Abstract
Asthma is a clinically complex condition but at present the pathologist recognises only one disease process. The airways in fatal asthma are occluded by tenacious plugs of exudate, mucus and cells. There is fragility of the airway surface epithelium and thickening of epithelial reticular basement membrane. Bronchial vessel dilation, congestion and oedema, an intense inflammatory cell infiltrate and enlargement of the mass of bronchial smooth muscle, and mucus-secreting gland each contribute to thickening of the airway wall. These changes contribute to the cardinal signs of inflammation (i.e. redness, heat, pain, swelling and secretion of mucus) and can profoundly modify the effects of airway contracture on airflow. The fragility and loss of surface epithelium, thickening of its underlying reticular layer and the presence of an inflammatory infiltrate, comprising activated T lymphocytes together with 'activated' and secreting eosinophils, are early events seen in biopsies of subjects with mild stable atopic asthma.
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