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Eur Respir J 2001; 17:934-938
Copyright ©ERS Journals Ltd 2001


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

K. Ansarin1, J.M. Chatkin1, I.M. Ferreira1, C.A. Gutierrez1, N. Zamel2 and K.R. Chapman2

1 Asthma Centre of the University Health Network, Toronto, Ontario, Canada and 2 Dept of Medicine, Division of Respiratory Medicine, University of Toronto, Toronto, Ontario, Canada

CORRESPONDENCE: K.R. Chapman, Suite 4-011 ECW, 399 Bathurst Street, Toronto, Ontario, Canada. Fax: 1 4166033456

Keywords: asthma, chronic obstructive pulmonary disease, diffusion capacity, forced expiratory volume in one second, nitric oxide

The following study was undertaken in order to determine how exhaled nitric oxide (eNO) levels in former smokers with chronic obstructive pulmonary disease (COPD) compared to eNO levels in patients with asthma and in healthy nonsmoking volunteers. The study also aimed to determine any relationship between eNO levels in COPD and: 1) conventional measures of lung function; and 2) inhaled corticosteroid (ICS) use.

In former smokers with COPD, nonsmokers with asthma and volunteers, eNO levels, spirometry, lung volumes, carbon monoxide diffusion capacity of the lung (DL,CO) and resting oxygen saturation (Sa,O2) were measured.

Median eNO was significantly higher among patients with COPD than among healthy volunteers (p=0.003) but lower than among patients with asthma (p<0.01). There was no significant difference in eNO levels between COPD patients using ICS and those not using ICS. By contrast, eNO was lower among asthma 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). Among patients with COPD, eNO was inversely correlated with forced expiratory volume in one second, DL,CO and Sa,O2, and was positively correlated with the residual lung volume/total lung capacity ratio. Among patients with asthma, no significant correlations were found.

Exhaled nitric oxide is increased in patients with chronic obstructive pulmonary disease, an increase that is influenced by structural abnormalities of tobacco-induced lung damage.







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