Abstract
The pathogenesis of emphysema is postulated to be mediated primarily by endogenous elastolytic enzymes. This theory suggests proteolysis of pulmonary tissue occurs when active pulmonary phagocytes release elastolytic enzymes in quantities which exceed the inhibitory capacity of the locally available antiproteases, either because of extensive enzyme release or because of congenital alpha1-antitrypsin deficiency. The destructive episodes occur over time at diffuse locations until identifiable functional alterations result and at that point clinical emphysema can be identified.
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