title: Effect of low-dose ciclesonide on allergen-induced responses in subjects with mild allergic asthma.
abstract: BACKGROUND
  Inhalation of allergens by sensitized patients with asthma induces reversible airway obstruction, airway hyperresponsiveness, and eosinophilic airway inflammation. Attenuation of allergen-induced bronchoconstriction and inflammation has been used to examine the efficacy of therapeutic agents such as inhaled corticosteroids in asthma. Ciclesonide, a nonhalogenated inhaled corticosteroid being developed for the treatment of persistent asthma, remains inactive until cleaved by esterases in the lung.
  
  
  OBJECTIVE
  This study examined the effect of low doses of inhaled ciclesonide, 40 microg and 80 microg, on allergen-induced bronchoconstriction, serum eosinophil cationic protein, and eosinophilic airway inflammation.
  
  
  METHODS
  Twenty-one nonsmokers with mild atopic asthma completed a multicenter, randomized, 3-way crossover study comparing the effects of 7-day treatment of ciclesonide or placebo. Allergen-induced responses, including the early and late fall in FEV1, peripheral blood eosinophils, serum eosinophil cationic protein levels, and eosinophils in induced sputum were measured.
  
  
  RESULTS
  Ciclesonide 80 microg attenuated the early and late asthmatic responses, including the change in FEV1, serum eosinophil cationic protein, and sputum eosinophils measured at 24 hours postchallenge (P < .025). Ciclesonide 40 microg attenuated the late asthmatic responses and sputum eosinophils measured at 24 hours postchallenge (P < .025), with no effect on the early allergen-induced bronchoconstriction, 24-hour FEV1, or serum eosinophil cationic protein levels (P < .025).
  
  
  CONCLUSIONS
  With the exception of 24-hour postchallenge peripheral blood eosinophils, a low dose of ciclesonide, 80 microg, was effective in blocking all allergen-induced responses measured.
authors.affiliation: Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Gail M
authors.initials: GM
authors.lastname: Gauvreau
authors.forename: Louis Philippe
authors.initials: LP
authors.lastname: Boulet
authors.forename: Dirkje S
authors.initials: DS
authors.lastname: Postma
authors.forename: Tomotaka
authors.initials: T
authors.lastname: Kawayama
authors.forename: Richard M
authors.initials: RM
authors.lastname: Watson
authors.forename: MyLinh
authors.initials: M
authors.lastname: Duong
authors.forename: Francine
authors.initials: F
authors.lastname: Deschesnes
authors.forename: Jan G R
authors.initials: JG
authors.lastname: De Monchy
authors.forename: Paul M
authors.initials: PM
authors.lastname: O'Byrne
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology*; D001249:Asthma / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D018592:Cross-Over Studies; D047150:Eosinophil Cationic Protein / Q000097:blood; D005260:Female; D005541:Forced Expiratory Volume / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D011282:Pregnenediones / Q000627:therapeutic use*
chemical_list: D000485:Allergens; D011282:Pregnenediones; D047150:Eosinophil Cationic Protein; C120481:ciclesonide