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      Sputum or blood eosinophil association with clinical measures of COPD severity in the SPIROMICS cohort

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          Abstract

          Background

          Eosinophils in blood and sputum in chronic obstructive pulmonary disease (COPD) have been associated with more frequent exacerbations, lower lung function, and corticosteroid responsiveness. We hypothesized increased eosinophils are associated with a severe COPD phenotype, including exacerbation frequency, and tested whether blood eosinophils reliably predict sputum eosinophils.

          Methods

          Comprehensive baseline data on SPIROMICS subjects, recruited for a range of COPD severity for smokers with ≥20 pack year history, included demographics, questionnaires, clinical assessments, quantitative computed tomography (QCT), blood and induced sputum.

          Findings

          Significantly, stratification by mean sputum eosinophils ≥1·25% (N=827) was associated with reduced FEV 1 % predicted (differences: 10% pre-bronchodilator, 4·7% post-bronchodilator), QCT density measures for emphysema and air trapping, and exacerbations treated with corticosteroids (p=0·002). In contrast, stratification by mean blood eosinophils ≥200/µL (N=2499) showed that FEV 1 % predicted was significant between low and high blood subgroups, but less than observed between sputum subgroups (blood eosinophil group differences: 4·2% pre-bronchodilator, 2·7% post-bronchodilator), slightly increased airway wall thickness (0·02 mm, p=0·032), greater symptoms (p=0·037), and wheezing (p=0·018), but no evidence of association with COPD exacerbations or other indices of severity. Blood eosinophils showed weak although significant association with sputum eosinophils (ROC AUC=0·64, p<0·001), but with a high false discovery rate (72%). Elevated sputum eosinophils, with or without blood eosinophils, were associated with lower lung function. Elevated blood eosinophils only in combination with elevated sputum eosinophils were associated with COPD exacerbations.

          Interpretation

          Stratification of SPIROMICS subjects by blood eosinophils alone showed minimal clinical differences and no association with exacerbations, whereas stratification by sputum eosinophils was associated with larger phenotypic differences and COPD exacerbations. Importantly, increased blood eosinophils did not reliably predict airway eosinophils in induced sputum.

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          Most cited references 22

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          Clinical Significance of Symptoms in Smokers with Preserved Pulmonary Function.

          Currently, the diagnosis of chronic obstructive pulmonary disease (COPD) requires a ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) of less than 0.70 as assessed by spirometry after bronchodilator use. However, many smokers who do not meet this definition have respiratory symptoms.
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            The clinical features of the overlap between COPD and asthma

            Background The coexistence of COPD and asthma is widely recognized but has not been well described. This study characterizes clinical features, spirometry, and chest CT scans of smoking subjects with both COPD and asthma. Methods We performed a cross-sectional study comparing subjects with COPD and asthma to subjects with COPD alone in the COPDGene Study. Results 119 (13%) of 915 subjects with COPD reported a history of physician-diagnosed asthma. These subjects were younger (61.3 vs 64.7 years old, p = 0.0001) with lower lifetime smoking intensity (43.7 vs 55.1 pack years, p = 0.0001). More African-Americans reported a history of asthma (33.6% vs 15.6%, p < 0.0001). Subjects with COPD and asthma demonstrated worse disease-related quality of life, were more likely to have had a severe COPD exacerbation in the past year, and were more likely to experience frequent exacerbations (OR 3.55 [2.19, 5.75], p < 0.0001). Subjects with COPD and asthma demonstrated greater gas-trapping on chest CT. There were no differences in spirometry or CT measurements of emphysema or airway wall thickness. Conclusion Subjects with COPD and asthma represent a relevant clinical population, with worse health-related quality of life. They experience more frequent and severe respiratory exacerbations despite younger age and reduced lifetime smoking history. Trial registration ClinicalTrials.gov: NCT00608764
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              The Asthma-COPD Overlap Syndrome.

              Although in textbooks asthma and chronic obstructive pulmonary disease (COPD) are viewed as distinct disorders, there is increasing awareness that many patients have features of both. This article reviews the asthma-COPD overlap syndrome.
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                Author and article information

                Journal
                101605555
                41464
                Lancet Respir Med
                Lancet Respir Med
                The Lancet. Respiratory medicine
                2213-2600
                2213-2619
                27 January 2018
                13 November 2017
                December 2017
                01 December 2018
                : 5
                : 12
                : 956-967
                Affiliations
                [1 ]Wake Forest School of Medicine, Winston-Salem, NC
                [2 ]Weill Cornell Medical College of Cornell University, New York, NY
                [3 ]VA Ann Arbor Healthcare System
                [4 ]University of Michigan, Ann Arbor, MI
                [5 ]University of North Carolina School of Medicine, Chapel Hill, NC
                [6 ]Johns Hopkins University, Baltimore, MD
                [7 ]University of California, San Francisco, CA
                [8 ]University of Arizona College of Medicine, Tucson, AZ
                [9 ]Columbia University/Presbyterian Hospital, New York, NY
                [10 ]University of North Carolina at Chapel Hill, Chapel Hill, NC
                [11 ]David Geffen School of Medicine, Los Angeles, CA
                [12 ]University of Iowa, Iowa City, IA
                [13 ]University of Utah Health Sciences Center, Salt Lake City, UT
                [14 ]Department of Veterans Affairs Medical Center, Salt Lake City, Utah
                Author notes
                Corresponding author: Annette T. Hastie, ahastie@ 123456wakehealth.edu , Center for Genomics and Personalized Medicine Research, One Medical Center Blvd, NRC-G70, Wake Forest School of Medicine, Winston-Salem, NC 27157, Phone: (336) 713-7522, Fax: (336) 713-7544
                Article
                NIHMS922126
                10.1016/S2213-2600(17)30432-0
                5849066
                29146301

                This manuscript version is made available under the CC BY-NC-ND 4.0 license.

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