[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.158.173.184. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
October 23, 1987

Pulmonary Medicine

JAMA. 1987;258(16):2267-2269. doi:10.1001/jama.1987.03400160121033
Abstract

In 1987, the prevention of chronic pulmonary disorders remains a major challenge.1 But to organize effective preventive therapy or treatment of early stages of disease, an understanding of disease mechanisms is required. Recent studies indicate that proteolytic and/or oxidative mechanisms insidiously damage alveoli and small airways and finally result in chronic obstructive pulmonary disease (COPD).2 This pathogenetic mechanism has been well established for emphysema associated with inherited α-antiprotease deficiency states,2 and similar pathogenetic processes may be active in adult respiratory distress syndrome3 and lung cancer.

Attempts at therapy have been initiated. Newly completed animal studies, for example, show that emphysema experimentally produced by human elastase derived from polymorphonuclear leukocytes can be ameliorated by intratracheal instillation of an antiprotease, eglin-c, produced by recombinant DNA technology. The antiprotease offered protection with no evidence of bronchial toxic reactions.4 Clinically, augmentation of α-antiprotease levels in antiprotease-deficient individuals has been

×