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Where current pharmacological therapies fall short in COPD: symptom control is not enough

CORRESPONDENCE: N. Roche Respiratory and Intensive Care MedicineHôtel-Dieu, 1, place du Parvis de Notre Dame, 75004 Paris, France, Fax: 33 142348448. E-mail: nicolas.roche{at}htd.aphp.fr

Chronic obstructive pulmonary disease (COPD) is a common and progressive condition that is currently the fourth leading cause of death worldwide. There is now a large body of evidence indicating that both pulmonary and systemic inflammation are present in patients with stable COPD and may underlie both respiratory symptoms and common comorbidities of this disease. Smoking cessation and long-term oxygen therapy have been shown to change the course of COPD and recent results obtained with the combination of fluticasone and salmeterol have indicated that it could decrease mortality and slow the decline in lung function in patients with this disease. However, some pharmacological treatments can significantly improve dyspnoea, exercise tolerance, limitations in activity, rate of exacerbations and quality of life (e.g. long-acting bronchodilators and inhaled corticosteroids combined with a long-acting ß₂-agonist). The ability of these agents to modify the rate of disease progression remains to be firmly established in large-scale, long-term trials.

The concept of disease modification itself in COPD may need to be revisited and more precisely defined in terms of markers and clinical outcomes, including extrarespiratory manifestations: agents that durably affect symptoms, activities, exacerbations and quality of life should probably be considered as disease modifiers. It is also reasonable to suggest that early diagnosis and treatment of patients with COPD might be the first and potentially most important disease-modifying intervention.

There is clearly a need for new therapies that directly target the specific inflammatory processes underlying chronic obstructive pulmonary disease and its pulmonary and extrapulmonary manifestations.

KEYWORDS: ß₂-agonists, chronic obstructive pulmonary disease, disease progression, inflammation, inhaled corticosteroid