Improvement in Bronchodilation Following Deep Inspiration After a Course of High-Dose Oral Prednisone in Asthma

Abstract

Bronchodilation following deep inspiration is usually impaired in patients with asthma. This might be due to changes in airway mechanics in the presence of inflammation or structural changes within the airways. Although inhaled corticosteroid treatment has been shown to improve airway responses to deep inspiration in patients with asthma, airway inflammation can persist despite inhaled corticosteroid treatment, and thus could still influence the airway mechanics during deep breaths. We hypothesized that oral steroid treatment further optimizes deep inspiration-induced bronchodilation in clinically stable asthmatic patients who are receiving therapy with inhaled corticosteroids. Twenty-four atopic patients with mild-to-moderate persistent asthma (FEV1, > 70% predicted; provocative concentration of methacholine causing a 20% fall in FEV1 [PC20], < 8 mg/mL), who were treated with 250 to 2,000 mug of beclomethasone-dipropionate or equivalent, participated in a parallel-design, double-blind study. Before and after treatment with 0.5 mg/kg/d prednisone or placebo for 14 days, a methacholine challenge was performed. Deep inspiration-induced bronchodilation was measured by the ratio of flow at 40% of FVC on the flow-volume curve after maximal inspiration/flow at 40% of FVC on the flow-volume curve after partial (60% of FVC) inspiration (M/P ratio). The M/P ratio significantly increased from a mean of 1.31 (range, 1.0 to 1.7) to 1.49 (range, 1.1 to 2.3) in the prednisone group. Interestingly, the improvement in the M/P ratio did not correlate with an accompanying significant increase in PC20 for methacholine (mean change, 1.02; SD doubling dose, 0.97) and a decrease in exhaled nitric oxide (mean change, 14 parts per billion [ppb]; SD, 33.4 ppb). Systemic antiinflammatory treatment in addition to maintenance therapy with inhaled corticosteroids increases bronchodilation by deep inspiration in patients with mild-to-moderate persistent asthma. This suggests that residual inflammation impairs airway mechanics in asthma patients.