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Thorax 67:A6 doi:10.1136/thoraxjnl-2012-202678.013
  • Spoken sessions
  • Targets for asthma therapy

S7 Influence of Beta-2 Adrenoceptor Genotype on Response to Regular Racemic or Levosalbutamol in Steroid Treated Asthmatics

  1. BJ Lipworth
  1. University of Dundee, Dundee, United Kingdom

Abstract

Background Asthmatic patients receiving inhaled corticosteroids often take frequent add-on therapy with albuterol despite on-demand prescription. We wished to evaluate trough methacholine airway hyper-responsiveness (the primary outcome) following regular treatment with racemic salbutamol and levosalbutamol compared to placebo, in steroid treated asthmatics stratified according to beta-2 adrenoceptor 16 genotype.

Methods We performed a randomised, double-blind, placebo-controlled, triple crossover trial comparing 2 weeks of regular therapy with inhaled racemic salbutamol (200µg qid); levosalbutamol (100µg qid); or placebo on methacholine PC20 6 hours post dose in 30 persistent asthmatics (15 homozygous Arg16 and Gly16) receiving inhaled corticosteroids.

Results There was no rebound worsening of trough airway hyper-responsiveness to methacholine after chronic exposure to either racemic (p=0.53) or levosalbutamol (p=0.84) compared to placebo; nor between genotypes - as doubling dilution (dd) difference in methacholine PC20 from placebo (Figure 1): salbutamol/Arg16= 0.36dd (95% CI: –0.43, 1.15); salbutamol/Gly16=0.01dd (95% CI: –0.47, 0.49); levosalbutamol/Arg16=–0.01dd (95% CI: –0.89, 0.87); levosalbutamol/Gly16=0.28dd (95% CI: –0.22, 0.77). Both active treatments improved morning PEF in Gly16 (p=0.04) but not Arg16 patients (p=0.50); while evening PEF improved in both Gly16 (p<0.001) and Arg16 patients (p=0.006).

Abstract S7 Figure 1

Conclusions Chronic exposure to either racemic or levosalbutamol added to inhaled corticosteroids did not cause rebound worsening of airway hyper-responsiveness at trough compared to placebo; with no difference seen between beta-2 adrenoceptor 16 genotypes.