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Effect of nasal triamcinolone acetonide on seasonal variations of bronchial hyperresponsiveness and bronchial inflammation in nonasthmatic children with seasonal allergic rhinitis.

AbstractBACKGROUND:
Recent evidence suggests that patients with allergic rhinitis have lower airway inflammation and a higher prevalence of bronchial hyperresponsiveness (BHR) regardless of asthma.
OBJECTIVE:
To investigate markers of lower airway inflammation in nonasthmatic children with seasonal allergic rhinitis (SAR) before and during pollen season and the effect of nasal triamcinolone acetonide on seasonal variations in these parameters.
METHODS:
Thirty-two nonasthmatic children with SAR in response to grass and/or weed pollens were recruited and separated into 2 groups. Group 1 was treated with triamcinolone acetonide (220 microg once daily) for 6 weeks, and group 2 received no intranasal corticosteroid treatment. Bronchial responsiveness to methacholine [concentration that caused a decrease in forced expiratory volume in 1 second of 20% (PC20)], eosinophil counts in sputum and peripheral blood, and eosinophil cationic protein (ECP) levels in sputum and serum were measured before and during grass pollen season.
RESULTS:
Twenty-eight patients completed the study. During the pollen season, methacholine PC20 significantly decreased in both groups when compared with the corresponding preseasonal values (P = .01 and P = .003, respectively). The mean percentage of sputum eosinophils increased significantly during the pollen season compared with preseasonal values in group 1 and group 2 (12.7% +/- 2.1% vs 16.5% +/- 2.1%, P = .007, and 11.0% +/- 2.0% vs 20.2% +/- 1.4%, P = .003, respectively). Median [interquartile ranges (IQR)] sputum ECP levels were significantly higher during the pollen season when compared with the preseasonal values in group 1 and group 2 [7.5 microg/L (3.5-36.0 microg/L) vs 35.5 microg/L (13.0-71.7 microg/L), P = .04, and 18.0 microg/L (6.0-36.0 microg/L) vs 69.0 microg/L (39.0-195.0 microg/L), P = .003, respectively], as were the serum ECP levels [6.0 microg/L (2.0-13.0 microg/L) vs 19.0 microg/L (14.0-43.5 microg/L), P = .004, and 6.0 microg/L (3.0-7.0 microg/L) vs 18.0 microg/L (6.0-36.0 microg/L), P = .001, respectively]. Although the mean number of eosinophils in blood increased during the pollen season in both groups, it was only significant in group 2 (70.0 +/- 20.0 vs 161.6 +/- 29.0, P = .02).
CONCLUSIONS:
Although prophylactic nasal corticosteroid treatment provides significant reduction of nasal symptoms and rescue antihistamine use, there is no significant prevention in the seasonal increase of bronchial inflammation and methacholine BHR.
AuthorsFazil Orhan, Bulent Enis Sekerel, Gonul Adalioglu, Munevver Pinar, Ayfer Tuncer
JournalAnnals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology (Ann Allergy Asthma Immunol) Vol. 92 Issue 4 Pg. 438-45 (Apr 2004) ISSN: 1081-1206 [Print] United States
PMID15104196 (Publication Type: Comparative Study, Evaluation Study, Journal Article)
Chemical References
  • Allergens
  • Biomarkers
  • Blood Proteins
  • Eosinophil Granule Proteins
  • Glucocorticoids
  • Ribonucleases
  • Triamcinolone Acetonide
Topics
  • Adolescent
  • Allergens (adverse effects)
  • Asthma (complications, drug therapy, physiopathology)
  • Biomarkers (blood)
  • Blood Proteins (metabolism)
  • Bronchial Hyperreactivity (drug therapy, etiology, physiopathology)
  • Bronchitis (complications, drug therapy, physiopathology)
  • Child
  • Child Welfare
  • Eosinophil Granule Proteins
  • Eosinophils (metabolism)
  • Female
  • Forced Expiratory Volume (drug effects)
  • Glucocorticoids (therapeutic use)
  • Humans
  • Leukocyte Count
  • Male
  • Pollen (adverse effects)
  • Respiratory Function Tests
  • Rhinitis, Allergic, Seasonal (complications, drug therapy, physiopathology)
  • Ribonucleases (metabolism)
  • Seasons
  • Sputum (chemistry, cytology, metabolism)
  • Statistics as Topic
  • Time Factors
  • Treatment Outcome
  • Triamcinolone Acetonide (therapeutic use)
  • Turkey

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