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ß2-adrenergic receptor polymorphisms, asthma and COPD: two large population-based studies.

https://arctichealth.org/en/permalink/ahliterature129736
Source
Eur Respir J. 2012 Mar;39(3):558-66
Publication Type
Article
Date
Mar-2012
Author
M. Thomsen
B G Nordestgaard
A A Sethi
A. Tybjærg-Hansen
M. Dahl
Author Affiliation
Dept of Clinical Biochemistry, Herlev Hospital, Herlev, Denmark.
Source
Eur Respir J. 2012 Mar;39(3):558-66
Date
Mar-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Asthma - epidemiology - genetics
Denmark - epidemiology
Female
Gene Frequency
Humans
Incidence
Lung - physiopathology
Male
Middle Aged
Polymorphism, Genetic
Prevalence
Pulmonary Disease, Chronic Obstructive - epidemiology - genetics
Receptors, Adrenergic, beta-2 - genetics
Young Adult
Abstract
The ß(2)-adrenergic receptor (ADRB2) is an important regulator of airway smooth muscle tone. We tested the hypothesis that three functional polymorphisms in the ADRB2 gene (Thr164Ile, Gly16Arg and Gln27Glu) are associated with reduced lung function, asthma or chronic obstructive pulmonary disease (COPD). We first genotyped 8,971 individuals from the Copenhagen City Heart Study for all three polymorphisms. To validate our findings, we genotyped an additional 53,777 individuals from the Copenhagen General Population Study for the Thr164Ile polymorphism. We identified 60,910 Thr164Ile noncarriers, 1,822 heterozygotes and 16 homozygotes. In the Copenhagen City Heart Study, the Thr164Ile genotype was associated with reduced forced expiratory volume in 1 s (FEV(1)) % predicted (trend p = 0.01) and FEV(1)/forced vital capacity (FVC) (p = 0.001): Thr164Ile heterozygotes had 3% and 2% reduced FEV(1) % pred and FEV(1)/FVC, respectively, compared with noncarriers. The odds ratio for COPD in Thr164Ile heterozygotes was 1.46 (95% CI 1.05-2.02). In the Copenhagen General Population Study, the Thr164 genotype associated with reduced FEV(1) % pred (p = 0.04) and FEV(1)/FVC (p
PubMed ID
22075484 View in PubMed
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Angiotensinogen mutations and risk for ischemic heart disease, myocardial infarction, and ischemic cerebrovascular disease. Six case-control studies from the Copenhagen City Heart Study.

https://arctichealth.org/en/permalink/ahliterature53929
Source
Ann Intern Med. 2001 May 15;134(10):941-54
Publication Type
Article
Date
May-15-2001
Author
A A Sethi
A. Tybjaerg-Hansen
M L Grønholdt
R. Steffensen
P. Schnohr
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry 54M1, Herlev University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
Source
Ann Intern Med. 2001 May 15;134(10):941-54
Date
May-15-2001
Language
English
Publication Type
Article
Keywords
Aged
Angiotensinogen - genetics
Brain Ischemia - genetics
Case-Control Studies
Female
Genetic Predisposition to Disease
Heterozygote
Homozygote
Humans
Male
Middle Aged
Mutation
Myocardial Infarction - genetics
Myocardial Ischemia - genetics
Regression Analysis
Research Support, Non-U.S. Gov't
Risk factors
Abstract
BACKGROUND: The M235T and T174M angiotensinogen mutations have been linked to increased risk for ischemic heart and cerebrovascular disease. OBJECTIVE: To determine whether angiotensinogen mutations are associated with ischemic heart disease, myocardial infarction, and ischemic cerebrovascular disease. DESIGN: Six case-control studies from the Copenhagen City Heart Study. SETTING: Copenhagen, Denmark. PARTICIPANTS: Participants in the Copenhagen City Heart Study and patients from the same hospital with ischemic heart disease (n = 866 and n = 943, respectively), myocardial infarction (n = 519 and n = 493, respectively), or ischemic cerebrovascular disease (n = 489 and n = 434, respectively) and 7975 controls without these conditions. MEASUREMENTS: Genotypes for the M235T and T174M angiotensinogen mutations were compared between controls and Copenhagen City Heart Study participants with ischemic heart disease, myocardial infarction, and cerebrovascular disease (studies 1a, 1b, and 1c) and patients from Copenhagen University Hospital with the same conditions (studies 2a, 2b, and 2c). RESULTS: Relative allele frequencies of 235T and 174M in the general population were 0.41 and 0.12, respectively. Genotype was not associated with increased risk for ischemic heart or ischemic cerebrovascular disease in studies of either mutation alone or combined in women or men. Among compound heterozygotes (235MT /174TM ), women in case-control study 2a had decreased risk for ischemic heart disease in age-adjusted analysis; however, this decreased risk was not seen in multifactorial-adjusted or matched analyses, in men, or in case-control study 1a. Among double homozygotes (235TT /174MM ), women in case-control study 2b had increased risk for myocardial infarction in matched analysis; however, this increased risk was not seen in age- or multifactorial-adjusted analyses, in men, or in case-control study 1b. Among single homozygotes (235TT /174TT ), men in case-control study 2b had increased risk for myocardial infarction in multifactorial-adjusted and matched analyses. This risk was not present in age-adjusted analysis, in women, or in case-control study 1b. In addition, male single homozygotes had decreased risk for ischemic cerebrovascular disease in case-control study 2c in age- and multifactorial-adjusted analyses, but this finding was not seen in matched analysis, in women, or in case-control study 1c. CONCLUSIONS: In six large case-control studies, the M235T and T174M angiotensinogen mutations were not consistently associated with increased (or decreased) risk for ischemic heart disease, myocardial infarction, or ischemic cerebrovascular disease. Statistically significant associations may represent chance findings rather than real phenomena.
PubMed ID
11352695 View in PubMed
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