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a Department of
Thoracic Medicine, b Department of
Cystic Fibrosis, c Imperial College School of Medicine at the
National Heart and Lung Institute, Dovehouse Street, London, SW3 6LY,
UK
Correspondence to: Professor P J Barnes.
Received 23 October 1998; Returned to authors 13 January 1999; Revised version received 18 June 1999; Accepted for publication 18 June 1999
BACKGROUND
Inflammation,
oxidative stress, and recurrent pulmonary infections are major
aggravating factors in cystic fibrosis. Nitric oxide (NO), a marker of
inflammation, is not increased, however, probably because it is
metabolised to peroxynitrite. Exhaled carbon monoxide (CO), a product
of heme degradation by heme oxygenase 1 (HO-1) which is induced by
inflammatory cytokines and oxidants, was therefore tested as a
non-invasive marker of airway inflammation and oxidative stress.
METHODSExhaled
CO and NO concentrations were measured in 29 patients (15 men)
with cystic fibrosis of mean (SD) age 25 (1) years, forced expiratory
volume in one second (FEV1) 43 (6)%, 14 of whom were
receiving steroid treatment.
RESULTSThe
concentration of exhaled CO was higher in patients with cystic fibrosis
(6.7 (0.6) ppm) than in 15 healthy subjects (eight men) aged 31 (3)
years (2.4 (0.4) ppm, mean difference 4.3 (95% CI 2.3 to 6.1),
p<0.001). Patients not receiving steroid treatment had higher CO
levels (8.4 (1.0) ppm) than treated patients (5.1 (0.5) ppm, mean
difference 3.3 (95% CI -5.7 to -0.9), p<0.01). Normal subjects had
higher NO levels (6.8 (0.4) ppb) than patients with cystic fibrosis
(3.2 (0.2) ppb, mean difference 3.8 (95% CI 2.6 to 4.9), p<0.05) and
were not influenced by steroid treatment (3.8 (0.4) ppb and 2.7 (0.3) ppb for treated and untreated patients, respectively, mean
difference 0.8 (95% CI -0.6 to 2.3), p>0.05). Patients homozygous
for the 
F508 CFTR mutation had higher CO and NO concentrations than
heterozygous patients (CO: 7.7 (1.8) ppm and 4.0 (0.6) ppm,
respectively, mean difference 3.7 (95% CI -7.1 to -0.3), p<0.05;
NO: 4.1 (0.5) ppb and 1.9 (0.7) ppb, respectively, mean difference
2.2 (95% CI -3.7 to -0.6), p<0.05).
CONCLUSIONSHigh
exhaled CO concentrations in patients with cystic fibrosis may reflect
induction of HO-1. Measurement of exhaled CO concentrations may be
clinically useful in the management and monitoring of oxidation and
inflammatory mediated lung injury.
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