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COPD is characterized by slowly progressive development of airflow limitation that is poorly reversible, in sharp contrast to asthma where there is variable airflow obstruction that is usually reversible spontaneously or with treatment (Barnes et al, 2000). A new definition of COPD has recently been formulated by the Global Initiative on Obstructive Lung Disease (GOLD): "a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases" (Pauwels et al, 2001). The disease is overviewed on-line in the Merck manual of diagnosis and therapy.

COPD encompasses chronic obstructive bronchitis, with obstruction of small airways, and emphysema with enlargement of airspaces and destruction of lung parenchyma, loss of lung elasticity and closure of small airways (see figures above). The relationship of the various major lung diseases is described in the inset to the right. The three overlapping circles represent patients with chronic bronchitis, emphysema, or asthma. The shaded area represents those with COPD. Patients with asthma whose airflow obstruction is completely reversible (subset 9) are not considered to have COPD. Often, patients with asthma whose airflow obstruction does not remit completely are almost impossible to differentiate from those who have chronic bronchitis and emphysema with partially reversible airflow obstruction and airway hyperreactivity. Therefore, patients with unremitting asthma are classified as having COPD (subsets 6, 7, and 8). Chronic bronchitis and emphysema with airflow obstruction usually occur together (subset 5), and some patients also have asthma (subset 8). Patients with asthma who are exposed to chronic irritation, as from cigarette smoke, may develop chronic productive cough, a feature of chronic bronchitis (subset 6). In the US, such patients are often said to have asthmatic bronchitis or asthmatic COPD. Patients with chronic bronchitis or emphysema without airflow obstruction (subsets 1, 2, and 11) are not classified as having COPD. The major feature of these conditions are productive cough of more than three months duration for more than two successive years; this reflects mucus hypersecretion. Patients with airway obstruction due to diseases with known etiology or specific pathology, such as cystic fibrosis or bronchiolitis fibrosa obliterans (subset 10), are not included in this definition.

COPD is one of the commonest chronic diseases word-wide, yet accurate statistics on its prevalence are hardly available. Recommended sources of information are the American Lung Association and the WHO. The WHO-World estimates that COPD currently represents the 6th most common disease (Lopez & Murray, 1998). Today, 600 million people suffer from COPD, with some three million dying from the disease each year. Air pollution (particularly indoor air pollution from burning fuels), poor diet, and occupational exposures all increase the risk of developing COPD. By far the greatest risk factor is however smoking which increases the risk of developing COPD by up to 10-fold and this habit is thought to account for 80-90% of COPD cases. There are 1100 million smokers in the world and this figure is increasing particularly in developing countries. This factor and the aging population had led to analysts suggesting that COPD will be the 5th most common cause of death by 2020 (Lopez & Murray, 1998). In the US up to 30-35 million people suffer from COPD and according to the American Lung Association up to half of these patients are undiagnosed. COPD is also common in Europe and in the UK for example, approximately 4% of men and 2% of women over 45 years are affected. It is a common cause of hospital admissions and one of the commonest causes of certified illness.

Rational therapy depends on understanding the underlying disease process. COPD is characterized by an accelerated decline of lung function. This occurs in all individuals as a natural process of aging however the process is more rapid in smokers especially in a sub-set of smokers who are for whatever reason more susceptible to loss of function. There has been only slow progress in understanding the cell and molecular mechanisms of COPD. However, it is now recognized that this disease involves a chronic inflammation in small airways and lung parenchyma, with the involvement of neutrophils, macrophages and cytotoxic (CD8+) T-lymphocytes. This inflammation results in fibrosis with narrowing of small airways (chronic obstructive bronchitis) and lung parenchymal destruction due to the action of various proteases, such as neutrophil elastase and matrix metalloproteinases (emphysema). This inflammation is quite different from that seen in asthma, indicating that different treatments are likely to be needed (Barnes et al, 2000b).

Current management of COPD is largely symptomatic and is described in the GOLD guidelines (Pauwels et al, 2001). It is important to encourage cessation of smoking and nicotine replacement therapy may help. The mainstay of current therapy is bronchodilators. Inhaled anticholinergics (ipratropium bromide four times daily or oxitropium bromide three times daily) are more effective than short-acting inhaled b 2-agonists and should be given on a regular basis, with short-acting b 2-agonists (salbutamol, terbutaline) as required for additional symptom control. Recently, the long-acting inhaled b 2-agonists salmeterol and formoterol have been shown to be effective bronchodilators for COPD and have additive effects with inhaled anticholinergics (Appleton et al, 2000). The bronchodilator response in COPD is small (<10% increase in FEV1), but the reduction in lung hyperinflation reduces dyspnoea and improves exercise performance. A combination inhaler of ipratropium bromide and salbutamol is useful, as these bronchodilators have an additive effect in COPD (Combivent inhlation study group, 1997). In more severe patients theophylline (slow release oral preparation b.d.) is also useful as an additional bronchodilator.

Inhaled corticosteroids are commonly prescribed for COPD, but their use is controversial. Some patients with COPD improve with corticosteroids and it is likely that these patients have coexistent asthma. Corticosteroids do not reduce the inflammatory response in COPD and several recent long-term studies have shown that they do not prevent the progression of the disease. Since there is a risk of systemic side effects when high doses are used inhaled corticosteroids should not be used routinely in the management of COPD (Barnes, 2000c). As COPD becomes more severe it may be necessary to consider long-term oxygen therapy in patients with chronic hypoxia and there are specific guidelines to determine which patients should be prescribed this expensive therapy (Barnes, 1999). In more severe disease pulmonary rehabilitation, a structured program of education, exercises and physiotherapy, has been shown in controlled trials to improve the exercise capacity and quality of life of patients with severe COPD (Lacasse et al, 1996).

Prophylactic antibiotics are not useful, but a broad-spectrum antibiotic is often used to treat exacerbations of COPD, although many exacerbations are now believed to be caused by viruses, rather than bacteria. Acute exacerbations are treated with supplemental oxygen, broad spectrum antibiotics (usually amoxycillin) and oral corticosteroids, which have been shown to accelerate recovery (Davies et al, 1996).