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BMJ 2006;332:1202-1204 (20 May), doi:10.1136/bmj.332.7551.1202
William MacNee, professor of respiratory and environmental medicine
ELEGI, Colt Research, MRC Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh.
| The first 150 words of the full text of this article appear below. |
Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs. The latter represents the innate and adaptive immune responses to long term exposure to noxious particles and gases, particularly cigarette smoke. All cigarette smokers have some inflammation in their lungs, but those who develop COPD have an enhanced or abnormal response to inhaling toxic agents. This amplified response may result in mucous hypersecretion (chronic bronchitis), tissue destruction (emphysema), and disruption of normal repair and defence mechanisms causing small airway inflammation and fibrosis (bronchiolitis).
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Sagital slice of lung removed from a patient who received a lung transplant for COPD. Centrilobular lesions have coalesced to produce severe lung destruction in the upper lobe
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These pathological changes result in increased resistance to airflow in the small conducting airways, increased compliance of the lungs, air trapping, and progressive airflow obstructionall characteristic features of COPD.
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