EFFECT OF REGULAR INHALED SALBUTAMOL ON AIRWAY RESPONSIVENESS AND AIRWAY INFLAMMATION IN RHINITIC NONASTHMATIC SUBJECTS

Citation
Dw. Evans et al., EFFECT OF REGULAR INHALED SALBUTAMOL ON AIRWAY RESPONSIVENESS AND AIRWAY INFLAMMATION IN RHINITIC NONASTHMATIC SUBJECTS, Thorax, 52(2), 1997, pp. 136-142
Citations number
25
Categorie Soggetti
Respiratory System
Journal title
ThoraxACNP
ISSN journal
00406376
Volume
52
Issue
2
Year of publication
1997
Pages
136 - 142
Database
ISI
SICI code
0040-6376(1997)52:2<136:EORISO>2.0.ZU;2-N
Abstract
Background - Regular, inhaled beta(2) agonists may increase airway res ponsiveness in asthmatic subjects. The mechanism is not known but may be via an increase in airway inflammation. A study was undertaken to e xamine the effect of regular inhaled salbutamol on airway responsivene ss to methacholine and hypertonic saline, on the maximal response plat eau to methacholine, and on inflammatory cells in induced sputum in rh initic non-asthmatic subjects. Methods - Thirty subjects with a baseli ne maximal response plateau of >15% fall in forced expiratory volume i n one second (FEV(1)) entered a randomised, placebo controlled, parall el trial consisting of two weeks run in, four weeks of treatment, and two weeks washout. Methacholine challenges were performed at the begin ning of the run in period, before treatment, after treatment, and afte r washout. Hypertonic saline challenges were performed before and afte r treatment and induced sputum samples were collected for differential cell counting. Results - There was no change in airway responsiveness , maximal response plateau to methacholine, or in induced sputum eosin ophils or mast cells. The maximum fall in FEV(1) after hypertonic sali ne increased in the salbutamol group (median change 6.0%, interquartil e range (IQR) 11.0) but did not change in the placebo group (median ch ange 1.3%, IQR 5.5). Conclusions - Regular inhaled salbutamol for four weeks increases airway responsiveness to hypertonic saline but does n ot alter airway responsiveness to methacholine or cells in induced spu tum in nonasthmatic individuals with rhinitis. The relevance of these findings to asthmatic subjects has not been established.