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      Vital capacity and COPD: the Swedish CArdioPulmonary bioImage Study (SCAPIS)

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          Abstract

          Background

          Spirometric diagnosis of chronic obstructive pulmonary disease (COPD) is based on the ratio of forced expiratory volume in 1 second (FEV 1)/vital capacity (VC), either as a fixed value <0.7 or below the lower limit of normal (LLN). Forced vital capacity (FVC) is a proxy for VC. The first aim was to compare the use of FVC and VC, assessed as the highest value of FVC or slow vital capacity (SVC), when assessing the FEV 1/VC ratio in a general population setting. The second aim was to evaluate the characteristics of subjects with COPD who obtained a higher SVC than FVC.

          Methods

          Subjects (n=1,050) aged 50–64 years were investigated with FEV 1, FVC, and SVC after bronchodilation. Global Initiative for Chronic Obstructive Lung Disease (GOLD) COPD FVC was defined as FEV 1/FVC <0.7, GOLDCOPD VC as FEV 1/VC <0.7 using the maximum value of FVC or SVC, LLNCOPD FVC as FEV 1/FVC below the LLN, and LLNCOPD VC as FEV 1/VC below the LLN using the maximum value of FVC or SVC.

          Results

          Prevalence of GOLDCOPD FVC was 10.0% (95% confidence interval [CI] 8.2–12.0) and the prevalence of LLNCOPD FVC was 9.5% (95% CI 7.8–11.4). When estimates were based on VC, the prevalence became higher; 16.4% (95% CI 14.3–18.9) and 15.6% (95% CI 13.5–17.9) for GOLDCOPD VC and LLNCOPD VC, respectively. The group of additional subjects classified as having COPD based on VC, had lower FEV 1, more wheeze and higher residual volume compared to subjects without any COPD.

          Conclusion

          The prevalence of COPD was significantly higher when the ratio FEV 1/VC was calculated using the highest value of SVC or FVC compared with using FVC only. Subjects classified as having COPD when using the VC concept were more obstructive and with indications of air trapping. Hence, the use of only FVC when assessing airflow limitation may result in a considerable under diagnosis of subjects with mild COPD.

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          Most cited references 15

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          Asthma and asthma-like symptoms in adults assessed by questionnaires. A literature review.

          The first widely used questionnaire in respiratory epidemiology was the questionnaire from the Medical Research Council (MRC) of Great Britain. In the first version, from 1960, there were only a few questions about wheezing, but in later editions, more questions about asthma and asthma-like symptoms were added. The MRC questionnaire initiated the development of other questionnaires such as the European Community for Coal and Steel (ECSC) questionnaire of respiratory symptoms and the questionnaire from the American Thoracic Society and the Division of Lung Diseases (ATS-DLD-78). In Tucson, Ariz, a questionnaire was developed in the 1970s that was focused on the subject's own report of asthma. In Great Britain, a questionnaire was developed in the 1980s with the intention of finding the most valid symptom-based items for identifying asthma, "the IUATLD (1984) questionnaire." When judging the validity of a questionnaire, it is essential to understand sensitivity and specificity. Sensitivity is the fraction of the truly diseased subjects found to be diseased using the questionnaire. Specificity is the fraction of the truly healthy subjects found to be healthy using the questionnaire. Regarding questionnaires dealing with asthma, the situation is confusing because of the absence of any gold standard for asthma. The most usual mode of validation has been to test the questionnaire against the results of a clinical physiologic investigation, often a nonspecific bronchial challenge test. Another approach has been to compare the answers from the questionnaire with the clinical diagnoses of asthma. When validated in relation to bronchial challenge tests, the questions about self-reported asthma have a mean sensitivity of 36 percent (range, 7 to 80 percent) and a mean specificity of 94 percent (range, 74 to 100 percent). The questions about "physician-diagnosed asthma" have even higher specificity, 99 percent. When validated in relation to a clinical diagnosis of asthma, the mean sensitivity for the question about self-reported asthma was 68 percent in the reviewed studies (range, 48 to 100 percent). The specificity was 94 percent (range, 78 to 100 percent). One problem in using the presence of bronchial hyperreactivity (BHR) as a gold standard for asthma is that many people with BHR report no respiratory complaints. In other words, the presence of BHR is a measure with high sensitivity but low specificity for asthma. The effect of using a methacholine challenge test as a standard for the disease will thus be an underestimation of the sensitivity of the questionnaire.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Large scale questionnaire survey on respiratory health in Sweden: effects of late- and non-response.

