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      International Journal of COPD (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

      39,063 Monthly downloads/views I 2.893 Impact Factor I 5.2 CiteScore I 1.16 Source Normalized Impact per Paper (SNIP) I 0.804 Scimago Journal & Country Rank (SJR)

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      A Proposed Approach to Chronic Airway Disease (CAD) Using Therapeutic Goals and Treatable Traits: A Look to the Future

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          Abstract

          Chronic airflow obstruction affects a wide range of airway diseases, the most frequent of which are asthma, COPD, and bronchiectasis; they are clearly identifiable in their extremes, but quite frequently overlap in some of their pathophysiological and clinical characteristics. This has generated the description of new mixed or overlapping disease phenotypes with no clear biological grounds. In this special article, a group of experts provides their perspective and proposes approaching the treatment of chronic airway disease (CAD) through the identification of a series of therapeutic goals (TG) linked to treatable traits (TT) – understood as clinical, physiological, or biological characteristics that are quantifiable using biomarkers. This therapeutic approach needs validating in a clinical trial with the strategy of identification of TG and treatment according to TT for each patient independently of their prior diagnosis.

          Most cited references55

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          T-helper type 2-driven inflammation defines major subphenotypes of asthma.

          Prescott G Woodruff, Barmak Modrek, David F Choy … (2009)
          T-helper type 2 (Th2) inflammation, mediated by IL-4, IL-5, and IL-13, is considered the central molecular mechanism underlying asthma, and Th2 cytokines are emerging therapeutic targets. However, clinical studies increasingly suggest that asthma is heterogeneous. To determine whether this clinical heterogeneity reflects heterogeneity in underlying molecular mechanisms related to Th2 inflammation. Using microarray and polymerase chain reaction analyses of airway epithelial brushings from 42 patients with mild-to-moderate asthma and 28 healthy control subjects, we classified subjects with asthma based on high or low expression of IL-13-inducible genes. We then validated this classification and investigated its clinical implications through analyses of cytokine expression in bronchial biopsies, markers of inflammation and remodeling, responsiveness to inhaled corticosteroids, and reproducibility on repeat examination. Gene expression analyses identified two evenly sized and distinct subgroups, "Th2-high" and "Th2-low" asthma (the latter indistinguishable from control subjects). These subgroups differed significantly in expression of IL-5 and IL-13 in bronchial biopsies and in airway hyperresponsiveness, serum IgE, blood and airway eosinophilia, subepithelial fibrosis, and airway mucin gene expression (all P < 0.03). The lung function improvements expected with inhaled corticosteroids were restricted to Th2-high asthma, and Th2 markers were reproducible on repeat evaluation. Asthma can be divided into at least two distinct molecular phenotypes defined by degree of Th2 inflammation. Th2 cytokines are likely to be a relevant therapeutic target in only a subset of patients with asthma. Furthermore, current models do not adequately explain non-Th2-driven asthma, which represents a significant proportion of patients and responds poorly to current therapies.
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            Low-dose inhaled corticosteroids and the prevention of death from asthma.

            S Suissa, P. Ernst, S Benayoun … (2000)
            Although inhaled corticosteroids are effective for the treatment of asthma, it is uncertain whether their use can prevent death from asthma. We used the Saskatchewan Health data bases to form a population-based cohort of all subjects from 5 through 44 years of age who were using antiasthma drugs during the period from 1975 through 1991. We followed subjects until the end of 1997, their 55th birthday, death, emigration, or termination of health insurance coverage; whichever came first. We conducted a nested case-control study in which subjects who died of asthma were matched with controls within the cohort according to the length of follow-up at the time of death of the case patient (the index date), the date of study entry, and the severity of asthma. We calculated rate ratios after adjustment for the subject's age and sex; the number of prescriptions of theophylline, nebulized and oral beta-adrenergic agonists, and oral corticosteroids in the year before the index date; the number of canisters of inhaled beta-adrenergic agonists used in the year before the index date; and the number of hospitalizations for asthma in the two years before the index date. The cohort consisted of 30,569 subjects. Of the 562 deaths, 77 were classified as due to asthma. We matched the 66 subjects who died of asthma for whom there were complete data with 2681 controls. Fifty-three percent of the case patients and 46 percent of the control patients had used inhaled corticosteroids in the previous year, most commonly low-dose beclomethasone. The mean number of canisters was 1.18 for the patients who died and 1.57 for the controls. On the basis of a continuous dose-response analysis, we calculated that the rate of death from asthma decreased by 21 percent with each additional canister of inhaled corticosteroids used in the previous year (adjusted rate ratio, 0.79; 95 percent confidence interval, 0.65 to 0.97). The rate of death from asthma during the first three months after discontinuation of inhaled corticosteroids was higher than the rate among patients who continued to use the drugs. The regular use of low-dose inhaled corticosteroids is associated with a decreased risk of death from asthma.
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              Outcomes in patients with chronic obstructive pulmonary disease and obstructive sleep apnea: the overlap syndrome.

