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      International Journal of COPD (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

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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.

          Most cited references104

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          Alternative projections of mortality and disability by cause 1990–2020: Global Burden of Disease Study

          The Lancet, 349(9064), 1498-1504
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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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              The nature of small-airway obstruction in chronic obstructive pulmonary disease.

              Chronic obstructive pulmonary disease (COPD) is a major public health problem associated with long-term exposure to toxic gases and particles. We examined the evolution of the pathological effects of airway obstruction in patients with COPD. The small airways were assessed in surgically resected lung tissue from 159 patients--39 with stage 0 (at risk), 39 with stage 1, 22 with stage 2, 16 with stage 3, and 43 with stage 4 (very severe) COPD, according to the classification of the Global Initiative for Chronic Obstructive Lung Disease (GOLD). The progression of COPD was strongly associated with an increase in the volume of tissue in the wall (P<0.001) and the accumulation of inflammatory mucous exudates in the lumen (P<0.001) of the small airways. The percentage of the airways that contained polymorphonuclear neutrophils (P<0.001), macrophages (P<0.001), CD4 cells (P=0.02), CD8 cells (P=0.038), B cells (P<0.001), and lymphoid aggregates containing follicles (P=0.003) and the absolute volume of B cells (P=0.03) and CD8 cells (P=0.02) also increased as COPD progressed. Progression of COPD is associated with the accumulation of inflammatory mucous exudates in the lumen and infiltration of the wall by innate and adaptive inflammatory immune cells that form lymphoid follicles. These changes are coupled to a repair or remodeling process that thickens the walls of these airways. Copyright 2004 Massachusetts Medical Society
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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
                c8f162c4-b6e5-4da3-99a1-a94427758153
                © 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.

                History
                : 15 May 2010
                Categories
                Review

                Respiratory medicine
                copd,emphysema,pulmonary function,beta-agonist,anti-inflammatory,pharmacotherapy in copd

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