M Hoshino1, Y Nakamura. 1. Second Department of Internal Medicine, Toho University School of Medicine, Tokyo, Japan.
Abstract
BACKGROUND:Azelastine is an oral antiallergic compound but there is no direct evidence of its anti-inflammatory actions in bronchial asthma. We examined the effect of azelastine on inflammatory cells infiltrating the bronchial mucosa and clinical symptoms in atopic asthma in a double-blind, parallel, randomized study. METHODS: The study was completed by 13 subjects in theazelastine (4 mg/day) group and 11 subjects in theplacebo group. Treatments were randomly administered for 3 months. Each subject recorded daily asthma symptoms and peak expiratory flow (PEF). Lung function and bronchial responsiveness to methacholine were measured before and after treatment. Fiberoptic bronchoscopy was performed and bronchial biopsies taken from segmental carinae before and after treatment with azelastine or placebo. Using each monoclonal antibody for eosinophils, mast cells, macrophages, and T lymphocytes we performed immunohistological staining on biopsy specimens. RESULTS: Compared with the placebo-treated group, the azelastine-treated group exhibited significant improvement of asthma symptoms (p<0.01), PEF (p<0.01), PEF diurnal variation (p<0.001), excluding forced expiratory volume in 1 s or airway responsiveness. This was accompanied by a reduction of EG2(+) eosinophils (p<0.01), CD3(+) (p<0.001), CD4(+) (p<0.05), CD8(+) (p<0.05) T lymphocytes, and CD25(+)-activated T lymphocytes (p<0.001) in the bronchial mucosa. Significant correlations were found between clinical data and immunohistochemical parameters. CONCLUSION: These results demonstrated that the beneficial effects ofazelastine in bronchial asthma may result from modulation of local bronchial inflammatory cell infiltration.
RCT Entities:
BACKGROUND:Azelastine is an oral antiallergic compound but there is no direct evidence of its anti-inflammatory actions in bronchial asthma. We examined the effect of azelastine on inflammatory cells infiltrating the bronchial mucosa and clinical symptoms in atopic asthma in a double-blind, parallel, randomized study. METHODS: The study was completed by 13 subjects in the azelastine (4 mg/day) group and 11 subjects in the placebo group. Treatments were randomly administered for 3 months. Each subject recorded daily asthma symptoms and peak expiratory flow (PEF). Lung function and bronchial responsiveness to methacholine were measured before and after treatment. Fiberoptic bronchoscopy was performed and bronchial biopsies taken from segmental carinae before and after treatment with azelastine or placebo. Using each monoclonal antibody for eosinophils, mast cells, macrophages, and T lymphocytes we performed immunohistological staining on biopsy specimens. RESULTS: Compared with the placebo-treated group, the azelastine-treated group exhibited significant improvement of asthma symptoms (p<0.01), PEF (p<0.01), PEF diurnal variation (p<0.001), excluding forced expiratory volume in 1 s or airway responsiveness. This was accompanied by a reduction of EG2(+) eosinophils (p<0.01), CD3(+) (p<0.001), CD4(+) (p<0.05), CD8(+) (p<0.05) T lymphocytes, and CD25(+)-activated T lymphocytes (p<0.001) in the bronchial mucosa. Significant correlations were found between clinical data and immunohistochemical parameters. CONCLUSION: These results demonstrated that the beneficial effects ofazelastine in bronchial asthma may result from modulation of local bronchial inflammatory cell infiltration.
Authors: G M Walsh; L Annunziato; N Frossard; K Knol; S Levander; J M Nicolas; M Taglialatela; M D Tharp; J P Tillement; H Timmerman Journal: Drugs Date: 2001 Impact factor: 9.546