BackgroundMost guidelines recommend either a long-acting beta-agonist (LABA) plus an inhaled glucocorticoid or a long-acting muscarinic antagonist (LAMA) as the first-choice treatment for patients with chronic obstructive pulmonary disease (COPD) who have a high risk of exacerbations The role of treatment with a LABA–LAMA regimen in these patients is unclear MethodsWe conducted a 52-week, randomized, double-blind, double-dummy, noninferiority trial Patients who had COPD with a history of at least one exacerbation during the previous year were randomly assigned to receive, by inhalation, either the LABA indacaterol (110 μg) plus the LAMA glycopyrronium (50 μg) once daily or the LABA salmeterol (50 μg) plus the inhaled glucocorticoid fluticasone (500 μg) twice daily The primary outcome was the annual rate of all COPD exacerbations ResultsA total of 1680 patients were assigned to the indacaterol–glycopyrronium group, and 1682 to the salmeterol–fluticasone group Indacaterol–glycopyrronium showed not onl

https://www.nejm.org/doi/suppl/10.1056/NEJMoa1516385/suppl_file/nejmoa1516385_appendix.pdf

Indacaterol–Glycopyrronium versus Salmeterol–Fluticasone for COPD

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(14)62410-7.pdf

Effect of roflumilast on exacerbations in patients with severe chronic obstructive pulmonary disease uncontrolled by combination therapy (REACT): a multicentre randomised controlled trial

Update on Clinical Aspects of COPD A pair of review articles examines our current understanding of the biology, diagnosis, and treatment of chronic obstructive pulmonary disease. This article focus...

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Update on Clinical Aspects of Chronic Obstructive Pulmonary Disease

α1-Antitrypsin deficiency (A1ATD) is an inherited disorder caused by mutations in SERPINA1, leading to liver and lung disease. It is not a rare disorder but frequently goes underdiagnosed or misdiagnosed as asthma, chronic obstructive pulmonary disease (COPD) or cryptogenic liver disease. The most frequent disease-associated mutations include the S allele and the Z allele of SERPINA1, which lead to the accumulation of misfolded α1-antitrypsin in hepatocytes, endoplasmic reticulum stress, low circulating levels of α1-antitrypsin and liver disease. Currently, there is no cure for severe liver disease and the only management option is liver transplantation when liver failure is life-threatening. A1ATD-associated lung disease predominately occurs in adults and is caused principally by inadequate protease inhibition. Treatment of A1ATD-associated lung disease includes standard therapies that are also used for the treatment of COPD, in addition to the use of augmentation therapy (that is, infusions of human plasma-derived, purified α1-antitrypsin). New therapies that target the misfolded α1-antitrypsin or attempt to correct the underlying genetic mutation are currently under development.

Diego J. Maselli

Papers

Hospitalized Exacerbations of COPD: Risk Factors and Outcomes in the ECLIPSE Cohort