JEFFREY I. WEITZ, M.D.; KATHRYN A. CROWLEY, M.D.; SHARON L LANDMAN, B.S.; BRIAN I. LIPMAN, M.D.; JOSEPH YU, M.D.
We compared plasma levels of the neutrophil elastase-derived fibrinopeptide A-alpha-1-21 in healthy cigarette smokers with those in nonsmokers. The mean A-alpha-1-21 concentration was fivefold higher (95% confidence interval [Cl], 3.0 to 9.6) in ten cigarette smokers than in 20 healthy nonsmokers (2.0 nmol/L compared with 0.4 nmol/L; p < 0.0001). To evaluate the acute effect of smoking on enzyme activity, a second group of ten smokers was studied. After refraining from smoking for 12 hours, each person smoked three cigarettes. The mean A-alpha-1-21 level in the second group of smokers was not different from that in the first group of smokers (1.8 nmol/L compared with 2.0 nmol/L) but was fivefold higher (95% Cl, 2.6 to 8.7) than that in the nonsmokers (1.8 nmol/L compared with 0.4 nmol/L; p < 0.0001). After smoking three cigarettes, subjects had a twofold elevation (95% Cl, 1.6 to 3.5) in the mean A-alpha-1-21 concentration (from 1.8 nmol/L to 4.1 nmol/L; p = 0.002). Our data show that cigarette smoking perturbs the in-vivo elastase-antielastase balance and thus may produce lung disease through this mechanism.
WEITZ JI, CROWLEY KA, LANDMAN SL, LIPMAN BI, YU J. Increased Neutrophil Elastase Activity in Cigarette Smokers. Ann Intern Med. 1987;107:680–682. doi: 10.7326/0003-4819-107-5-680
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Published: Ann Intern Med. 1987;107(5):680-682.
Cardiology, Coronary Risk Factors, Smoking.
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