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Editorials: Point and Counterpoint |

Rebuttal From Dr Barnes

Peter J. Barnes, DM, Master FCCP
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURE: The authors have reported to CHEST the following: P. J. B. has served on the scientific advisory boards of AstraZeneca, Boehringer-Ingelheim, Chiesi, GlaxoSmithKline, Glenmark, Johnson & Johnson, Napp, Novartis, Takeda, Pfizer, Prosonix, Respivert, Teva, and Zambon and has received research funding from AstraZeneca, Boehringer-Ingelheim, Chiesi, Novartis, and Takeda.

Airway Disease Section, National Heart and Lung Institute, Imperial College, London, England

CORRESPONDENCE TO: Peter J. Barnes, DM, Master FCCP, Airway Disease Section, National Heart and Lung Institute, Dovehouse St, London SW3 6LY, UK


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(1):21-22. doi:10.1016/j.chest.2016.09.025
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We both agree that poor adherence is the major reason for poor control of asthma and that true severe refractory asthma is rare. Asthma may also be difficult to control because of poor inhaler technique, comorbidities, and exposure to exacerbating factors. Dr O’Byrne suggests that patients with truly refractory asthma compose 5% to 8% of all patients with asthma, but recent accurate estimates suggest a figure of less than 4%. Of these patients, only a proportion (about 30%) have increased eosinophils in induced sputum, whereas others have increased neutrophils, a mixed granulocytic pattern, or no increase in inflammatory cells and therefore are presumably much less likely to respond to a specific anti-eosinophilic therapy. However, to classify the inflammatory phenotype of asthma, it is necessary to study induced sputum. This is technically demanding (especially in patients with severe disease), time consuming, and expensive with respect to staff costs, and not all patients with asthma are able to produce a suitable sputum sample. Another problem is that these inflammatory phenotypes of asthma are not stable; in a recent study, the phenotype in about half of patients with asthma changed on repeated testing. This means that induced sputum analysis is not practical in clinical practice. Determination of fractional exhaled nitric oxide is less invasive, is easy to perform in the clinic, and reflects airway eosinophilic inflammation, but results are affected by several factors, particularly cigarette smoking and the use of inhaled corticosteroids. Indeed, fractional exhaled nitric oxide is often used currently as a measurement of adherence to corticosteroid therapy. However, nitric oxide analyzers are relatively expensive so may not be available in most clinical practices. The simplest approach would be to measure eosinophils in blood, which is a readily available test, but the relationship between eosinophils in blood (total or differential counts) to eosinophils in sputum and the airways is not yet clear. Furthermore, inhaled corticosteroid therapy reduces eosinophils in blood.

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