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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.

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      Blood Eosinophil Count and Hospital Readmission in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

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          Abstract

          Purpose

          This retrospective, observational cohort study investigated the association of blood eosinophil counts within 1 week of hospitalization for acute exacerbation of COPD (AECOPD) with subsequent risk of all-cause and COPD-related readmission from a large integrated health system.

          Patients and Methods

          Electronic medical records were extracted for index hospitalization for AECOPD at all Intermountain Healthcare hospitals. The primary outcome was the relationship of blood eosinophil count to 30-day all-cause readmission; secondary outcomes were 60-day, 90-day, and 12-month all-cause readmission, COPD-related readmission, and empiric derivation of the eosinophil count with the highest area under the curve (AUC) for predicting 30-day all-cause readmission.

          Results

          Of 2445 included patients, 1935 (79%) had a blood eosinophil count <300 cells/µL and 510 (21%) had a count ≥300 cells/µL. Using a 300-cells/μL threshold, there was no significant difference between high and low eosinophil groups in 30-day (odds ratio [OR]=1.05, 95% confidence interval [CI]=0.75–1.47) or 60-day (OR=1.15, 95% CI=0.88–1.51) all-cause readmissions. However, patients with greater (versus lesser) eosinophil counts had increased 90-day and 12-month all-cause readmissions (OR=1.35, 95% CI=1.06–1.72, and OR=1.32, 95% CI=1.07–1.62). COPD-related readmission rates were significantly greater for patients with greater (versus lesser) eosinophil counts at 30, 60, and 90 days and 12 months (OR range=1.52–1.97). A total of 70 cells/µL had the most discriminatory power to predict 30-day all-cause readmission (highest AUC).

          Conclusion

          Eosinophil counts in patients with COPD were not associated with a difference in 30-day all-cause readmissions. However, greater eosinophil counts were associated with increased risk of all-cause readmission at 90 days and 12 months and COPD-related readmission at 30, 60, and 90 days and 12 months. Patients with eosinophils <70 cells/μL had the lowest risk for 30-day all-cause readmission. Blood eosinophils in patients hospitalized with AECOPD may be a useful biomarker for the risk of hospital readmission.

          Most cited references37

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          Once-Daily Single-Inhaler Triple versus Dual Therapy in Patients with COPD

          The benefits of triple therapy for chronic obstructive pulmonary disease (COPD) with an inhaled glucocorticoid, a long-acting muscarinic antagonist (LAMA), and a long-acting β2-agonist (LABA), as compared with dual therapy (either inhaled glucocorticoid-LABA or LAMA-LABA), are uncertain.
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            Blood eosinophil count and exacerbations in severe chronic obstructive pulmonary disease after withdrawal of inhaled corticosteroids: a post-hoc analysis of the WISDOM trial

            Blood eosinophil counts might predict response to inhaled corticosteroids (ICS) in patients with chronic obstructive pulmonary disease (COPD) and a history of exacerbations. We used data from the WISDOM trial to assess whether patients with COPD with higher blood eosinophil counts would be more likely to have exacerbations if ICS treatment was withdrawn.
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              Acute exacerbations of chronic obstructive pulmonary disease: identification of biologic clusters and their biomarkers.

              Exacerbations of chronic obstructive pulmonary disease (COPD) are heterogeneous with respect to inflammation and etiology. Investigate biomarker expression in COPD exacerbations to identify biologic clusters and determine biomarkers that recognize clinical COPD exacerbation phenotypes, namely those associated with bacteria, viruses, or eosinophilic airway inflammation. Patients with COPD were observed for 1 year at stable and exacerbation visits. Biomarkers were measured in sputum and serum. Viruses and selected bacteria were assessed in sputum by polymerase chain reaction and routine diagnostic bacterial culture. Biologic phenotypes were explored using unbiased cluster analysis and biomarkers that differentiated clinical exacerbation phenotypes were investigated. A total of 145 patients (101 men and 44 women) entered the study. A total of 182 exacerbations were captured from 86 patients. Four distinct biologic exacerbation clusters were identified. These were bacterial-, viral-, or eosinophilic-predominant, and a fourth associated with limited changes in the inflammatory profile termed “pauciinflammatory.” Of all exacerbations, 55%, 29%, and 28% were associated with bacteria, virus, or a sputum eosinophilia. The biomarkers that best identified these clinical phenotypes were sputum IL-1β, 0.89 (area under receiver operating characteristic curve) (95% confidence interval [CI], 0.83–0.95); serum CXCL10, 0.83 (95% CI, 0.70–0.96); and percentage peripheral eosinophils, 0.85 (95% CI, 0.78–0.93), respectively. The heterogeneity of the biologic response of COPD exacerbations can be defined. Sputum IL-1β, serum CXCL10, and peripheral eosinophils are biomarkers of bacteria-, virus-, or eosinophil-associated exacerbations of COPD. Whether phenotype-specific biomarkers can be applied to direct therapy warrants further investigation.
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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
                23 October 2020
                2020
                : 15
                : 2629-2641
                Affiliations
                [1 ]Pulmonary and Critical Care Medicine Division, Intermountain Medical Center , Murray, UT, USA
                [2 ]Pulmonary and Critical Care Medicine, University of Utah , Salt Lake City, UT, USA
                [3 ]Intermountain Heart Institute at Intermountain Healthcare , Salt Lake City, UT, USA
                [4 ]Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine , Stanford, CA, USA
                [5 ]Health Economics Outcomes Research, AstraZeneca , Wilmington, DE, USA
                [6 ]Enterprise Analytics, Intermountain Healthcare , Salt Lake City, UT, USA
                Author notes
                Correspondence: Matthew J Hegewald Pulmonary and Critical Care Medicine Division, Intermountain Medical Center , 5121 S Cottonwood Street, Murray, UT84107, USATel +1-801-507-4870Fax +1-801-507-4792 Email matt.hegewald@imail.org
                Author information
                http://orcid.org/0000-0002-4163-5841
                http://orcid.org/0000-0002-2656-0263
                http://orcid.org/0000-0003-1587-4774
                Article
                251115
                10.2147/COPD.S251115
                7591040
                33122901
                e969530d-5cf4-4bf6-ba68-a2114ebf2a0c
                © 2020 Hegewald 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).

                History
                : 12 June 2020
                : 07 October 2020
                Page count
                Figures: 3, Tables: 9, References: 38, Pages: 13
                Funding
                Funded by: AstraZeneca (Wilmington, DE, USA);
                This study was funded by AstraZeneca (Wilmington, DE, USA).
                Categories
                Original Research

                Respiratory medicine
                aecopd,phenotype,biomarkers,eosinophils,electronic medical records
                Respiratory medicine
                aecopd, phenotype, biomarkers, eosinophils, electronic medical records

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