Serum Myeloperoxidase and Nitric Oxide Levels in Acute Exacerbation and Stable COPD Compared with Healthy Controls: A...

Background and Objectives: Oxidative stress and nitric oxide (NO)-related inflammatory activity contribute to chronic obstructive pulmonary disease (COPD), particularly during acute exacerbation of COPD (AECOPD). Myeloperoxidase (MPO) reflects neutrophil-related oxidative activity, whereas NO is involved in airway inflammation, endothelial regulation, and systemic inflammatory responses. This study compared serum MPO and NO levels among patients with AECOPD, patients with stable COPD, and healthy controls, and explored their discriminatory performance for distinguishing AECOPD from stable COPD. Materials and Methods: This cross-sectional comparative observational study prospectively enrolled 90 participants: 30 patients with AECOPD, 30 patients with stable COPD, and 30 healthy adult controls. COPD was confirmed by post-bronchodilator spirometry. Serum MPO and NO levels were measured using commercially available enzyme-linked immunosorbent assay kits. Group comparisons, exploratory subgroup analyses, correlation analyses, regression models, and receiver operating characteristic (ROC) curve analyses were performed. Results: Serum NO and MPO levels increased stepwise from healthy controls to stable COPD and AECOPD. Median serum NO levels were 109.79, 170.05, and 227.95 µmol/L, respectively, and median serum MPO levels were 4.14, 8.00, and 9.98 ng/mL, respectively (both p < 0.001). GOLD stage 3-4 disease was associated with higher levels of both biomarkers than GOLD stage 1-2 disease (both p < 0.001). In COPD-only exploratory logistic regression, serum NO and MPO were associated with AECOPD status. ROC analysis showed AUC values of 0.911 for serum NO and 0.811 for serum MPO, with no significant AUC difference by DeLong's test (p = 0.187). Conclusions: Serum MPO and NO levels were progressively higher across healthy control, stable COPD, and AECOPD states. These exploratory findings suggest that systemic oxidative and NO-associated inflammatory activity may reflect COPD clinical state; however, sample-specific ROC cut-offs require external validation before diagnostic use.