DECREASED CONCENTRATION OF EXHALED NITRIC-OXIDE (NO) IN PATIENTS WITHCYSTIC-FIBROSIS

Citation
H. Grasemann et al., DECREASED CONCENTRATION OF EXHALED NITRIC-OXIDE (NO) IN PATIENTS WITHCYSTIC-FIBROSIS, Pediatric pulmonology, 24(3), 1997, pp. 173-177
Citations number
37
Categorie Soggetti
Respiratory System",Pediatrics
Journal title
ISSN journal
87556863
Volume
24
Issue
3
Year of publication
1997
Pages
173 - 177
Database
ISI
SICI code
8755-6863(1997)24:3<173:DCOEN(>2.0.ZU;2-Y
Abstract
Nitric oxide (NO) is produced by various cell types in the human respi ratory tract. Endogenously produced nitric oxide is detectable in the exhaled air of healthy individuals. Exhaled NO has been shown to be in creased in airway inflammation, most probably due to cytokine-mediated activation of NO synthases. To assess whether NO can serve as a marke r of inflammation in cystic fibrosis (CF) lung disease, we measured ex haled NO in CF patients with a chemiluminescence analyser. Single brea th measurements were performed in 27 stable CF patients (age range, 6- 40 years) and 30 non-smoking controls (age range, 6-37 years). Exhaled NO concentrations were 9.1 +/- 3.6 ppb in the controls and 5.9 +/- 2. 6 ppb (P < 0.001) in CF patients. To account for room air NO concentra tions on the measurement of exhaled NO, we also calculated the differe nce between exhaled NO and ambient NO concentrations. Difference value s were also significantly lower in CF compared with controls (P < 0.00 01). In CF patients there was a positive correlation between exhaled N O and forced vital capacity (r = 0.43, P = 0.033), suggesting that exh aled NO is lower in patients with severe lung disease than in those wi th mild disease. We conclude that measurements of exhaled NO in CF doe s not reflect activity of CF airway inflammation. The decreased concen trations of exhaled NO may be due to inhibitory effects of inflammator y cytokines on NO synthases in the airways and alveolar epithelial cel ls or to increased retention in airway secretions. (C) 1997 Wiley-Liss . Inc.