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33 records – page 1 of 4.

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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ß2 -adrenergic receptor Thr164IIe polymorphism, blood pressure and ischaemic heart disease in 66?750 individuals.

https://arctichealth.org/en/permalink/ahliterature131722
Source
J Intern Med. 2012 Mar;271(3):305-14
Publication Type
Article
Date
Mar-2012
Author
M. Thomsen
M. Dahl
A. Tybjaerg-Hansen
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Copenhagen, Denmark.
Source
J Intern Med. 2012 Mar;271(3):305-14
Date
Mar-2012
Language
English
Publication Type
Article
Keywords
Aged
Blood Pressure - genetics
Cross-Sectional Studies
Denmark
Female
Genetic Predisposition to Disease - genetics
Genotype
Humans
Hypertension - genetics
Male
Middle Aged
Muscle, Skeletal
Myocardial Ischemia - genetics
Myocytes, Smooth Muscle
Polymorphism, Single Nucleotide
Prospective Studies
Questionnaires
Receptors, Adrenergic, beta-2 - genetics
Sex Factors
Abstract
The ß(2) -adrenergic receptor (ADRB2) is located on smooth muscle cells and is an important regulator of smooth muscle tone. The Thr164Ile polymorphism (rs1800888) in the ADRB2 gene is rare but has profound functional consequences on receptor function and could cause lifelong elevated smooth muscle tone. We tested the hypothesis that Thr164Ile is associated with increased blood pressure, increased frequency of hypertension and increased risk of cardiovascular disease (CVD).
A total of 66 750 individuals from two large Danish general population studies were genotyped, and 1943 Thr164Ile heterozygotes and 16 homozygotes were identified.
Thr164Ile genotype was associated with increased systolic and diastolic blood pressure in women (trend: P = 0.04 and 0.02): systolic and diastolic blood pressure increased by 5% and 2%, respectively, in female homozygotes compared with female noncarriers. All female Thr164Ile homozygotes had hypertension compared with 58% of female heterozygotes and 54% of female noncarriers (chi-square: P = 0.001). Female Thr164Ile homozygotes and heterozygotes had odds ratios for ischaemic heart disease (IHD) of 2.93 (0.56-15.5) and 1.28 (1.03-1.61), respectively, compared with female noncarriers (trend: P = 0.007). These differences were not observed in men. Furthermore, Gly16Arg (rs1042713) and Gln27Glu (rs1042714) in the ADRB2 gene were not associated with blood pressure, hypertension or CVD either in the population overall or in women and men separately.
ADRB2 Thr164Ile is associated with increased blood pressure, increased frequency of hypertension and increased risk of IHD amongst women in the general population. These findings, particularly for homozygotes, are novel.
PubMed ID
21883537 View in PubMed
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25-Hydroxyvitamin D concentrations and risk of venous thromboembolism in the general population with 18,791 participants.

