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(Chest. 2004;126:138S-149S.)
© 2004 American College of Chest Physicians

Therapeutic Responses in Asthma and COPD*

Corticosteroids

Michael J. Larj, MD, FCCP and Eugene R. Bleecker, MD, FCCP

* From the Center for Human Genomics, Division of Pulmonary and Critical Care Medicine, Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to: Eugene Bleecker, MD, FCCP, Co-Director, Center for Human Genomics, Professor of Medicine, Wake Forest University School of Medicine, Center for Human Genomics, Medical Center Blvd, Winston-Salem, NC 27157-1008; e-mail: ebleeck{at}wfubmc.edu

The effects of inhaled corticosteroids (ICSs) in asthma include reduced severity of symptoms, improved pulmonary function, diminished bronchial hyperresponsiveness (BHR), prevention of exacerbations, and possible prevention of airway wall remodeling. Compared with an inhaled ß2-agonist, ICSs improve airway function and BHR, reduce bronchial-epithelium abnormalities, decrease bronchial inflammation, and reduce inflammatory-cell infiltration into the bronchial lamina propria; thus, they may prevent airway remodeling. In children, early use of ICSs may result in improved airway function over time. ICSs reduce use of prednisone, asthma medications, hospitalizations, and urgent-care visits. The primary side effects of ICSs in children are limited to transient reduction in growth. Compared with a leukotriene receptor antagonist (LTRA), ICSs produced a greater change from baseline in FEV1 and greater reductions in symptoms. A long-acting ß2-agonist (LABA) combined with an ICS produced greater improvements than does therapy with ICSs even at higher doses. In COPD, the therapeutic value of ICSs is not as clear. While clinical trials in patients with mild COPD have not shown a reduction in decline in FEV1 over time, other studies have shown that ICS therapy reduces exacerbations in patients with more severe COPD. Combination therapy with both ICS and LABA has recently been shown to be effective in COPD, where studies have documented additive improvement in FEV1. Overall, the same therapeutic approaches show clinical effectiveness in both asthma and COPD. This supports the hypothesis that there are some similarities in these obstructive airway diseases. Future approaches should further define phenotypes, perhaps based in part on pharmacogenetic factors that will guide anti-inflammatory therapy in asthma and COPD.

Key Words: bronchial hyperreactivity • COPD • FEV1 • inhaled corticosteroids • long-acting ß2-agonists • leukotriene receptor antagonists






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