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Oxidative stress in chronic obstructive pulmonary disease. Oxidative Stress Study Group.

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Published:1st Aug 1997
Author: Repine JE, Bast A, Lankhorst I.
Availability: Free full text
Ref.:Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):341-57.
DOI:10.1164/ajrccm.156.2.9611013

Chronic obstructive pulmonary disease (COPD) is a major worldwide health problem that has an increasing prevalence and mortality (1, 2). Oxidative stress, which can be defined as an increased exposure to oxidants and/or decreased antioxidant capacities, is widely recognized as a central feature of many diseases (3, 4). Considerable evidence now links COPD with increased oxidative stress (5, 6). The purpose of this review is to describe the role and origin of the oxidant–antioxidant disturbances that participate in the development of COPD. Our presentation also addresses ways of assessing the contribution of oxidants and identifies therapeutic approaches that could improve cellular oxidant–antioxidant balance in the lungs of COPD patients.

COPD is an obstructive airway disorder characterized by a slowly progressive and irreversible decrease in FEV1 (1, 2, 7). FEV1 decreases are caused by a narrowing of airway lumen diameters that develops as a result of varying perturbations in both airway and interstitial lung tissue. Airway abnormalities consist of increased wall thickening, intraluminal mucus accumulation, smooth muscle hypertrophy, and small airway lining fluid changes. Additional early lesions include inflammatory cell infiltration and goblet cell metaplasia.

The tissue component of emphysema is defined anatomically as the permanent destructive enlargement of airspaces distal to the terminal bronchioles with a concomitant loss of alveolar attachments (7). Emphysema is recognized in vivo by a decreased diffusing capacity (Dl CO) and reduced lung parenchymal density on chest radiograph and high-resolution computerized tomography.

Chronic bronchitis, a frequent feature of COPD, is a persistent recurrent bronchial hypersecretion that causes expectoration on most days for a minimum of 3 mo per year for at least two successive years (7). The pathology of chronic bronchitis is not unequivocal but primarily includes large airway mucus gland hyperplasia and inflammation; however, hypersecretion may occur without airway obstruction.

Patients with COPD often manifest some reversibility of airway obstruction following treatment with bronchodilators and airway hyperresponsiveness when given constrictor stimuli (8). These similar features often cause difficulties in differentiating COPD from asthma, especially in older patients. However, asthma is usually not related to cigarette smoking, and the reversibility of the obstructive pattern and airway hyperresponsiveness is a more common and more prominent occurrence in asthma than in COPD. In addition, emphysema and chronic hypoxemia are usually absent in asthma (8, 9).

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