title: Effect of nasal triamcinolone acetonide on lower airway inflammatory markers in patients with allergic rhinitis.
abstract: BACKGROUND
  Allergic rhinitis (AR) and asthma are commonly associated, and similar underlying inflammatory processes link both diseases. AR, even in the absence of asthma, is associated with increased levels of exhaled nitric oxide (ENO) and hydrogen peroxide (H(2)O(2)) in exhaled breath condensate, 2 noninvasive markers of lower airway inflammation.
  
  
  OBJECTIVE
  We sought to evaluate the effect of treatment with the nasal steroid triamcinolone acetonide on ENO and exhaled H(2)O(2) in subjects with AR.
  
  
  METHODS
  We allocated 23 subjects in a randomized, double-blind, parallel-controlled fashion to 4-week treatment with triamcinolone acetonide (220 microg/d) or matching placebo.
  
  
  RESULTS
  ENO levels were greater in the subgroup with concomitant asthma (16/23 subjects) and decreased significantly with triamcinolone acetonide treatment in this subgroup of patients in comparison with patients receiving placebo. Breath condensate levels of H(2)O(2) were higher in patients with AR without asthma than in those with asthma but decreased significantly with triamcinolone acetonide treatment in both subgroups. No changes were observed in bronchial hyperresponsiveness, nasal and asthma symptoms, or peak expiratory flow with active treatment or placebo.
  
  
  CONCLUSIONS
  We conclude that treatment of AR with triamcinolone acetonide results in decrease of 2 noninvasive markers of lower airway inflammation, ENO and H(2)O(2), supporting that upper and lower airway inflammation should be seen as a continuum in subjects with AR with and without asthma. ENO might be a more specific marker of the lower airway inflammation present in asthma.
authors.affiliation: Asthma and Airway Centre of the Toronto Western Hospital, University Health Network, Division of Respiratory Medicine, University of Toronto, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada.
authors.forename: Alessandra
authors.initials: A
authors.lastname: Sandrini
authors.forename: Ivone M
authors.initials: IM
authors.lastname: Ferreira
authors.forename: Jose R
authors.initials: JR
authors.lastname: Jardim
authors.forename: Noe
authors.initials: N
authors.lastname: Zamel
authors.forename: Kenneth R
authors.initials: KR
authors.lastname: Chapman
mesh_terms: D000281:Administration, Intranasal; D000293:Adolescent; D000328:Adult; D000368:Aged; D001249:Asthma / Q000150:complications; D015415:Biomarkers; D016535:Bronchial Hyperreactivity / Q000188:drug therapy; D004311:Double-Blind Method; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D012119:Respiration; D012221:Rhinitis, Allergic, Perennial / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D006255:Rhinitis, Allergic, Seasonal / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D014222:Triamcinolone Acetonide / Q000008:administration & dosage*
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D009569:Nitric Oxide; D006861:Hydrogen Peroxide; D014222:Triamcinolone Acetonide