Source: Annual Congress 2002 - Asthma and COPD: pharmacology
Disease area: Airway diseases

Abstract

Background Studies show a dose-related interaction between SABAs and airway inflammation. SABAs enhance TH2 pathways, and conversely inflammatory cytokines impair beta receptor function. We aimed to study whether any negative effects of BA are enhanced in patients with increasing airway inflammation. Design. A randomised, double-blind, placebo-controlled trial. Run-in (2 weeks): all BA withheld. Phase 1 (2 weeks): patients received either salbutamol/ipratropium 100ug/20μ g (BA) or ipratropium 20μ g (placebo), each 4 puffs 4 times daily. Phase 2: same study treatments continued but inhaled steroids (ICS) stopped until loss of control occurred (LOC, determined using a priori criteria). Measurements Exhaled NO, spirometry, PD₂₀ methacholine, and AUC for post-methacholine FEV₁ salbutamol response were measured after the run-in, Phase 1, and Phase 2. Results. 5/36 patients were excluded because Phase 2 eNO did not rise. Results for 31 patients (16 BA; 15 placebo) were analysed. FEV₁ fell significantly during Phase 1 with BA but not placebo (0.27 vs 0.05 litres; p=0.006). During Phase 2, FEV₁ fell in both groups, but significantly more with BA (0.54 vs 0.33 litres; p=0.032). Changes in eNO were identical (10.4 and 10.9 ppb respectively). Time to LOC was significantly shorter with BA: 8.9 versus 16.8 days (p=0.03). There were no significant differences in AUC_0-45 or PD₂₀. Conclusion. Continuous use of high doses of inhaled SABA causes reduced lung function which is potentiated by increasing airway inflammation. The rate of onset of symptoms in such circumstances is also enhanced with BA. This emphasizes the risks of excessive SABA use in patients with unstable asthma and/or if compliance with ICS therapy is poor.

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J. M. Wraight, A. D. Smith, J. O. Cowan, E. M. Flannery, G. P. Herbison, D. R. Taylor (Dunedin, New Zealand). Short-acting beta-agonist (SABA) and airway inflammation: dynamic negative interaction. Eur Respir J 2002; 20: Suppl. 38, 752

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