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      Influencing the decline of lung function in COPD: use of pharmacotherapy

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          Abstract

          Chronic obstructive pulmonary disease (COPD) is a common and deadly disease. One of the hallmarks of COPD is an accelerated decline in lung function, as measured by spirometry. Inflammation, oxidative stress and other pathways are hypothesized to be important in this deterioration. Because progressive airflow obstruction is associated with considerable morbidity and mortality, a major goal of COPD treatment has been to slow or prevent the accelerated decline in lung function. Until recently, the only known effective intervention was smoking cessation. However, newly reported large clinical trials have shown that commonly used medications may help slow the rate of lung function decline. The effect of these medications is modest (and thus required such large, expensive trials) and to be of clinical benefit, therapy would likely need to start early in the course of disease and be prolonged. Such a treatment strategy aimed at preservation of lung function would need to be balanced against the side effects and costs of prolonged therapy. A variety of newer classes of medications may help target other pathophysiologically important pathways, and could be used in the future to prevent lung function decline in COPD.

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          Most cited references 12

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          Targeted treatment in COPD: a multi-system approach for a multi-system disease

          Chronic obstructive pulmonary disease is a varied condition when examined from a number of different perspectives including factors which influence disease development, pathological process and clinical features. There may be a complex interaction between the degree by which each of these processes influences the development of COPD and the subsequent clinical phenotype with which the patient presents. The varied host response and subsequent clinical phenotype has generated much interest in recent years. It is possible that failure of treatment to impact on mortality and reverse the disease process is because of the heterogeneous nature of the condition. Identification and targeted treatment of clinical and pathological phenotypes within the broad spectrum of COPD may therefore improve outcome. This article will review previous work which has attempted to phenotype COPD and identify if specific treatment for these phenotypes has been shown to be of benefit. It will examine the work on pathological processes and clinical manifestations, both pulmonary and systemic, and will focus on pharmacological therapies.
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            Growth and aging of the normal human lung.

            The lung grows primarily by alveolar multiplication, but alveoli also double in size from infancy to adult life. The time at which alveolar multiplication ceases is obscure. As the lung ages it loses alveolar surface area due to alteration in the internal geometry of the lung. Alveolar wall tissue is also lost, thought to reflect loss of capillary bed.
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              Unexpected failure of anti-tumor necrosis factor therapy in chronic obstructive pulmonary disease.

               Peter Barnes (2007)
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2010
                2010
                3 June 2010
                : 5
                : 153-164
                Affiliations
                [1 ]Harvard Combined Pulmonary and Critical Care Fellowship, Harvard Medical School, Boston, MA, USA;
                [2 ]Pulmonary and Critical Care and Sleep Divisions, Brigham and Women’s Hospital, MA, USA
                Author notes
                Correspondence: Robert L Owens, Clinical and Research Fellow, Pulmonary and Critical Care and Sleep Divisions, Brigham and Women’s Hospital, 221 Longwood Avenue, Boston, MA 02115, USA, Tel +1 (617) 525-8711, Fax +1 (617) 732-7337, Email rowens@ 123456partners.org
                Article
                copd-5-153
                2898088
                20631815
                © 2010 Gladysheva et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

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