Bronchial reactivity, smoking, and alpha1-antitrypsin. A population-based study of middle-aged men.
1982; National Institutes of Health; Volume: 126; Issue: 5 Linguagem: Inglês
10.1164/arrd.1982.126.5.864
AutoresM. U. Kabiraj, Bo Simonsson, S. Groth, Anneli Björklund, K Bülow, S.‐E. Lindell,
Tópico(s)Protease and Inhibitor Mechanisms
ResumoWe assessed bronchial reactivity to increasing doses of inhaled methacholine (MCH) in a population-based study on alpha1-antitrypsin. We compared 34 consecutive 48- to 50-yr-old heterozygous (Pi-MZ) men with 31 men of the same age with normal Pi phenotype (Pi-M) matched for smoking habits. There was no significant difference between control FEV1 or in MCH reactivity between the Pi-MZ and the Pi-M group. Twelve Pi-MZ subjects and 11 Pi-M subjects showed a fall of greater than or equal to 15% of FEV1 (PC 15%). Smokers showed increased sensitivity to MCH in both phenotype groups, although there was no significant difference in control FEV1 between the smoking and nonsmoking groups. Eleven smokers and ex-smokers, 5 with histories of asthma or sputum production, showed bronchial hyperreactivity, i.e., PC 15% FEV1, to 0.1% MCH or lower concentrations. Among nonsmokers there was 1 reactor and 1 hyperreactor. We conclude that heterozygous alpha1-antitrypsin deficiency (Pi-MZ) does not increase bronchial reactivity and that smoking does.
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