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Thorax 1999;54:917-920 doi:10.1136/thx.54.10.917
  • Original article

Increased carbon monoxide in exhaled air of patients with cystic fibrosis

  1. P Paredia,
  2. P L Shahb,
  3. P Montuschia,
  4. P Sullivanb,
  5. M E Hodsonb,
  6. S A Kharitonova,
  7. P J Barnesa
  1. aDepartment of Thoracic Medicine, bDepartment of Cystic Fibrosis, cImperial College School of Medicine at the National Heart and Lung Institute, Dovehouse Street, London, SW3 6LY, UK
  1. Professor P J Barnes.
  • Received 23 October 1998
  • Revision requested 13 January 1999
  • Revised 18 June 1999
  • Accepted 18 June 1999

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 non-invasive 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 (FEV1) 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 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 ΔF508 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).

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.

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