Reviews and feature articleTherapeutic approaches to asthma–chronic obstructive pulmonary disease overlap syndromes
Section snippets
Treating eosinophilic COPD
The presence of increased eosinophil counts in sputum (>3%) or blood (>400/dL) might predict a clinical response to inhaled corticosteroids (ICSs), and these patients can have increased airway reversibility.4, 5, 6, 7 These patients can have both asthma and COPD (because these are both common diseases), or they might represent a variant of COPD. It is appropriate to treat these patients with bronchodilators and ICSs. However, even high doses of oral corticosteroids might not suppress
Targeting neutrophilic inflammation
Increased airway neutrophils counts are found in patients with COPD, some patients with severe asthma, and smoking asthmatic patients, but it is not clear to what extent this inflammation contributes to disease expression. Neutrophils release reactive oxygen species, proteases, and inflammatory mediators, which might exacerbate the disease and are poorly responsive to corticosteroids. This suggests that reducing neutrophilic inflammation might provide clinical benefit, but this must be balanced
Reversing corticosteroid resistance
Resistance to the anti-inflammatory effects of corticosteroids might be an important factor in determining asthma severity and is a major barrier to effective therapy in patients with severe asthma, smoking asthmatic patients, and patients with COPD. Several molecular mechanisms have now been described to account for corticosteroid resistance in asthmatic patients, including activation of p38 MAPK, JNK and ERK activity, increased expression of an alternatively spliced variant of glucocorticoid
Bronchodilatation
Long-acting inhaled bronchodilators, including long-acting β2-agonists (LABAs) and long-acting muscarinic antagonists/anticholinergics (LAMAs), are the mainstay of treatment in patients with COPD and are equally effective because they reduce air trapping by relaxing airway smooth muscle as a result of reducing the effects of intrinsic cholinergic tone.154 Air trapping increases with exertion (dynamic hyperinflation), leading to exertional dyspnea, which is the major symptom of COPD.155 In
Future directions
The recognition that there are several phenotypes of asthma, COPD, and ACOS suggest that more specific treatments might be beneficial, particularly in patients whose symptoms are not controlled by maximal doses of currently recommended treatments, such as ICSs and bronchodilators. To select appropriate therapy will require biomarkers that are predictive of response to specific therapy. These include blood biomarkers, such as eosinophil counts and levels of plasma periostin and fraction of
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2023, Journal of Allergy and Clinical ImmunologyEpidemiology of Asthma-Chronic Obstructive Pulmonary Disease Overlap
2022, Immunology and Allergy Clinics of North AmericaCitation Excerpt :As our knowledge of the clinical phenotypes and underlying mechanisms within asthma, COPD, and Asthma-COPD Overlap improve, the epidemiology will continue to evolve. Given the continued lack of consensus definition for ACO a “diagnostic label–free” (ie, COPD vs asthma vs ACO) approach has been recommended 62 and others propose focusing on the unique phenotypes that have therapeutic and/or prognostic implications.63,64 Regardless, a consensus approach to the diagnosis of ACO is essential for generating meaningful and consistent worldwide epidemiologic information about this condition.
Prospects for COPD treatment
2021, Current Opinion in Pharmacologyp38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics
2023, Cell Communication and Signaling
Series editors: Joshua A. Boyce, MD, Fred Finkelman, MD, and William T. Shearer, MD, PhD
Supported by the NIHR Respiratory Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London, United Kingdom.
Disclosure of potential conflict of interest: P. J. Barnes has received research support from GlaxoSmithKline, AstraZeneca, Pfizer, Chiesi, Takeda, Nycomed/Takeda, Novartis, and Aquinox; has received consulting fees or honoraria from AstraZeneca, Chiesi, Novartis, Zambon, and Boehringer Ingelheim; has received fees for participation in review activities from GlaxoSmithKline; is on Scientific Advisory Boards for Boehringer Ingelheim and Pfizer; has consultant arrangements with Glenmark and Sun Pharma; has provided expert testimony on behalf of Boehringer Ingelheim and Teva; and has received payment for lectures from AstraZeneca, Nycomed, Chiesi, Novartis, and Pfizer.
Terms in boldface and italics are defined in the glossary on page 532.