title: In patients with chronic bronchitis a four week trial with inhaled steroids does not attenuate airway inflammation.
abstract: Systemic corticosteroids have been recommended as a therapeutic option in patients with moderate to severe COPD. In an early stage of the disease, i.e. chronic bronchitis with mild or no airflow obstruction, a trial with inhaled steroids could reveal potential benefits, particularly in terms of a modulation of airway inflammation. We therefore investigated the effect of inhaled fluticasone (1000 microg day(-1)) on markers of airway inflammation in 19 patients with chronic bronchitis (mean+/-SEM FEV1, 83.4+/-3.0% predicted; FEV1/VC, 67.5+/-2.4%) in a double-blind, cross-over, placebo-controlled manner. Visits were performed before and after two 4-week treatment periods. separated by a 4-week washout period. Lung function, the concentration of exhaled nitric oxide, differential cell counts in induced sputum and the number of cells positive for iNOS, as well as the levels of LDH, ECP, neutrophil elastase and IL-8 in sputum supernatants were determined. Although the total cell number decreased significantly after fluticasone (geometric mean 12.3 vs. 7.7 x 10(6)/ml; P<0.05) it was not significantly different from the change observed after placebo (14.2 vs. 10.6 x 10(6)/ml; n.s.). None of the other parameters showed statistically significant changes after fluticasone or placebo and the results did not depend on the presence of airway hyperresponsiveness. We conclude that in patients with chronic bronchitis short-term treatment with inhaled corticosterids did not improve lung function or inflammatory parameters to an extent which was statistically significant as compared to spontaneous variability.
authors.affiliation: Krankenhaus Grosshansdorf, Zentrum für Pneumologie und Thoraxchirurgie, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Loppow
authors.forename: M B
authors.initials: MB
authors.lastname: Schleiss
authors.forename: F
authors.initials: F
authors.lastname: Kanniess
authors.forename: C
authors.initials: C
authors.lastname: Taube
authors.forename: R A
authors.initials: RA
authors.lastname: Jörres
authors.forename: H
authors.initials: H
authors.lastname: Magnussen
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000730:Androstadienes / Q000008:administration & dosage* / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D015415:Biomarkers / Q000032:analysis; D001944:Breath Tests; D001991:Bronchitis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002452:Cell Count; D002908:Chronic Disease; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D000068298:Fluticasone; D005541:Forced Expiratory Volume; D006801:Humans; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000032:analysis; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D013183:Sputum / Q000166:cytology / Q000201:enzymology; D013997:Time Factors; D017211:Treatment Failure; D014797:Vital Capacity
chemical_list: D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D009569:Nitric Oxide; D000068298:Fluticasone; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II