Exhaled nitric oxide in pulmonary diseases: a comprehensive review.
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.
Barnes
Peter J
PJ
Airway Disease Section, Imperial College London, National Heart and Lung Institute, London, England.
Dweik
Raed A
RA
Gelb
Arthur F
AF
Gibson
Peter G
PG
George
Steven C
SC
Grasemann
Hartmut
H
Pavord
Ian D
ID
Ratjen
Felix
F
Silkoff
Philip E
PE
Taylor
D Robin
DR
Zamel
Noe
N
D001249:Asthma / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D001944:Breath Tests; D045853:Exhalation / Q000502:physiology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D009569:Nitric Oxide / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology / Q000628:therapy
D009569:Nitric Oxide