            Participation rates in epidemiologic studies conducted with postal questionnaires have steadily declined since 1970s. This can lead to an increased risk for selection bias. The aim of this study was to examine cause and effect of non-response in a large cross sectional study assessing respiratory health in western Sweden. The study sample was 29,218. The response rate to the initial postal questionnaire was 33%. The response rates to subsequent postal reminders were 15%, 7% and 7% of eligible participants totalling a participation of 62%. Of those who did not respond to the postal survey, a random sample of 400 subjects were identified and contacted for interview by telephone. Non-responders did not differ significantly in prevalence of airway diseases or symptoms when compared with responders. Male sex, young age and smokers were underestimated among non-responders. No clear trends in prevalence of respiratory symptoms and report of asthma were found with delayed response to the postal survey. The proportion of smokers and men increased with increasing number of reminders. Letters reminding subjects about the study did increase the participation rate but did not alter the risk estimates. We conclude that with a response rate of 62%, our estimate of disease and symptom prevalence was not biased in this Swedish population. However, smoking was underestimated. No general trend for late-responders was seen and therefore we conclude that extrapolation of results to non-responders is not possible in our study. Causes of non-response were mainly due to circumstantial factors.
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              An official American Thoracic Society/European Respiratory Society statement: research questions in COPD.

              Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity, mortality, and resource use worldwide. The goal of this official American Thoracic Society (ATS)/European Respiratory Society (ERS) research statement is to describe evidence related to diagnosis, assessment and management; identify gaps in knowledge; and make recommendations for future research. It is not intended to provide clinical practice recommendations on COPD diagnosis and management. Clinicians, researchers, and patient advocates with expertise in COPD were invited to participate. A literature search of Medline was performed, and studies deemed relevant were selected. The search was not a systematic review of the evidence. Existing evidence was appraised and summarised, and then salient knowledge gaps were identified. Recommendations for research that addresses important gaps in the evidence in all areas of COPD were formulated via discussion and consensus. Great strides have been made in the diagnosis, assessment and management of COPD, as well as understanding its pathogenesis. Despite this, many important questions remain unanswered. This ATS/ERS research statement highlights the types of research that leading clinicians, researchers, and patient advocates believe will have the greatest impact on patient-centred outcomes. Copyright ©ATS/ERS 2015.
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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
                2016
                02 May 2016
                : 11
                : 927-933
                Affiliations
                [1 ]Section of Occupational and Environmental Medicine, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
                [2 ]Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University, Umeå, Sweden
                [3 ]Department of Radiology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
                [4 ]Department of Clinical Science, Malmö, Lund University, Lund, Sweden
                [5 ]Department of Respiratory Medicine and Department of Medicine and Health Sciences, Linköping University, Linköping, Sweden
                [6 ]Respiratory Medicine Unit, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden
                [7 ]Department of Internal Medicine/Lung Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
                [8 ]Department of Medical Sciences, Clinical Physiology and Respiratory, Allergy and Sleep Research, Uppsala University, Uppsala, Sweden
                [9 ]Department of Translational Medicine, Lund University, Malmö, Sweden
                [10 ]Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
                Author notes
                Correspondence: Kjell Torén, Department of Molecular and Clinical Medicine, Section of Occupational and Environmental Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 414, S-405 30 Gothenburg, Sweden, Email kjell.toren@ 123456amm.gu.se
                Article
                copd-11-927
                10.2147/COPD.S104644
                4859418
                27194908
                © 2016 Torén 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.

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