Practical Pearls from the GOLD Guidelines on COPD

By Juan Garcia, MD, FCCP; and Stephen Jenkinson, MD, FCCP

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General Knowledge Concerning COPD in the United States

The incidence of COPD has risen continuously over the last 30 years, and data-based information from a 1998 survey suggest that 13 million Americans have been diagnosed with COPD (3 million with emphysema and 10 million with chronic bronchitis).^2,3 Many more millions of patients are thought to be exhibiting early symptoms of COPD but have not yet been diagnosed or treated. COPD is the term used to refer to patients with airflow obstruction due to either emphysema, chronic bronchitis, or a combination of both disorders. COPD was the fourth leading cause of death in the United States in 1998, and death rates rose steadily between 1965 and 1998. The data from 1998 showed that COPD accounted for > 100,000 deaths and > 600,000 hospital discharges. The majority of patients are male, but an increasing prevalence of the disease in women has been noted in the last 5 years.

Emphysema is defined according to anatomical pathology as abnormal, permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis. This tissue destruction results in enlargement of proximal and distal airspaces and can ultimately form bullae out in the lung parenchyma. These bullae result in loss of surface area for gas exchange in the involved lungs.

Chronic bronchitis is defined as the presence of a chronic, productive cough for 3 months during each of 2 consecutive years, and for which other causes of chronic cough have been excluded.⁴ The other common causes of chronic cough include asthma, gastric reflux, or postnasal drip secondary to sinus disease.⁵ The pathologic findings of chronic bronchitis include enlargement of tracheobronchial mucus glands, as well as variable amounts of airway smooth-muscle hyperplasia, inflammation, and bronchial wall thickening. Abnormalities of small airways may also be present, and are accompanied by fibrosis and the presence of a mononuclear inflammatory process.

Pearl: The decrease in the pulmonary function FEV₁ of the patient is inversely proportional to the number of inflammatory cells in the airways.

Pearl: A genetically inherited form of emphysema occurs, resulting from a1-antitrypsin (AAT) deficiency. This disorder accounts for < 1 to 2% of COPD cases in the United States.¹ AAT is a protease inhibitor produced by the liver that circulates into tissues. Active proteases are released into the lung by lung macrophages and neutrophils, which can contribute to the development of emphysema.

Pearl: All patients developing emphysema who form bullae before age 45 should be evaluated for AAT deficiency. A normal serum level of AAT is > 11 mmol/L. Patients with low levels of AAT should be evaluated by a pulmonologist and may be candidates for AAT replacement therapy.

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