The Journal Club: COPD Exacerbations

Abstract

In this issue, I review articles that provide further insights into the pathogenesis and/or management of chronic obstructive pulmonary disease (COPD) exacerbations. Exacerbations remain a significant source of cost, morbidity and progression of disease. The current Global initiative for chronic Obstructive Lung Disease (GOLD) guidelines1 focus on symptoms and exacerbations as the major factors to consider in treatment escalation. In the earlier editions of COPD recommendations and guidelines, inhaled corticosteroids (ICSs) have played a central role in dealing with acute exacerbations. The most recent iteration of the (GOLD) guidelines suggests that long-acting muscarinic antagonists (LAMAs) are first line therapy for patients with a history of 2 or more exacerbations in the previous 12 months. If these fail then a combination with a long-acting beta-agonist (LABA) is recommended. The recommendation to try LAMAs or a LABA/LAMA combination before an ICS/LABA combination for treatment of exacerbations appears to be related in large part to evidence that there may be an increased risk of pneumonia with use of inhaled corticosteroids for at least some COPD patients. In the last Journal Club, I highlighted that there remains an ongoing debate with regard to whether there is a subset of patients for whom ICS/LABAs may be a preferred first choice. The first paper presented in this Journal Club, the TRINITY Trial, compares a new triple combination ICS/LABA/LAMAs versus the use of LAMA alone for prevention of COPD exacerbations. The second paper reviewed is the most recent American Thoracic Society/European Respiratory Society guidelines for treatment of acute exacerbations. It provides a thorough review of the literature regarding the evidence for some of the most common practices in the treatment of acute exacerbations, from use of oral steroids and antibiotics to in-home management with non-invasive ventilation. Finally, I have included an interesting paper that examines the potential role of secretory IgA deficiency in select small airways as a potential pathogenic mechanism for persistent small airway inflammation and reinfection in patients with frequent COPD exacerbations.