Inhaled corticosteroids in COPD - Author's reply (2)

AUTHORS’ REPLY We would like to thank Drs Brightling and Pavord for their interesting comments. As stated in our article, we enrolled only patients with stable COPD, diagnosed according to a recent European Consensus Conference, and none of them had a previous history of asthma.1 The percentage of sputum eosinophils in the global COPD study population (34 subjects; mean (SE) 2.7 (0.7)) was not significantly different from that of the healthy subjects (16 subjects; mean (SE) 0.98 (0.2)) by the Mann-Whitney U test (p = 0.08). Indeed, if we consider the treated and control groups separately, a significant increase in the proportion of sputum eosinophils is seen in both COPD groups compared with the healthy subjects (p = 0.02). We suggest that the sputum eosinophilia in our patients with smoking related COPD could be explained by their current smoking habit. In fact, recent experimental and clinical data seem to support the hypothesis that exposure to cigarette smoke can induce eosinophilic airway inflammation both in animals and humans.2 3 Although there was no overall change in the sputum eosinophil count after two months of treatment with beclomethasone dipropionate, we have analysed separately the seven subjects with eosinophils of >2% in the treated group. In these subjects, not only neutrophils but also sputum eosinophils decreased (from a mean (SE) of 4.5 (1.2)% to 2.0 (0.4)%) after two months of treatment, although the difference did not reach statistical significance (p = 0.06). Moreover, these subjects did not show a significant increase in FEV1 after two months of treatment with inhaled corticosteroids (from 60.1 (5.6)% to 64.9 (4.1)% predicted). We also analysed separately the subgroup of treated patients with COPD with sputum eosinophils