Abstract

Asthma is a chronic inflammatory disease of the airways characterized by reversible airway constriction and airway hyperresponsiveness. It is a common disease, affecting S-IO% of adults. Chronic inflammatory reactions are central to the disease process and underly the functional airway abnormalities in asthma. Chronically inflamed airways are hyperresponsive and become obstructed as airflow is limited by smooth muscle contraction, oedema, excess mucus production and infiltrating inflammatory cells. Changes in the airways in asthma have been assessed in a number of ways. Post-mortem examination of the lungs of patients who have died with asthma permits direct analysis of the cell types infiltrating the airways and the structure and composition of the airway wall. Direct in vivo sampling techniques such as biopsies, induced sputum, bronchoalveolar lavage (BAL), bronchial washes and bronchial brushing have proved useful in providing important information on the airway changes that characterize asthma. Most studies have focused on the large conducting airways, as these are more accessible both for histological examination and in vivo sampling. The small airways (those less than 2 mm diameter) contribute only 10% of total airway resistance and have been termed the ‘silent zone’ (1). Due to difficulty of sampling and lack of specific tests for small airways function, changes in the small airways in asthma have been largely under-evaluated. More recently, however, sensitive methods of airway analysis, such as high-resolution computed tomography (HRCT), have shown that the inflammatory and structural changes in asthma occur in both the large and small airways (2). Moreover, the low resistance of the small airways means that they can be extensively damaged and severely obstructed before the patient experiences any symptoms (3). The growing importance of small involvement in the pathogenesis of asthma is, therefore, becoming clearer.

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