“For now we see through a glass darkly;”

Corinthians I: 13 v.12

Research into chronic obstructive pulmonary disease (COPD), for so long the Cinderella disorder of respiratory medicine, has undergone something of a renaissance in the last 10 years, with an increased awareness of its high prevalence1 as well as its growing importance as a cause of death in the developing world.2Having achieved a measure of consensus on the most appropriate definition,3-5 more mechanistic studies have shown that inflammatory cell infiltration in the walls of large airways6 and the presence of pro-inflammatory cytokines in induced sputum are frequent findings in patients with COPD.7 ,8 The characteristics of the cellular and biochemical changes differ from those seen in asthma with a predominance of alveolar macrophages and a relative neutrophilia, whilst the lymphocytes in the airway wall show no evidence of the CD4+ predominance seen in asthmatic airways.6 Data from a variety of groups using different sampling methods confirm that active inflammation is present in the airways and in the alveoli9of patients with COPD at almost any stage of the disease. Inevitably, this begs the question of whether these processes can be modified and, given the substantial benefits seen in bronchial asthma, what might be the role of inhaled corticosteroids in the patient with COPD.

Data on the inflammatory changes seen in the airways of patients with COPD have been available for many years,10 although the scientific importance was not fully appreciated. Clinicians were aware that some patients with COPD improved dramatically after a course of oral corticosteroids—not just for exacerbations11 but even when clinically stable—and, as a result, empirical trials of corticosteroids have been recommended.12 Between 10% and 20% of patients show a “response” to this therapy with …