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      Influence of Comorbidities on the Survival of COPD Patients According to Phenotypes

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          Abstract

          Background

          Chronic obstructive pulmonary disease (COPD) usually occurs alongside other conditions. Few studies on comorbidities have taken into account the phenotypes of COPD patients. The objective of this study is to evaluate the prevalence of comorbidities included in the Charlson index and their influence on the survival of patients with COPD, taking phenotypes into account.

          Methods

          An observational study was conducted on a group of 273 patients who had COPD and underwent spirometry in the first half of 2011, with a median prospective follow-up period of 68.15 months. The survival of these patients was analyzed according to the presence of various comorbidities.

          Results

          Of the 273 patients, 93 (34.1%) died within the follow-up period. An increased presence of chronic ischemic heart disease (CIHD), chronic heart failure (CHF), chronic kidney disease (CKD), and malignancy was found in deceased patients. All of these conditions shorten the survival of COPD patients globally; however, when considering phenotypes, only CHF influences the exacerbator with chronic bronchitis phenotype, CKD influences the non-exacerbator phenotype, and malignancy influences the positive bronchodilator test (BDT) and exacerbator with chronic bronchitis phenotypes. In the multivariate model, advanced age (hazard ratio, HR: 1.05; p=0.001), CHF (HR: 1.74; p=0.030), and the presence of malignancy (HR: 1.78; p=0.010) were observed as independent mortality risk factors.

          Conclusion

          The survival is shorter in the presence of CIHD in overall COPD patients and also CHF, CKD, and malignancy for certain phenotypes. It is important to pay attention to these comorbidities in the comprehensive care of COPD patients.

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          Most cited references 33

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          Prevalence and outcomes of diabetes, hypertension and cardiovascular disease in COPD.

          Chronic obstructive pulmonary disease (COPD) is associated with important chronic comorbid diseases, including cardiovascular disease, diabetes and hypertension. The present study analysed data from 20,296 subjects aged > or =45 yrs at baseline in the Atherosclerosis Risk in Communities Study (ARIC) and the Cardiovascular Health Study (CHS). The sample was stratified based on baseline lung function data, according to modified Global Initiative for Obstructive Lung Disease (GOLD) criteria. Comorbid disease at baseline and death and hospitalisations over a 5-yr follow-up were then searched for. Lung function impairment was found to be associated with more comorbid disease. In logistic regression models adjusting for age, sex, race, smoking, body mass index and education, subjects with GOLD stage 3 or 4 COPD had a higher prevalence of diabetes (odds ratio (OR) 1.5, 95% confidence interval (CI) 1.1-1.9), hypertension (OR 1.6, 95% CI 1.3-1.9) and cardiovascular disease (OR 2.4, 95% CI 1.9-3.0). Comorbid disease was associated with a higher risk of hospitalisation and mortality that was worse in people with impaired lung function. Lung function impairment is associated with a higher risk of comorbid disease, which contributes to a higher risk of adverse outcomes of mortality and hospitalisations.
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            Oxidative stress in COPD.

            Oxidative stress is now recognized as a major predisposing factor in the pathogenesis of COPD. Existing therapies for COPD are ineffective at halting disease progression, with bronchodilators being the mainstay of pharmacotherapy, providing symptomatic relief only. It is, therefore, important for a better understanding of the underlying mechanisms by which oxidative stress drives disease pathogenesis to develop novel and more effective therapies. Antioxidant capacity in COPD is substantially reduced as a result of cigarette smoking and exacerbations, with oxidative stress persisting long after the cessation of cigarette smoking or exacerbation, due to the continued production of reactive oxygen species from endogenous sources. We discuss (1) how oxidative stress arises in the lung, (2) how it is neutralized, (3) what genetic factors may predispose to the development of COPD, and (4) how this impacts inflammation and autoimmunity in the development of emphysema and small airways disease. Finally, various strategies have been considered to neutralize the increased oxidative burden present in COPD. This review highlights why current antioxidant strategies have so far failed and what promising alternatives are on the horizon. Moreover, a number of studies have shown that there is no single "magic bullet" to combat oxidative stress, but instead a combination therapy, targeting oxidative stress in the various subcellular compartments, may prove to be more effective in COPD.
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              Identification and prospective validation of clinically relevant chronic obstructive pulmonary disease (COPD) subtypes.

              Chronic obstructive pulmonary disease (COPD) is increasingly considered a heterogeneous condition. It was hypothesised that COPD, as currently defined, includes different clinically relevant subtypes. To identify and validate COPD subtypes, 342 subjects hospitalised for the first time because of a COPD exacerbation were recruited. Three months after discharge, when clinically stable, symptoms and quality of life, lung function, exercise capacity, nutritional status, biomarkers of systemic and bronchial inflammation, sputum microbiology, CT of the thorax and echocardiography were assessed. COPD groups were identified by partitioning cluster analysis and validated prospectively against cause-specific hospitalisations and all-cause mortality during a 4 year follow-up. Three COPD groups were identified: group 1 (n=126, 67 years) was characterised by severe airflow limitation (postbronchodilator forced expiratory volume in 1 s (FEV(1)) 38% predicted) and worse performance in most of the respiratory domains of the disease; group 2 (n=125, 69 years) showed milder airflow limitation (FEV(1) 63% predicted); and group 3 (n=91, 67 years) combined a similarly milder airflow limitation (FEV(1) 58% predicted) with a high proportion of obesity, cardiovascular disorders, diabetes and systemic inflammation. During follow-up, group 1 had more frequent hospitalisations due to COPD (HR 3.28, p<0.001) and higher all-cause mortality (HR 2.36, p=0.018) than the other two groups, whereas group 3 had more admissions due to cardiovascular disease (HR 2.87, p=0.014). In patients with COPD recruited at their first hospitalisation, three different COPD subtypes were identified and prospectively validated: 'severe respiratory COPD', 'moderate respiratory COPD', and 'systemic COPD'.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                copd
                copd
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove
                1176-9106
                1178-2005
                30 October 2020
                2020
                : 15
                : 2759-2767
                Affiliations
                [1 ]Pulmonology Service, Gregorio Marañón General University Hospital , Madrid, Spain
                [2 ]Faculty of Medicine, Complutense University of Madrid , Madrid, Spain
                [3 ]Pulmonology Section, Infanta Leonor University Hospital , Madrid, Spain
                [4 ]Research Support Service, Gregorio Marañón Health Research Institute , Madrid, Spain
                [5 ]Preventive Medicine and Public Health Teaching and Research Unit, Health Sciences Faculty, Rey Juan Carlos University , Alcorcón, Madrid, Spain
                [6 ]Public Health and Maternal and Child Health Department, Faculty of Medicine, Complutense University of Madrid , Madrid, Spain
                [7 ]Gregorio Marañón Health Research Institute , Madrid, Spain
                Author notes
                Correspondence: Zichen Ji Pulmonology Service, Gregorio Marañón University General Hospital , Madrid28007, SpainTel +34 617 882 547 Email jizich72@gmail.com
                Article
                270770
                10.2147/COPD.S270770
                7608550
                © 2020 Ji et al.

                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).

                Page count
                Figures: 2, Tables: 12, References: 34, Pages: 9
                Funding
                Menarini supported this study with an unconditional scholarship. This research is a part of the work funded by the Madrid Society of Pneumology and Thoracic Surgery (XVIII Awards Edition, 2018) and the Spanish Society of Pneumology and Thoracic Surgery (project no. 733 of the 2018 edition).
                Categories
                Original Research

                Respiratory medicine

                survival, risk factors, comorbidities, phenotypes, copd, mortality

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