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      A new approach to assess COPD by identifying lung function break-points

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          Abstract

          Purpose

          COPD is a progressive disease, which can take different routes, leading to great heterogeneity. The aim of the post-hoc analysis reported here was to perform continuous analyses of advanced lung function measurements, using linear and nonlinear regressions.

          Patients and methods

          Fifty-one COPD patients with mild to very severe disease (Global Initiative for Chronic Obstructive Lung Disease [GOLD] Stages I–IV) and 41 healthy smokers were investigated post-bronchodilation by flow-volume spirometry, body plethysmography, diffusion capacity testing, and impulse oscillometry. The relationship between COPD severity, based on forced expiratory volume in 1 second (FEV 1), and different lung function parameters was analyzed by flexible nonparametric method, linear regression, and segmented linear regression with break-points.

          Results

          Most lung function parameters were nonlinear in relation to spirometric severity. Parameters related to volume (residual volume, functional residual capacity, total lung capacity, diffusion capacity [diffusion capacity of the lung for carbon monoxide], diffusion capacity of the lung for carbon monoxide/alveolar volume) and reactance (reactance area and reactance at 5Hz) were segmented with break-points at 60%–70% of FEV 1. FEV 1/forced vital capacity (FVC) and resonance frequency had break-points around 80% of FEV 1, while many resistance parameters had break-points below 40%. The slopes in percent predicted differed; resistance at 5 Hz minus resistance at 20 Hz had a linear slope change of −5.3 per unit FEV 1, while residual volume had no slope change above and −3.3 change per unit FEV 1 below its break-point of 61%.

          Conclusion

          Continuous analyses of different lung function parameters over the spirometric COPD severity range gave valuable information additional to categorical analyses. Parameters related to volume, diffusion capacity, and reactance showed break-points around 65% of FEV 1, indicating that air trapping starts to dominate in moderate COPD (FEV 1 =50%–80%). This may have an impact on the patient’s management plan and selection of patients and/or outcomes in clinical research.

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          Most cited references 19

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          Reference spirometric values using techniques and equipment that meet ATS recommendations.

          Forced expiratory volumes and flows were measured in 251 healthy nonsmoking men and women using techniques and equipment that meet American Thoracic Society (ATS) recommendations. Linear regression equations using height and age alone predict spirometric parameters as well as more complex equations using additional variables. Single values for 95% confidence intervals are acceptable and should replace the commonly used method of subtracting 20% to determine the lower limit of normal for a predicted value. Our study produced predicted values for forced vital capacity and forced expiratory volume in one second that were almost identical to those predicted by Morris and associates (1) when the data from their study were modified to be compatible with the back extrapolation technique recommended by the ATS. The study of Morris and colleagues was performed at sea level in rural subjects, whereas ours was performed at an altitude of 1,400 m in urban subjects. Either the present study or the study of Morris and co-workers, modified to back extrapolation, could be recommended for predicting normal values.
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            Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction.

            Chronic obstructive pulmonary disease is a leading global cause of morbidity and mortality that is characterised by inexorable deterioration of small airways obstruction with emphysema associated with cellular inflammation and structural remodelling. Other features include apoptosis as well as proliferation of cells, and both tissue repair and lack of tissue repair. Metalloprotease release, together with that of apoptotic factors, may underlie the emphysema, and, conversely, fibrosis of the small airways may be accounted for by the effects of growth factor activation. In advanced disease, influential factors include the development of autoimmunity, with activation of dendritic cells and T-helper cells of both type 1 and 2, and the senescence response. An inability of macrophages to ingest apoptosed cells and bacteria may exacerbate inflammatory responses. Systemic inflammation with concomitant cardiovascular disease and metabolic syndrome may reflect the effect of cigarette smoke on nonpulmonary cells. Corticosteroid resistance may be secondary to oxidative stress mechanisms, such as inactivation of histone deacetylases. The mechanisms of chronic obstructive pulmonary disease may be heterogeneous, according to severity, and clinical phenotypes need to be correlated with cellular and pathological processes. Treatments may be targeted to patients with specific mechanisms.
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              Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease

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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2015
                14 October 2015
                : 10
                : 2193-2202
                Affiliations
                [1 ]Respiratory Medicine and Allergology, Department of Clinical Sciences, Lund University, Lund, Sweden
                [2 ]Regional Cancer Center South, Skåne University Hospital, Lund, Sweden
                Author notes
                Correspondence: Göran Eriksson, Respiratory Medicine and Allergology, Department of Clinical Sciences, Lund University, 221 84 Lund, Sweden, Tel +46 733 299 929, Email goran.eriksson@ 123456med.lu.se
                [*]

                These authors contributed equally to this work

                Article
                copd-10-2193
                10.2147/COPD.S86059
                4610777
                © 2015 Eriksson et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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