https://arctichealth.org/en/permalink/ahliterature117634
Source
J Thromb Haemost. 2013 Mar;11(3):423-31
Publication Type
Article
Date
Mar-2013
Author
P. Brøndum-Jacobsen
M. Benn
A. Tybjaerg-Hansen
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark.
Source
J Thromb Haemost. 2013 Mar;11(3):423-31
Date
Mar-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Biological Markers - blood
Denmark
Down-Regulation
Female
Humans
Incidence
Kaplan-Meier Estimate
Linear Models
Male
Middle Aged
Multivariate Analysis
Proportional Hazards Models
Prospective Studies
Risk assessment
Risk factors
Seasons
Time Factors
Venous Thromboembolism - blood - diagnosis - epidemiology
Vitamin D - analogs & derivatives - blood
Vitamin D Deficiency - blood - diagnosis - epidemiology
Abstract
Vitamin D has potential antithrombotic effects, suggesting that vitamin D analogs could be used as adjunctive antithrombotic agents. However, epidemiologic evidence of an association between reduced 25-hydroxyvitamin D concentrations and the risk of venous thromboembolism is lacking.
To test the hypothesis that reduced plasma 25-hydroxyvitamin D concentrations are associated with an increased risk of venous thromboembolism in the general population.
We prospectively studied 18 791 participants from the Copenhagen City Heart Study and the Copenhagen General Population Study. During up to 30 years of follow-up, 950 participants were diagnosed with venous thromboembolism. Plasma 25-hydroxyvitamin D concentrations were adjusted for seasonal variation.
The cumulative incidence of venous thromboembolism as a function of age increased with decreasing tertiles of seasonally adjusted plasma 25-hydroxyvitamin D (log-rank trend: P = 4 × 10(-4) ). On comparison of participants in the lowest and the highest tertile of plasma 25-hydroxyvitamin D concentrations, the crude risk estimate in a model adjusted for age and sex was a 37% (95% confidence interval [CI] 15-64%) increased risk of venous thromboembolism. The corresponding risk increase in a model adjusted for age, sex, body mass index, smoking and cancer was 26% (95% CI 5-51%), and in a multivariable-adjusted model also including physical activity, hormone replacement therapy, menopausal status, oral contraception use and lipid-lowering therapy it was 28% (95% CI 6-53%). Furthermore, corresponding risk increases with attempts to correct for regression dilution bias were 103% (95% CI 37-202%), 70% (95% CI 14-155%) and 73% (95% CI 15-160%) in the three models, respectively.
In these large general population studies, we observed a stepwise increasing risk of venous thromboembolism with decreasing tertiles of seasonally adjusted plasma 25-hydroxyvitamin D concentrations.
PubMed ID
23279309 View in PubMed
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ACE gene polymorphism as a risk factor for ischemic cerebrovascular disease.

https://arctichealth.org/en/permalink/ahliterature48152
Source
Ann Intern Med. 1997 Sep 1;127(5):346-55
Publication Type
Article
Date
Sep-1-1997
Author
B. Agerholm-Larsen
A. Tybjaerg-Hansen
R. Frikke-Schmidt
M L Grønholdt
G. Jensen
B G Nordestgaard
Author Affiliation
Herlev University Hospital, Denmark.
Source
Ann Intern Med. 1997 Sep 1;127(5):346-55
Date
Sep-1-1997
Language
English
Publication Type
Article
Keywords
Alleles
Brain Ischemia - enzymology - genetics
Cross-Sectional Studies
Denmark
Female
Genotype
Humans
Logistic Models
Male
Middle Aged
Mutation
Odds Ratio
Peptidyl-Dipeptidase A - genetics
Polymorphism, Genetic
Research Support, Non-U.S. Gov't
Risk
Risk factors
Abstract
BACKGROUND: Researchers have suggested that the deletional allele of the ACE (angiotensin-converting enzyme) gene insertion-deletion polymorphism is a potent risk factor for myocardial infarction. This association could not be confirmed in the Copenhagen City Heart Study, in which 10,150 persons were studied. The ACE gene polymorphism has also recently been suggested as a potent risk factor for ischemic cerebrovascular disease. OBJECTIVE: To investigate the association between ACE gene polymorphism and ischemic cerebrovascular disease. DESIGN: Two case-referent studies and a cross-sectional study. SETTING: University hospital in Copenhagen, Denmark. PARTICIPANTS: Case-referent study 1: 35 women and 38 men who developed ischemic cerebrovascular disease before 50 years of age compared with 1454 women and 1737 men from a general population sample. Case-referent study 2: 82 women and 137 men with ischemic cerebrovascular disease and carotid stenosis greater than 40% compared with 4273 women and 3091 men from the general population sample. Cross-sectional study of the general population sample: 67 women and 93 men with ischemic cerebrovascular disease compared with 4077 women and 3156 men without such disease. MEASUREMENTS: Genotype; age; body mass index; smoking habits; levels of lipids, lipoproteins, apolipoproteins, and fibrinogen; and diagnosis of hypertension, diabetes mellitus, and ischemic cerebrovascular disease. RESULTS: Odds ratios for ischemic cerebrovascular disease by ACE genotype classes were not significantly different from 1.0 in women or men in any of the three studies, separately or combined. In a logistic regression analysis that controlled for age and conventional cardiovascular risk factors, odds ratios in either sex still did not significantly differ from 1.0 in any study, separately or combined. CONCLUSION: In two case-referent studies, a cross-sectional study, and the three studies combined, no statistically significant difference was found in the development of ischemic cerebrovascular disease between genotype classes of the ACE gene polymorphism in women or men.
PubMed ID
9273825 View in PubMed
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ACE gene polymorphism explains 30-40% of variability in serum ACE activity in both women and men in the population at large: the Copenhagen City Heart Study.

