Exhaled nitric oxide in chronic obstructive pulmonary disease: relationship to pulmonary function

Citation
K. Ansarin et al., Exhaled nitric oxide in chronic obstructive pulmonary disease: relationship to pulmonary function, EUR RESP J, 17(5), 2001, pp. 934-938
Citations number
14
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
EUROPEAN RESPIRATORY JOURNAL
ISSN journal
09031936 → ACNP
Volume
17
Issue
5
Year of publication
2001
Pages
934 - 938
Database
ISI
SICI code
0903-1936(200105)17:5<934:ENOICO>2.0.ZU;2-X
Abstract
The following study was undertaken in order to determine how exhaled nitric oxide (eNO) levels in former smokers with chronic obstructive pulmonary di sease (COPD) compared to eNO levels in patients with asthma and in healthy nonsmoking volunteers. The study also aimed to determine any relationship b etween eNO levels in COPD and: 1) conventional measures of lung function; a nd 2) inhaled corticosteroid (ICS) use. In former smokers with COPD, nonsmokers with asthma and volunteers, eNO lev els, spirometry, lung volumes, carbon monoxide diffusion capacity of the lu ng (DL,CO) and resting oxygen saturation (Sa,O-2) were measured. Median eNO was significantly higher among patients with COPD than among hea lth), volunteers (p=0.003) but lower than among patients with asthma (p <0. 01). There was no significant difference in eNO levels between COPD patient s using ICS and those not using ICS. By contrast, eNO was lower among asthm a patients who used ICS (median 32 parts per billion (ppb); 25-75% range 16 -54) than among asthma patients who did not (51 ppb; 32-87) (p=0.034). Amon g patients with COPD, eNO was inversely correlated with forced expiratory v olume in one second, DL,CO and Sa,O-2, and was positively correlated with t he residual lung volume/total lung capacity ratio. Among patients with asth ma, no significant correlations were found. Exhaled nitric oxide is increased in patients with chronic obstructive pulm onary disease, an increase that is influenced by structural abnormalities o f tobacco-induced lung damage.