BACKGROUND: Although beta2-adrenoceptor agonists are widely used in the treatment of asthma, a number of studies have suggested that their long-term use may exacerbate the condition. One possible mechanism for this stems from the in vitro observation that beta2-agonists increase IgE synthesis by human blood mononuclear cells. OBJECTIVE: We sought to examine the effect of regular beta2-agonist therapy on IgE production in vivo in human volunteers. METHODS:Placebo or salbutamol (8 mg BD) tablets were given in a double-blind, randomized fashion to 25 volunteers allergic to grass pollen throughout a period encompassing the UK grass pollen season (April through September). Levels of serum IgE were measured monthly, and nasal IgE was measured at the height and end of the season. Efficacy was assessed through monthly recordings of symptoms of blocked nose (vascular) and other symptoms of rhinitis (nonvascular). RESULTS: For the whole group the geometric mean of serum IgE levels rose from a baseline of 58.7 IU/mL (range, 0 to 1027 IU/mL) to 140 IU/mL (range, 12 to 878 IU/mL) at the height of the pollen season (P =.0001). There was no significant difference between the magnitude of the rise in IgE between the groups with a ratio of increase for salbutamol/placebo of 1.17 (confidence interval = 0.78 to 1.75). There was no change in nasal IgE levels. Total and nonvascular symptom scores were reduced by salbutamol, reaching statistical significance at the height of the pollen season (P <.05). CONCLUSION: An oral dose of the beta2-agonist salbutamol, sufficient to maintain therapeutic levels and provide clinical benefit, does not accentuate the seasonal increase of IgE in human atopic volunteers.
RCT Entities:
BACKGROUND: Although beta2-adrenoceptor agonists are widely used in the treatment of asthma, a number of studies have suggested that their long-term use may exacerbate the condition. One possible mechanism for this stems from the in vitro observation that beta2-agonists increase IgE synthesis by human blood mononuclear cells. OBJECTIVE: We sought to examine the effect of regular beta2-agonist therapy on IgE production in vivo in human volunteers. METHODS: Placebo or salbutamol (8 mg BD) tablets were given in a double-blind, randomized fashion to 25 volunteers allergic to grass pollen throughout a period encompassing the UK grass pollen season (April through September). Levels of serum IgE were measured monthly, and nasal IgE was measured at the height and end of the season. Efficacy was assessed through monthly recordings of symptoms of blocked nose (vascular) and other symptoms of rhinitis (nonvascular). RESULTS: For the whole group the geometric mean of serum IgE levels rose from a baseline of 58.7 IU/mL (range, 0 to 1027 IU/mL) to 140 IU/mL (range, 12 to 878 IU/mL) at the height of the pollen season (P =.0001). There was no significant difference between the magnitude of the rise in IgE between the groups with a ratio of increase for salbutamol/placebo of 1.17 (confidence interval = 0.78 to 1.75). There was no change in nasal IgE levels. Total and nonvascular symptom scores were reduced by salbutamol, reaching statistical significance at the height of the pollen season (P <.05). CONCLUSION: An oral dose of the beta2-agonist salbutamol, sufficient to maintain therapeutic levels and provide clinical benefit, does not accentuate the seasonal increase of IgE in human atopic volunteers.