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Beta agonist dose reduction in asthma
  1. Head, Division of Medicine
  2. The Queen Elizabeth Hospital Campus
  3. Woodville South
  4. South Australia 5011
    1. Division of Respiratory Medicine
    2. City Hospital
    3. Nottingham NG5 1PB
    4. UK

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      I write with regard to the article by Harrisonet al 1 who described their findings of reducing β agonist use in asthma patients with a methodology involving placebo inhalers. This study describes an interesting design as well as interesting outcomes with an apparent reduction in β agonist use without loss of control.

      There are several pieces of information which would make the article more useful in understanding how widely these results may be extrapolated. Firstly, the baseline inhaled corticosteroid use and the distribution between the two groups is important information. It would also help if the authors of the paper could clarify whether the patients continued on their usual maintenance inhaled corticosteroids throughout the study and whether the budesonide that was added at weeks 4–6 was in addition to baseline steroid use. The next issue concerns the instructions the patients were given about the use of β agonists. How many of them were told to use doses on a four times a day basis rather than as required? I also would like to know the proportion of patients who recognised they were receiving placebo with no active medication compared with those who were not aware that they had been switched to placebo. Finally, were specific instructions given to patients that they might need to ignore some some symptoms of breathlessness to enable the reduction in the use of β agonists?

      The above information would be helpful in understanding more completely the population and how applicable this dosage reduction scheme may be to other patients with asthma.


      author’s reply We thank Dr Ruffin for his interest and comments on our randomised placebo controlled trial of β agonist dose reduction in asthma.1-1 The mean (range) baseline inhaled steroid dose was 600 (300–1000) μg/day in the β agonist reduction group and 757 (200–1200) μg/day in the control group (difference not significant). Six subjects were taking budesonide, one fluticasone propionate, and the remainder beclomethasone dipropionate, and all but one via a metered dose inhaler. Dr Ruffin is correct in stating that the two weeks of budesonide was in addition to the subjects’ usual inhaled steroid, the dose of which was unchanged for the duration of the study. All subjects were given their usual dose of β agonist as terbutaline in four divided doses with additional terbutaline as required. We are unable to comment on the number of subjects who correctly guessed they were on placebo, but since the use of as required terbutaline was similar in each group there was probably not an important difference. Finally, subjects were not given any special instructions about ignoring their symptoms but all were informed that they had a 50% chance that their “regular” study inhaler would contain placebo. Clearly, one explanation for our findings is that many subjects take their β agonist out of habit or for non-asthma symptoms and can therefore withdraw it without leading to a deterioration in lung function or an increase in asthma symptoms.


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