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      Chronic obstructive pulmonary disease

      , Prof, MD a , * , , MD a , , MD b

      Lancet (London, England)

      Elsevier Ltd.

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          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: β 2 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.

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          Most cited references 110

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          Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper.

           W MacNee,  ,  B Celli (2004)
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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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              Immunology of asthma and chronic obstructive pulmonary disease.

               Peter Barnes (2008)
              Asthma and chronic obstructive pulmonary disease (COPD) are both obstructive airway diseases that involve chronic inflammation of the respiratory tract, but the type of inflammation is markedly different between these diseases, with different patterns of inflammatory cells and mediators being involved. As described in this Review, these inflammatory profiles are largely determined by the involvement of different immune cells, which orchestrate the recruitment and activation of inflammatory cells that drive the distinct patterns of structural changes in these diseases. However, it is now becoming clear that the distinction between these diseases becomes blurred in patients with severe asthma, in asthmatic subjects who smoke and during acute exacerbations. This has important implications for the development of new therapies.
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                Author and article information

                Contributors
                Journal
                Lancet
                Lancet
                Lancet (London, England)
                Elsevier Ltd.
                0140-6736
                1474-547X
                5 February 2012
                7-13 April 2012
                5 February 2012
                : 379
                : 9823
                : 1341-1351
                Affiliations
                [a ]Respiratory Division, University Hospital, University of Leuven, Leuven, Belgium
                [b ]Fundació Clinic, Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Ciber de Enfermedades Respiratorias (Ciberes), Hospital Clinic, Barcelona, Spain
                Author notes
                [* ]Correspondence to: Prof Marc Decramer, Respiratory Division, University Hospital, University of Leuven, Herestraat 49, 3000 Leuven, Belgium marc.decramer@ 123456uzleuven.be
                Article
                S0140-6736(11)60968-9
                10.1016/S0140-6736(11)60968-9
                7172377
                22314182
                Copyright © 2012 Elsevier Ltd. All rights reserved.

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                Medicine

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