title: Elevated levels of expired breath hydrogen peroxide in bronchiectasis.
abstract: Airway inflammation is important in the development and progression of many lung diseases, including bronchiectasis. Activation of inflammatory cells such as neutrophils, eosinophils, and macrophages induces a respiratory burst resulting in the production of reactive oxygen species such as hydrogen peroxide (H2O2). We have measured exhaled H2O2 in patients with documented bronchiectasis and investigated whether the concentration of H2O2 is related to the disease severity, as defined by lung function. We also investigated whether the concentrations of expired H2O2 were different in bronchiectatic patients who received inhaled corticosteroids compared with steroid-naïve patients. In 37 patients with bronchiectasis (mean age, 45 +/- 2.5 yr; FEV1, 59 +/- 3% pred), mean H2O2 concentration in exhaled breath condensate was significantly elevated as compared with the values in 25 age-matched (mean age, 42 +/- 2 yr) normal subjects (0.87 +/- 0.01 versus 0.26 +/- 0.04 microM, p < 0.001). There was a significant negative correlation between H2O2 and FEV1 (r = -0.76, p < 0.0001). Patients treated with inhaled corticosteroids had values of H2O2 similar to those of steroid-naïve patients (0.8 +/- 0.1 versus 0.9 +/- 0.1, p > 0.05). We conclude that H2O2 is elevated in exhaled air condensate of patients with bronchiectasis and is correlated with disease severity. Measurement of H2O2 may be used as a simple noninvasive method to monitor airway inflammation and oxidative stress.
authors.affiliation: Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College of Medicine, London, United Kingdom.
authors.forename: S
authors.initials: S
authors.lastname: Loukides
authors.forename: I
authors.initials: I
authors.lastname: Horvath
authors.forename: T
authors.initials: T
authors.lastname: Wodehouse
authors.forename: P J
authors.initials: PJ
authors.lastname: Cole
authors.forename: P J
authors.initials: PJ
authors.lastname: Barnes
mesh_terms: D000280:Administration, Inhalation; D000287:Administration, Topical; D000328:Adult; D000730:Androstadienes / Q000008:administration & dosage / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001987:Bronchiectasis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001991:Bronchitis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D018450:Disease Progression; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D000068298:Fluticasone; D005541:Forced Expiratory Volume / Q000502:physiology; D005938:Glucocorticoids; D006801:Humans; D006861:Hydrogen Peroxide / Q000032:analysis*; D008168:Lung / Q000503:physiopathology; D016676:Macrophages, Alveolar / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012119:Respiration; D016897:Respiratory Burst / Q000502:physiology
chemical_list: D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; D000068298:Fluticasone