Kerstjens and associates [1] found no effect after 18 months of inhaled steroids on the decrease in forced expiratory volume in 1 second (FEV₁) in a randomized controlled trial that included a similar number of patients treated with inhaled steroids. However, Dompeling and coworkers [2] reported a significantly slower rate of decline in prebronchodilator FEV₁ during 18 months of inhaled corticosteroid treatment in 56 patients with asthma (n = 28) or chronic obstructive pulmonary disease (COPD) (n = 28), compared with the same group before initiation of inhaled steroid treatment. They interpreted this result as evidence that inhaled corticosteroids "slowed the unfavorable course of asthma or COPD seen with bronchodilator therapy alone".

I question the validity of their interpretation that a decreased rate of decline of prebronchodilator FEV₁ indicates improvement in the unfavorable course of obstructive airway disease seen with bronchodilators alone. Spirometric evidence for irreversible airway obstruction, which develops at an accelerated rate in asthmatic patients, is best determined after maximal bronchodilator therapy [3]. Therefore, analysis of postbronchodilator FEV₁ rate of decline should be a more realistic reflection of the rate of change of maximal airway function than measurement of prebronchodilator FEV₁.

To illustrate this point, I have added postbronchodilator FEV₁ slopes to Figure 3 of the article by Dompeling and colleagues [2]. They interpreted their Figure as indicating that inhaled steroids may double the time before low levels of lung function are reached (Figure 1). As can be seen from the redrawn figure, their theoretical comparison requires that prebronchodilator FEV₁ be greater than postbronchodilator FEV₁ after year 8 or 9. This result occurs because the rate of decline in postbronchodilator FEV₁ was actually greater after initiation of inhaled steroids ( –120 mL/year) than before treatment with inhaled steroids ( –98 mL/year). This paradox casts doubt on the validity of their extrapolation.

View larger version (15K): [in this window] [in a new window]   Figure 1. Theoretical comparison between the effects of beclomethasone therapy and bronchodilator therapy on the time to development of chronic airflow limitation. Thin lines = prebronchodilator results from Dompeling and colleagues' [1] (Figure 3). Thick lines = postbronchodilator results, using the same data and assumptions of Dompeling and colleagues.

It is well established that therapy with inhaled corticosteroids improves asthma symptoms. The study of Dompeling and colleagues [2] showed decreased bronchial hyper-responsiveness in asthmatics and alleviation of symptoms and a decrease in the number of exacerbations in both asthmatics and patients with COPD, thus supporting this role for inhaled steroids. I suggest that the improvements in prebronchodilator FEV (₁) found in their study probably relate to these changes in bronchial hyper-reactivity, symptoms and exacerbations of asthma and COPD, rather than to the irreversible inflammatory damage that presumably underlies accelerated declines in maximal FEV₁ noted among asthmatic patients.