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      Chronic obstructive pulmonary disease with mild airflow limitation: current knowledge and proposal for future research – a consensus document from six scientific societies

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          Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality and morbidity worldwide, with high and growing prevalence. Its underdiagnosis and hence under-treatment is a general feature across all countries. This is particularly true for the mild or early stages of the disease, when symptoms do not yet interfere with daily living activities and both patients and doctors are likely to underestimate the presence of the disease. A diagnosis of COPD requires spirometry in subjects with a history of exposure to known risk factors and symptoms. Postbronchodilator forced expiratory volume in 1 second (FEV 1)/forced vital capacity <0.7 or less than the lower limit of normal confirms the presence of airflow limitation, the severity of which can be measured by FEV 1% predicted: stage 1 defines COPD with mild airflow limitation, which means postbronchodilator FEV 1 ≥80% predicted. In recent years, an elegant series of studies has shown that “exclusive reliance on spirometry, in patients with mild airflow limitation, may result in underestimation of clinically important physiologic impairment”. In fact, exercise tolerance, diffusing capacity, and gas exchange can be impaired in subjects at a mild stage of airflow limitation. Furthermore, growing evidence indicates that smokers without overt abnormal spirometry have respiratory symptoms and undergo therapy. This is an essential issue in COPD. In fact, on one hand, airflow limitation, even mild, can unduly limit the patient’s physical activity, with deleterious consequences on quality of life and even survival; on the other hand, particularly in younger subjects, mild airflow limitation might coincide with the early stage of the disease. Therefore, we thought that it was worthwhile to analyze further and discuss this stage of “mild COPD”. To this end, representatives of scientific societies from five European countries have met and developed this document to stimulate the attention of the scientific community on COPD with “mild” airflow limitation. The aim of this document is to highlight some key features of this important concept and help the practicing physician to understand better what is behind “mild” COPD. Future research should address two major issues: first, whether mild airflow limitation represents an early stage of COPD and what the mechanisms underlying the evolution to more severe stages of the disease are; and second, not far removed from the first, whether regular treatment should be considered for COPD patients with mild airflow limitation, either to prevent progression of the disease or to encourage and improve physical activity or both.

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          Most cited references 115

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            The natural history of chronic airflow obstruction.

            A prospective epidemiological study of the early stages of the development of chronic obstructive pulmonary disease was performed on London working men. The findings showed that forced expiratory volume in one second (FEV1) falls gradually over a lifetime, but in most non-smokers and many smokers clinically significant airflow obstruction never develops. In susceptible people, however, smoking causes irreversible obstructive changes. If a susceptible smoker stops smoking he will not recover his lung function, but the average further rates of loss of FEV1 will revert to normal. Therefore, severe or fatal obstructive lung disease could be prevented by screening smokers' lung function in early middle age if those with reduced function could be induced to stop smoking. Infective processes and chronic mucus hypersecretion do not cause chronic airflow obstruction to progress more rapidly. There are thus two largely unrelated disease processes, chronic airflow obstruction and the hypersecretory disorder (including infective processes).
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              Chronic obstructive pulmonary disease

              Summary Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow obstruction that is only partly reversible, inflammation in the airways, and systemic effects or comorbities. The main cause is smoking tobacco, but other factors have been identified. Several pathobiological processes interact on a complex background of genetic determinants, lung growth, and environmental stimuli. The disease is further aggravated by exacerbations, particularly in patients with severe disease, up to 78% of which are due to bacterial infections, viral infections, or both. Comorbidities include ischaemic heart disease, diabetes, and lung cancer. Bronchodilators constitute the mainstay of treatment: β2 agonists and long-acting anticholinergic agents are frequently used (the former often with inhaled corticosteroids). Besides improving symptoms, these treatments are also thought to lead to some degree of disease modification. Future research should be directed towards the development of agents that notably affect the course of disease.

                Author and article information

                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
                29 August 2017
                : 12
                : 2593-2610
                [1 ]Pulmonary Unit, University of Verona, Verona, Italy
                [2 ]Respiratory Department, University Hospital Centre, Zagreb, Croatia
                [3 ]Pathology Unit, University of Verona, Verona, Italy
                [4 ]Department of Respiratory Medicine, Hospital Son Espases-IdISPa and CIBERES, Palma, Spain
                [5 ]University Clinic of Respiratory and Allergic Diseases, Golnik, Slovenia
                [6 ]First Department of Respiratory Medicine, Medical School of National and Kapodistrian University of Athens, Greece
                [7 ]Respiratory Medicine, Hospital Universitario Miguel Servet, CIBERES & IISAragon, Zaragoza, Spain
                [8 ]Pulmonary Unit, ULSS 22 Bussolengo, Italy
                [9 ]Jordanovac Department for Respiratory Diseases, University of Zagreb School of Medicine, University Hospital Centre, Zagreb, Croatia
                [10 ]First Department of Critical Care and Pulmonary Services, Evangelismos Hospital, University of Athens, Greece
                [11 ]Pneumology Department, Hospital Universitary Vall d’Hebron, Barcelona, Spain
                Author notes
                Correspondence: Andrea Rossi, UOC Pneumologia, Azienda Ospedaliera-Universitaria Integrata, 1 Piazzale Stefani, Verona 37126, Italy, Tel +39 045 812 2438, Email andrea.rossi@
                © 2017 Rossi et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( 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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