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The American review of respiratory disease

Serum antiproteases in smokers and nonsmokers. Relationships to smoking status and pulmonary function.


PMID 3878111

Abstract

In this study of 50 relatively young male smokers and an equal number of age- and race-matched male nonsmokers, smokers had a 13.3% (p = 0.007) increase in mean serum alpha 1-proteinase inhibitor (alpha 1-Pl) concentration. This increase in serum alpha 1-Pl concentration was accompanied by increases in both the serum trypsin inhibitory capacity (TIC) (9.9%, p = 0.002) and the elastase inhibitory capacity (EIC) (12.4%, p = 0.001). That cigarette smoking increases serum alpha 1-Pl concentration and total protease inhibitory capacity was further supported by a significant association of alpha 1-PI, TIC, and EIC with increased pack-years smoking history, plasma nicotine, and plasma cotinine concentrations. Pulmonary function did not correlate with serum alpha 1-PI concentration. However, higher serum TIC and EIC did correlate with tests of small airways dysfunction. Highly significant correlations (r greater than or equal to 0.6, p = 0.001) were observed between TIC (or EIC) and alpha 1-PI concentrations. The linear relationships between TIC (or EIC) and serum alpha 1-PI concentration were not significantly different in smokers and nonsmokers. Further, no significant differential effect of smoking on either the TIC or EIC could be demonstrated. A decreased apparent functional activity of alpha 1-PI (i.e., nanomoles of protease inhibited per nanomole of alpha 1-PI) was associated with its higher serum concentration, a phenomenon observed in both smokers and nonsmokers. Thus, although cigarette smoking increases serum alpha 1-PI concentration and total protease inhibitory capacity, no evidence was obtained to suggest that the functional activity of serum alpha 1-PI (against either trypsin or elastase) was directly affected by smoking.

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