Morten Dahl, MD; Anne Tybjærg-Hansen, MD, DMSc; Peter Lange, MD, DMSc; Jørgen Vestbo, MD, DMSc; Børge G. Nordestgaard, MD, DMSc
Acknowledgments: The authors thank Anne-Merete Bengtsen, Charlotte Worm, and Hanne Damm for technical assistance and the participants of the Copenhagen City Heart Study for their willingness to participate.
Grant Support: By the Danish Lung Association, the Danish Heart Foundation, the Danish Medical Research Council, Løvens Kemiske Fabrik's Forskningsfond, and the Beckett Fund.
Requests for Single Reprints: Børge G. Nordestgaard, MD, DMSc, Department of Clinical Biochemistry, Herlev University Hospital, DK-2730 Herlev, Denmark; e-mail, email@example.com.
Current Author Addresses: Drs. Dahl and Nordestgaard: Department of Clinical Biochemistry 54M1, Herlev University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
Dr. Tybjærg-Hansen: Department of Clinical Biochemistry KB3011, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, DK-2100, Copenhagen Ø, Denmark.
Drs. Lange and Vestbo: Department of Respiratory Medicine 121, Hvidovre University Hospital, Kettegård Allé 30, DK-2650 Hvidovre, Denmark.
Author Contributions: Conception and design: M. Dahl, A. Tybjærg-Hansen, P. Lange, J. Vestbo, B.G. Nordestgaard.
Analysis and interpretation of the data: M. Dahl, A. Tybjærg-Hansen, P. Lange, J. Vestbo, B.G. Nordestgaard.
Drafting of the article: M. Dahl.
Critical revision of the article for important intellectual content: M. Dahl, A. Tybjærg-Hansen, P. Lange, J. Vestbo, B.G. Nordestgaard.
Final approval of the article: M. Dahl, A. Tybjærg-Hansen, P. Lange, J. Vestbo, B.G. Nordestgaard.
Statistical expertise: M. Dahl, A. Tybjærg-Hansen, P. Lange, J. Vestbo, B.G. Nordestgaard.
Obtaining of funding: A. Tybjærg-Hansen, B.G. Nordestgaard.
Collection and assembly of data: M. Dahl, A. Tybjærg-Hansen, B.G. Nordestgaard.
Dahl M, Tybjærg-Hansen A, Lange P, Vestbo J, Nordestgaard BG. Change in Lung Function and Morbidity from Chronic Obstructive Pulmonary Disease in α1-Antitrypsin MZ Heterozygotes: A Longitudinal Study of the General Population. Ann Intern Med. 2002;136:270-279. doi: 10.7326/0003-4819-136-4-200202190-00006
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Published: Ann Intern Med. 2002;136(4):270-279.
Chronic obstructive pulmonary disease (COPD) is one of the most important health problems worldwide (1, 2). More than 90% of COPD cases are caused by smoking, but only a fraction of smokers develop this disease. The variability in COPD expression among smokers could be due to differences in the environment, in genetic predisposition, or both.
So far, severe α1-antitrypsin deficiency has been the best described genetic risk factor for COPD (2, 3). When lung tissue is α1-antitrypsin deficient, protection from neutrophil elastase is impaired and elastic tissue is slowly destroyed, ultimately leading to reduced lung function and development of COPD (4). Severe α1-antitrypsin deficiency is almost entirely caused by the presence of the Z alleles in the α1-antitrypsin gene rather than the normal M allele. Relative plasma α1-antitrypsin concentrations are approximately 16% for persons with the ZZ genotype, 83% for persons with the MZ genotype, and 100% for persons with the MM genotype (5). A deteriorating effect of severe α1-antitrypsin deficiency (the ZZ genotype) on lung function has been known for many years (2-4), whereas the role of intermediate deficiency (the MZ genotype) remains uncertain (6, 7).
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Pulmonary/Critical Care, Chronic Obstructive Airway Disease.
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