JEFFREY I. WEITZ, M.D.; KATHRYN A. CROWLEY, M.D.; SHARON L LANDMAN, B.S.; BRIAN I. LIPMAN, M.D.; JOSEPH YU, M.D.
Grant support: by grants to Jeffrey Weitz, M. D., from the National Institutes of Health (HL-15486), the Ontario Heart and Stroke Foundation, The Medical Research Council of Canada, and the Ciba-Geigy Foundation. Jeffrey Weitz is a Scholar of the Ontario Heart and Stroke Foundation.
▸Requests for reprints should be addressed to Jeffrey I. Weitz, M.D.; Fourth Floor, McMaster Clinic, Henderson General Hospital, 711 Concession Street; Hamilton, Ontario L8V 1C3, Canada.
WEITZ J., CROWLEY K., LANDMAN S., LIPMAN B., 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.
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.
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Cardiology, Coronary Risk Factors, Smoking.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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