Purpose Our study aimed to evaluate the relationship between exhaled nitric oxide (eNO) markers and obstructive sleep apnea (OSA) severity and verify the changes in eNO profiles among mild, moderate, and severe OSA subgroups. Methods This study was a cross-sectional and in-hospital population-based study. We investigated 123 OSA patients (17 mild, 23 moderate and, 83 severe OSA) in the department of respiratory diseases. Studied data included anthropometry, respiratory polygraphy, biological markers, spirometry, and multi-flow eNO measurements. Data analysis implied linear correlation, non-parametric ANOVA, and pair-wise comparison. Results No significant difference could be found among 3 OSA severity subgroups for FENO at – four sampling flow rates (50–350 mL/s). The bronchial production rate of NO (J’awNO) was proportionally increased, with median values of 11.2, 33.9, and 36.2 in mild, moderate, and severe OSA, respectively (p=0.010). The alveolar concentration of NO (CANO) changed with a non-linear pattern; it was increased in moderate (6.49) vs mild (7.79) OSA but decreased in severe OSA (5.20, p = 0.015). The only correction that could be established between OSA severity and exhaled nitric oxide markers is through J’AWNO (rho=0.25, p=0.02) and CANO (rho= 0.18, p=0.04). There was no significant correlation between FENO measured at three different flow rates and the OSA severity. We also found a weak but significant correlation between FENO 100 and averaged SpO2 (rho = 0.07, p= 0.03). Conclusion The present study showed that J’AWNO, which represents eNO derived from the central airway, is proportionally increased in more severe OSA, while eNO from alveolar space, indicated by CANO, was also associated with OSA severity and relatively lower in the most severe OSA patients. In contrast, stand-alone FENO metrics did not show a clear difference among the three severity subgroups.
Objective: The aim of the present study was to measure the correlation between the level of exhaled Nitric Oxide (NO) and Obstructive Sleep Apnea (OSA) severity and to evaluate its modification after Continuous Positive Airway Pressure (CPAP) treatment in severe OSA patients. Methods: It was a descriptive and cross-sectional study. Subjects were classified by mild-moderate or severe OSA. CPAP was used for severe OSA patients and followed up for 3 months. Exhaled NO was measured in the morning after the previous night of Respiratory Polygraphy (RPG) recording. Results: This study recruited 123 subjects, including 40 mild-moderate and 83 severe OSA patients. The level of maximum bronchial NO production (J’awNO) in patients with severe OSA was significantly higher than mild-moderate OSA [36.2 (6.1–92.2) vs. 19.6 (1.6-73.0) ppb; p=0.001)]. The level of concentration of NO in the gas phase of the alveolar (CANO) in patients with severe OSA was lower than mild-moderate OSA [5.2 (1.2-12.7) vs. 6.9 (0.8-14.0) ppb; p=0.002). The total flux of NO in the conducting airway compartment (J’awNO) and CANO were correlated with an apnea-hypopnea index (AHI) (rho=0.25 and p=0.02; rho= 0.18 and p=0.04, respectively). There was a weak significant correlation between J’awNO and nadir SpO2 in patients with OSA (rho = -0.22 and p= 0.023). After 3-month treatment with CPAP, the level of J’awNO was significantly reduced in patients with severe OSA [23.4 (12.9-44.5) vs. 33.1 (21.2-55.0); p<0.001. Conclusion: J'awNO is proportionally increased in patients with severe OSA and reduced after treatment with CPAP. Thus, J’awNO may be used as a relevant and surrogate biomarker of severe OSA.
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