pg/mL). Correlation analysis showed that circulating endocan had a negative correlation to FEV1 /FVC, FEV1 /predictive and FVC (adjusted r =-0.213, P =0.03; adjusted r =-0.209, P =0.034; and adjusted r =-0.300, P =0.002, respectively), and had a positive correlation to Fas (adjusted r =0.280, P =0.004).
Conclusion: Our study shows that elevated circulating endocan levels are associated with reduced lung ventilation function in COPD and AECOPD patients. In addition, endocan may influence apoptosis in COPD, suggesting that endocan may play a role in COPD pathogenesis.
Methods: In total, 27 healthy volunteers, 55 COPD patients and 36 acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients were included in the study. Basic demographic characteristics, clinical features and blood samples were collected. Magnetic luminex screening assays were used to detect the concentration of endocan, Fas and Fas ligand (Fas-L) in plasma. Differences between groups were compared using an Independent sample t -test, Welch's t -test, chi-squared test and Wilcoxon rank sum test. The correlations of plasma endocan with lung function parameters, Fas and Fas-L were analyzed by Pearson's partial correlation test (adjusted for age, gender, body mass index and smoking history) and multiple linear regression.
Results: Plasma endocan levels in COPD patients were significantly higher than those in healthy volunteers (509.7±18.25 pg/mL vs 434.8±18.98 pg/mL ( P =0.0124)), and AECOPD patients had the highest levels of endocan (524.7±27.18 pg/mL). Correlation analysis showed that circulating endocan had a negative correlation to FEV1 /FVC, FEV1 /predictive and FVC (adjusted r =-0.213, P =0.03; adjusted r =-0.209, P =0.034; and adjusted r =-0.300, P =0.002, respectively), and had a positive correlation to Fas (adjusted r =0.280, P =0.004).
Conclusion: Our study shows that elevated circulating endocan levels are associated with reduced lung ventilation function in COPD and AECOPD patients. In addition, endocan may influence apoptosis in COPD, suggesting that endocan may play a role in COPD pathogenesis.
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