Journal
CHEST
Volume 138, Issue 3, Pages 682-692Publisher
ELSEVIER
DOI: 10.1378/chest.09-2090
Keywords
-
Categories
Funding
- GE Analytical Instruments, Inc.
- Aperion Inc.
- Aerocrine, Ltd.
- Aerocrine, Ltd. Sweden
Ask authors/readers for more resources
The upregulation of nitric oxide (NO) by inflammatory cytokines and mediators in central and peripheral airway sites can be monitored easily in exhaled air. It is now possible to estimate the predominant site of increased fraction of exhaled NO (FENO) and its potential pathologic and physiologic role in various pulmonary diseases. In asthma, increased FENO reflects eosinophilic-mediated inflammatory pathways moderately well in central and/or peripheral airway sites and implies increased inhaled and systemic corticosteroid responsiveness. Recently, five randomized controlled algorithm asthma trials reported only equivocal benefits of adding measurements of FENO to usual clinical guideline management including spirometry; however, significant design issues may exist. Overall, FENO measurement at a single expiratory flow rate of 50 mL/s may be an important adjunct for diagnosis and management in selected cases of asthma. This may supplement standard clinical asthma care guidelines, including spirometry, providing a noninvasive window into predominantly large-airway-presumed eosinophilic inflammation. In COPD, large/central airway maximal NO flux and peripheral/small airway/alveolar NO concentration may be normal and the role of FENO monitoring is less clear and therefore less established than in asthma. Furthermore, concurrent smoking reduces FENO. Monitoring FENO in pulmonary hypertension and cystic fibrosis has opened up a window to the role NO may play in their pathogenesis and possible clinical benefits in the management of these diseases. CHEST 2010; 138(3):682-692
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available