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First published online on February 8, 2008
Chest, doi:10.1378/chest.07-2405
doi:10.1378/chest.07-2405
(Chest. 2008; 133:1095-1100)
© 2008 American College of Chest Physicians
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Longitudinal Decline of Diffusing Capacity of the Lung for Carbon Monoxide in Community Subjects With the PiMZ {alpha}1-Antitrypsin Phenotype*

Graciela E. Silva, PhD, MPH; Stefano Guerra, MD, PhD, MPH; Sam Keim, MD; Robert A. Barbee, MD and Duane L. Sherrill, PhD

* From the College of Nursing and Healthcare Innovation (Dr. Silva), Arizona State University, Phoenix; Arizona Respiratory Center (Drs. Guerra and Barbee), Tuscon; Mel and Enid Zuckerman College of Public Health (Dr. Sherrill), University of Arizona, Tuscon; and College of Medicine (Dr. Keim), University of Arizona, Tucson, AZ.

Correspondence to: Graciela E. Silva, PhD, MPH, Arizona State University, College of Nursing and Healthcare Innovation, 500 N Third St, Phoenix, AZ 85004-0698; e-mail: graciela.silva{at}asu.edu

Abstract

Background: It is well known that homozygous deficiency of {alpha}1-antitrypsin, PiZZ, is associated with an increased risk of emphysema. However, studies evaluating associations between the heterozygous form PiMZ with emphysema and impaired lung function have provided conflicting results.

Study objective: The goal of this study was to determine if the phenotype PiMZ is associated with an accelerated decline in diffusing capacity of the lung for carbon monoxide (DLCO).

Design and methods: The Tucson Epidemiologic Study of Airway Obstructive Disease is a prospective, population-based cohort study initiated in 1972. Participants completed standardized questionnaires in up to 12 periodic surveys and DLCO assessments in up to 4 surveys. Random-effects models were used to determine the effects of {alpha}1-antitrypsin phenotypes on percentage of predicted (% predicted) DLCO levels among 1,075 subjects ≥ 18 years old.

Results: % predicted DLCO declined more rapidly in subjects who smoked compared to nonsmoking subjects. Additionally, in smokers, the PiMZ phenotype was associated with borderline % predicted DLCO deficits at age 40 years (8.6%; p = 0.075) and significant % predicted DLCO deficits at age 60 years (15.2%; p = 0.001) and 80 years (21.9%; p = 0.003), as compared with the PiMM phenotype.

Conclusions: DLCO may be a more sensitive indicator of the long-term effects of intermediate levels of {alpha}1-antitrypsin on lung function especially in subjects who smoke.

Key Words: {alpha}1-antitrypsin deficiency • antitrypsin • pulmonary epidemiology






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