Increased carbon monoxide in exhaled air of patients with cystic fibrosis

Abstract

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 noninvasive marker of airway inflammation and oxidative stress. Methods-Exhaled 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 (FEV 1 ) 43 (6)%, 14 of whom were receiving steroid treatment. Results-The 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 diVerence 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 diVerence 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 diVerence 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 diVerence 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 diVerence 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 diVerence 2.2 (95% CI -3.7 to -0.6), p<0.05). Conclusions-High 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. (Thorax 1999;54:917-920)

Assessment of exhaled carbon monoxide in exacerbations of chronic obstructive pulmonary disease

“…Thus, although marker levels in ex-smoker subjects should be interpreted with caution, smokers can be reliably discriminated from exsmokers using this device. Consequently, this eCO measurement methodology is widely accepted by experts on this field of research (12,13,21,26,(29)(30)(31)(32).…”

“…Increased concentration of eCO has been demonstrated in several inflammatory lung diseases including asthma (12), bronchiectasis (13), and cystic fibrosis (CF) (21). Several recent studies have reported the elevated levels of eCO in COPD as well (18,20).…”

“Haemoxygenase-1 induction and exhaled markers of oxidative stress in lung diseases”, summary of the ERS Research Seminar in Budapest, Hungary, September, 1999

“…The levels of exhaled CO are increased in patients with bronchiectasis and it is not reduced in patients treated with inhaled corticosteroids [46]. In cystic fibrosis (CF) there is an increase in the level of exhaled CO and this is further increased during infective exacerbations [47,48]. While in patients with stable CF inhaled steroids do not appear to affect the level of CO, oral corticosteroids are associated with lower values.…”

Breath Analysis: Potential for Clinical Diagnosis and Exposure Assessment

“…Recently, Montuschi (54 ) reviewed EBC analyses in patients with COPD and listed related breath markers, including H 2 O 2 , eicosanoids (leukotrienes, prostanoids, and isoprostanes), NO-derived products (S-nitrosothiols, nitrite, and nitrate), pH, aldehydes, and others. Moreover, CO has also been studied as a breath marker of asthma (55)(56)(57) and CF (58,59 ); H 2 O 2 as a breath marker of asthma (60,61 ), COPD (62,63 ), and CF (64,65 ); isoprostanes as breath markers of asthma (66 ), COPD (67 ), and CF (68 ); and nitrite/nitrate as breath markers of asthma (69 ) and CF (70,71 ).…”