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Chronic obstructive pulmonary disease

  • Nature Reviews Disease Primers 1, Article number: 15076 (2015)
  • doi:10.1038/nrdp.2015.76
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Abstract

Chronic obstructive pulmonary disease (COPD) is a common disease with high global morbidity and mortality. COPD is characterized by poorly reversible airway obstruction, which is confirmed by spirometry, and includes obstruction of the small airways (chronic obstructive bronchiolitis) and emphysema, which lead to air trapping and shortness of breath in response to physical exertion. The most common risk factor for the development of COPD is cigarette smoking, but other environmental factors, such as exposure to indoor air pollutants — especially in developing countries — might influence COPD risk. Not all smokers develop COPD and the reasons for disease susceptibility in these individuals have not been fully elucidated. Although the mechanisms underlying COPD remain poorly understood, the disease is associated with chronic inflammation that is usually corticosteroid resistant. In addition, COPD involves accelerated ageing of the lungs and an abnormal repair mechanism that might be driven by oxidative stress. Acute exacerbations, which are mainly triggered by viral or bacterial infections, are important as they are linked to a poor prognosis. The mainstay of the management of stable disease is the use of inhaled long-acting bronchodilators, whereas corticosteroids are beneficial primarily in patients who have coexisting features of asthma, such as eosinophilic inflammation and more reversibility of airway obstruction. Apart from smoking cessation, no treatments reduce disease progression. More research is needed to better understand disease mechanisms and to develop new treatments that reduce disease activity and progression.

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Acknowledgements

The authors thank J. Allinson from Imperial College, London, UK, for the design of Figure 8.

Figure 8: Mechanisms and effects of COPD exacerbations.
Figure 8

Increased inflammation caused by bacteria, viruses or pollutants results in inflammation of the airways that causes further airway narrowing and systemic inflammation. COPD, chronic obstructive pulmonary disease.

Author information

Affiliations

  1. Airway Disease Section, National Heart and Lung Institute, Imperial College, Dovehouse Street, London SW3 6LY, UK.

    • Peter J. Barnes
    •  & Jadwiga A. Wedzicha
  2. Division of Medical Genetics and Population Health, National Heart and Lung Institute, Imperial College, London, UK.

    • Peter G. J. Burney
  3. Channing Division of Network Medicine and Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

    • Edwin K. Silverman
  4. Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

    • Bartolome R. Celli
  5. Centre of Respiratory Medicine and Allergy, Manchester Academic Science Centre, University Hospital South Manchester NHS Foundation Trust, Manchester, UK.

    • Jørgen Vestbo
  6. Department of Respiratory Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.

    • Emiel F. M. Wouters

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Contributions

Introduction (P.J.B.); Epidemiology (P.G.J.B.); Mechanisms/pathophysiology (E.K.S. and P.J.B.); Diagnosis, screening and prevention (B.R.C.); Management (J.A.W. and J.V.); Quality of life (E.F.M.W.); Outlook (P.J.B.); Overview of Primer (P.J.B.).

Competing interests

P.J.B. has served on scientific advisory boards of AstraZeneca, Boehringer Ingelheim, Chiesi, Daiichi Sankyo, GlaxoSmithKline, Glenmark, Johnson & Johnson, Merck, Novartis, Takeda, Pfizer, Prosonix, RespiVert, Sun Pharmaceuticals, Teva and UCB, and has received research funding from Aquinox Pharmaceuticals, AstraZeneca, Boehringer Ingelheim, Chiesi, Daiichi Sankyo, GlaxoSmithKline, Novartis, Takeda, Pfizer and Sun Pharmaceuticals. He is also a cofounder of RespiVert (now part of Johnson & Johnson), which has discovered novel inhaled anti-inflammatory treatments for asthma and COPD. P.G.J.B. has received grants from the Medical Research Council, the Wellcome Trust, Public Health England and the British Lung Foundation, and serves on an advisory board for Novartis. B.R.C. has received grants to the Pulmonary and Critical Care Division of the Brigham and Women's Hospital to complete research studies in COPD from AstraZeneca. He has also received compensation for advisory board participation and/or consultancy from GlaxoSmithKline, Boehringer Ingelheim, Almirall, AstraZeneca, MedImmune, Takeda and Novartis. He does not have shares or interest in any company, nor does any member of his family. He has not received or had any relationship with the tobacco industry and has not participated in promotional talks. E.K.S. has received, in the past 3 years, honoraria and consulting fees from Merck and grant support and consulting fees from GlaxoSmithKline. J.V. has received funding for advising and presenting from AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Novartis, Takeda and Teva, and has received research funding from GlaxoSmithKline. J.A.W. has received research grant funding from Novartis, Takeda, Johnson & Johnson, Vifor Pharma and GlaxoSmithKline. She has received honoraria for lectures and/or advisory boards before January 2015 from GlaxoSmithKline, Novartis, Boehringer Ingelheim, AstraZeneca, Almirall, Pfizer, Chiesi and RespiVert. E.F.M.W. declares no competing interests.

Corresponding author

Correspondence to Peter J. Barnes.