Chest
Clinical InvestigationsANTITRYPSINA Longitudinal Study of α1-Antitrypsin Phenotypes and Decline in FEV1 in a Community Population
Section snippets
Materials and Methods
Details of the study design have been published previously.1121 Briefly, the data are derived from the Tucson Epidemiologic Study of Airways Obstructive Diseases. The study included subjects who were selected from a random, stratified cluster sample of white, non-Mexican-American households in Tucson, AZ, in 1972. There were 12 follow-up surveys over a period of 20 to 22 years. Standardized questionnaires assessing respiratory symptoms and disease history, occupation, smoking history, and
Results
The basic α1-antitrypsin phenotype distribution was similar to frequencies reported by other authors,101418 and did not differ significantly by sex, smoking status, emphysema, chronic bronchitis, or asthma diagnoses. The frequency for PiMZ did not differ significantly between rapid-decliners and nondecliners (Table 1). Means for FEV1 slope, initial FEV1 measurements, age at initial survey, and number of years of follow-up were not significantly different among the different phenotypes (Table 2
Discussion
Sandford et al20 analyzed the association between the increased risk of rapid decline in lung function and having the PiMZ phenotype. The odds ratio (OR) was 2.8 comparing 283 rapid decliners (mean ΔFEV1, −154 ± 3 mL per year) to 308 nondecliners (mean ΔFEV1, +15 ± 2 mL per year). This association was stronger when family history of COPD was taken into account (OR, 9.7). Potential confounders like age, sex, and initial level of lung function were adjusted for in a logistic regression. Study
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Cited by (34)
Hereditary pulmonary emphysema
2019, Emery and Rimoin's Principles and Practice of Medical Genetics and Genomics: Cardiovascular, Respiratory, and Gastrointestinal DisordersPortuguese consensus document for the management of alpha-1-antitrypsin deficiency
2018, PulmonologyCitation Excerpt :Although S homozygotes are not associated with a significant risk of emphysema, SZ heterozygotes have an increased risk, particularly if associated with cigarette smoking.40–43 Moreover, several studies performed so far, with differences in terms of sample sizing, have provided contradictory results about an increased risk of COPD in MZ individuals.31,44–47 However, more recent studies based in large populations of patients and controls support an increased risk of COPD mainly influenced by exposure to cigarette smoke.48
Hereditary Pulmonary Emphysema
2013, Emery and Rimoin's Principles and Practice of Medical Geneticsα<inf>1</inf>-antitrypsin protease inhibitor MZ heterozygosity is associated with airflow obstruction in two large cohorts
2010, ChestCitation Excerpt :The results of published longitudinal studies of decline in lung function over time also have been inconsistent. A general population study in Copenhagen, Denmark, found the annual decrease in FEV1 to be slightly greater in PI MZ individuals than in PI MM individuals,17 but another longitudinal study of the general population in Arizona failed to confirm these findings.18 A 5-year follow-up of smokers in the Lung Health Study demonstrated that rapid decline of FEV1 was associated with PI MZ, and this association was stronger when PI MZ subjects also had a family history of COPD.19
Longitudinal decline of diffusing capacity of the lung for carbon monoxide in community subjects with the PiMZ α<inf>1</inf>-antitrypsin phenotype
2008, ChestCitation Excerpt :However, it would seem improbable that there would be any systemic bias in hemoglobin concentration in our randomly selected community sample. Using the same cohort of the TESAOD study, we have previously shown that subjects with the PiMZ phenotype were not at increased risk for a diagnosis of COPD or showing an accelerated decline of FEV1.11 Those findings were confirmed in the current study, in which, despite the effects of the PiMZ phenotype on Dlco, no association between α1-antitrypsin phenotypes and % predicted FEV1 was found.
Deficient alpha-1-antitrypsin phenotypes and persistent airflow limitation in severe asthma
2006, Respiratory Medicine
This research was supported in part by National Institutes of Health fellowship grant No. HL10506–02 (to GES).