“…Airways that respond only slightly to bronchodilators after a significant decline in lung function may have some degree of damage, such as loss of lung elastic recoil, hypertrophy of airway smooth muscle and thickening of the basement membrane, which may, in some instances, not be reversed either by bronchodilators or by corticosteroids [28,29]. It is not only in long-term studies that the acute bronchodilating response has been shown to be an important predictor of Short-term studies [11] 12 Beclomethasone Double-blind/"cross-over" -FEV1 ↑, but less than with prednisone 1,600, 2 weeks comparison [12] 83 Beclomethasone Double-blind/"cross-over" -FEV1, FVC and PEFR ↑, but less than with 1,500, 2 weeks comparison prednisolone [13,14] 127 Beclomethasone Double-blind/"cross-over" -FEV1, FVC and PEFR ↑, but less than with 1,500, 2 weeks comparison prednisolone [15] 107 Beclomethasone Double-blind/"cross-over" -FEV1, FVC and PEFR ↑, but less effective 1,500, 2 weeks comparison than prednisone in emphysema [16] 105 the long-term response to inhaled steroids. In short-term studies with systemic corticosteroids in patients with COPD, a significant relationship was also found between the bronchodilating response and the response to steroids [30][31][32].…”