              Santiago Carrizo, Ray M. Marín, Bartolome R Celli … (2010)
              Patients with chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) (overlap syndrome) are more likely to develop pulmonary hypertension than patients with either condition alone. To assess the relation of overlap syndrome to mortality and first-time hospitalization because of COPD exacerbation and the effect of continuous positive airway pressure (CPAP) on these major outcomes. We included 228 patients with overlap syndrome treated with CPAP, 213 patients with overlap syndrome not treated with CPAP, and 210 patients with COPD without OSA. All were free of heart failure, myocardial infarction, or stroke. Median follow-up was 9.4 years (range, 3.3-12.7). End points were all-cause mortality and first-time COPD exacerbation leading to hospitalization. After adjustment for age, sex, body mass index, smoking status, alcohol consumption, comorbidities, severity of COPD, apnea-hypopnea index, and daytime sleepiness, patients with overlap syndrome not treated with CPAP had a higher mortality (relative risk, 1.79; 95% confidence interval, 1.16-2.77) and were more likely to suffer a severe COPD exacerbation leading to hospitalization (relative risk, 1.70; 95% confidence interval, 1.21-2.38) versus the COPD-only group. Patients with overlap syndrome treated with CPAP had no increased risk for either outcome compared with patients with COPD-only. The overlap syndrome is associated with an increased risk of death and hospitalization because of COPD exacerbation. CPAP treatment was associated with improved survival and decreased hospitalizations in patients with overlap syndrome.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Chron Obstruct Pulmon Dis
                Journal ID (iso-abbrev): Int J Chron Obstruct Pulmon Dis
                Journal ID (publisher-id): copd
                Journal ID (pmc): copd
                Title: International Journal of Chronic Obstructive Pulmonary Disease
                Publisher: Dove
                ISSN (Print): 1176-9106
                ISSN (Electronic): 1178-2005
                Publication date (Electronic): 04 September 2020
                Publication date Collection: 2020
                Volume: 15
                Pages: 2091-2100
                Affiliations
                [1 ]Pneumology Service, University Hospital Lucus Augusti , Lugo, EOXI Cervo, Lugo, Monforte, Spain
                [2 ]Pneumology Service, Hospital Universitari Vall d’Hebron, Vall d’Hebron Institut de Recerca (VHIR), Vall d’Hebron Barcelona Hospital Campus, CIBERES , Barcelona, Spain
                [3 ]Pneumology Service, Hospital Universitario Virgen del Rocio , Seville, Spain
                [4 ]Pneumology Service, La Princesa University Hospital, Madrid, Research Institute La Princesa IIP , Madrid, Spain
                [5 ]Pneumology Service, Ramón y Cajal Hospital (Ramon y Cajal Health Research Institute, IRYCIS) , Madrid, Spain
                [6 ]Pneumology Service, Hospital Universitario Dr Peset , Valencia, Spain
                [7 ]Faculty of Medicine at the University of Santiago de Compostela, Pneumology Service of the University Clinical Hospital of Santiago de Compostela, CIBERES , Santiago de Compostela, Spain
                [8 ]Pneumology Service, Hospital de la Santa Creu i Sant Pau , Barcelona, Spain
                [9 ]Division of Respirology and Sleep Medicine, Queen's University , Canada, ON, Canada
                [10 ]Pneumology Service, Hospital Universitario Nuestra Señora de Candelaria , Santa Cruz De Tenerife, Spain
                [11 ]Pneumology Service, Hospital de Laredo , Laredo, Spain
                [12 ]Pneumology Service and Faculty of Medicine, Hospital Clínico San Carlos, Complutense University of Madrid , Madrid, Spain
                [13 ]Pneumology Service, Hospital Arnau de Vilanova , Valencia, Spain
                [14 ]Pneumology Service, Son Espases University Hospital, IdISBa, CIBERES, Clínica Quirón-Rotger , Palma, Spain
                Author notes
                Correspondence: Borja G Cosio Pneumology Service, Hospital Universitario Son Espases, IdISBa, CIBERES, Clínica Quirón-Rotger , Ctra. de Valldemossa 79, Palma de Mallorca07010, SpainTel +34 871 206714 Ext 76714Fax +34 871 909724 Email borja.cosio@ssib.es
                Author information
                http://orcid.org/0000-0003-2652-6847
                http://orcid.org/0000-0002-9850-9520
                http://orcid.org/0000-0002-0175-2824
                http://orcid.org/0000-0002-1689-3347
                http://orcid.org/0000-0001-5847-4784
                http://orcid.org/0000-0002-9615-6557
                http://orcid.org/0000-0003-2567-5496
                http://orcid.org/0000-0003-1703-1367
                http://orcid.org/0000-0003-0552-2484
                http://orcid.org/0000-0002-3890-2742
                http://orcid.org/0000-0002-6388-8209
                Article
                Publisher ID: 263430
                DOI: 10.2147/COPD.S263430
                PMC ID: 7481271
                PubMed ID: 32943862
                SO-VID: 5bc02c94-ecf2-4972-a265-5f0ca0d44a2e
                Copyright © © 2020 Pérez de Llano et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 19 May 2020
                Date accepted : 20 July 2020
                Page count
                Figures: 1, Tables: 2, References: 81, Pages: 10
                Categories
                Subject: Perspectives

                ScienceOpen disciplines: Respiratory medicine
                Keywords: airflow obstruction,biomarker,personalised medicine,copd asthma overlap
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: airflow obstruction, biomarker, personalised medicine, copd asthma overlap

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