The association between allergic rhinitis and airway dysfunction and nasal endothelial damage and oxidative stress.

Abstract

Although lower airway hyperresponsiveness is present in approximately one in three patients with allergic rhinitis (AR), the underlying mechanism remains unclear. To evaluate nasal patency and pulmonary functions in AR independently of the presence of asthma and to investigate the relationships between these and nasal oxidative stress parameters and endothelial damage. Seventy adolescents with AR (AR group - 27 with asthma and 43 without asthma) and 30 healthy controls (HC group) were included in this prospective, cross-sectional study. Endocan and oxidative biomarkers [total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI)] in nasal lavage fluid specimens; peak nasal inspiratory flow (PNIF); fractional exhaled nitric oxide (FeNO), and impulse oscillometry (zR5, zR20, and R5-20 for resistance and zX5 and zX20 for reactance) were investigated. Nasal endocan, TOS, and OSI values were higher in the AR group and TAS in the HC group. There was no difference between AR groups with and without asthma in terms of nasal endocan and oxidative biomarkers. FeNO levels and airway resistance (zR5, zR20, and R5-20) were higher in the AR group than in the HC group. However, there was no difference between the groups in PNIF. X5 was higher among the AR without asthma than in the other groups. Correlation between OSI and R5-20 was observed in the AR group. In the linear regression model, (logged) OSI was significantly predicted (logged) R5-20. The airways of adolescents with AR without asthma were as much affected as those of the AR with asthma, and this effect was associated with nasal endothelial damage and an increase in oxidative stress.