THE EFFECT OF REGULAR SALBUTAMOL ON LUNG-FUNCTION AND BRONCHIAL HYPERRESPONSIVENESS IN NORMAL SUBJECTS AND NONASTHMATIC ATOPIC SUBJECTS WITH ALLERGIC RHINITIS

Citation
D. Boothmanburrell et al., THE EFFECT OF REGULAR SALBUTAMOL ON LUNG-FUNCTION AND BRONCHIAL HYPERRESPONSIVENESS IN NORMAL SUBJECTS AND NONASTHMATIC ATOPIC SUBJECTS WITH ALLERGIC RHINITIS, Chest, 112(1), 1997, pp. 12-18
Citations number
31
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
112
Issue
1
Year of publication
1997
Pages
12 - 18
Database
ISI
SICI code
0012-3692(1997)112:1<12:TEORSO>2.0.ZU;2-S
Abstract
Background: The effects of regular inhaled beta-agonist treatment on l ung function remain a controversial issue. In an earlier study, the ad ministration of regular inhaled salbutamol resulted in negative change s in FEV1 not only in asthmatics, but also in nonasthmatic atopic subj ects. Objective: The aim of this study was to confirm these findings a nd also to examine whether regular inhaled salbutamol would increase b ronchial hyperresponsiveness in atopic or normal individuals. Design: The study was a randomized, double-blind, placebo-controlled, crossove r investigation. Participants: There were two groups: 10 normal health subjects (group A) and nine nonasthmatic atopic subjects (group B). I nterventions: Subjects received inhaled salbutamol or identical placeb o for periods of 6 weeks, the dose being increased in stepwise fashion at 2-week intervals. Measurements: Changes in lung function were asse ssed by measuring spirometric values, airways conductance, and changes in complete and partial expiratory flow volume curves. Changes in the se parameters following a methacholine challenge were used to assess b ronchial hyperresponsiveness. Results: No statistically significant di fferences in lung function or bronchial hyperresponsiveness were noted to occur as the result of treatment in either group. Conclusion: Our results do not support the view that regular inhaled salbutamol in nor mal or atopic subjects without asthma causes adverse changes in tbe ai rways.