https://arctichealth.org/en/permalink/ahliterature199818
Source
Atherosclerosis. 1999 Dec;147(2):425-7
Publication Type
Article
Date
Dec-1999

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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Apolipoprotein E genotype: epsilon32 women are protected while epsilon43 and epsilon44 men are susceptible to ischemic heart disease: the Copenhagen City Heart Study.

https://arctichealth.org/en/permalink/ahliterature54115
Source
J Am Coll Cardiol. 2000 Apr;35(5):1192-9
Publication Type
Article
Date
Apr-2000
Author
R. Frikke-Schmidt
A. Tybjaerg-Hansen
R. Steffensen
G. Jensen
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev University Hospital, Denmark.
Source
J Am Coll Cardiol. 2000 Apr;35(5):1192-9
Date
Apr-2000
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Apolipoproteins E - genetics
Case-Control Studies
Denmark - epidemiology
Female
Genetic Predisposition to Disease - genetics
Genotype
Heterozygote
Humans
Male
Middle Aged
Myocardial Ischemia - blood - epidemiology - genetics
Polymorphism, Genetic - genetics
Research Support, Non-U.S. Gov't
Risk factors
Sex Characteristics
Sex Distribution
Abstract
OBJECTIVES: We tested the hypothesis that risk of ischemic heart disease (IHD) differs as a function of apolipoprotein E (APOE) genotype in women and men. BACKGROUND: Apolipoprotein E genotype influences lipids and lipoproteins and, therefore, possibly the risk of IHD. METHODS: We genotyped 9,241 white women and men from the general population and 940 white women and men with IHD. RESULTS: Test of interaction suggested that APOE genotype may influence risk of IHD differently in women and men (p = 0.07). After age adjustment, the odds ratio (OR) for IHD for epsilon32 versus epsilon33 women was 0.57 (95% confidence interval [CI]: 0.35 to 0.94) while epsilon43 and epsilon44 versus epsilon33 men had ORs of 1.16 (0.96 to 1.41) and 1.58 (1.01 to 2.45). After adjustment for age and other conventional cardiovascular risk factors, the equivalent ORs were for epsilon32 women 0.38 (0.18 to 0.79), for epsilon43 men 1.35 (1.02-1.78) and for epsilon44 men 1.58 (0.80 to 3.08). Equivalent ORs for epsilon43 and epsilon44 versus epsilon33 women and for epsilon32 versus epsilon33 men were all close to 1.0 and nonsignificant. Of the total risk of IHD relative to the epsilon33 genotype, the fraction attributed to epsilon32 in women was -9%, while the fractions attributed to epsilon43 and epsilon44 in men were +8% and +2%. CONCLUSIONS: Relative to epsilon33 individuals, epsilon32 women are protected while epsilon43 and epsilon44 men are particularly susceptible to IHD.
Notes
Comment In: J Am Coll Cardiol. 2001 Jan;37(1):329-3111153762
PubMed ID
10758960 View in PubMed
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Association of mutations in the apolipoprotein B gene with hypercholesterolemia and the risk of ischemic heart disease.

https://arctichealth.org/en/permalink/ahliterature54398
Source
N Engl J Med. 1998 May 28;338(22):1577-84
Publication Type
Article
Date
May-28-1998
Author
A. Tybjaerg-Hansen
R. Steffensen
H. Meinertz
P. Schnohr
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev University Hospital, University of Copenhagen, Denmark.
Source
N Engl J Med. 1998 May 28;338(22):1577-84
Date
May-28-1998
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Apolipoproteins B - blood - genetics
Cholesterol - blood
Female
Heterozygote
Humans
Hypercholesterolemia, Familial - genetics
Male
Middle Aged
Myocardial Ischemia - genetics
Odds Ratio
Point Mutation
Prevalence
Research Support, Non-U.S. Gov't
Risk factors
Abstract
BACKGROUND: Familial hypercholesterolemia leads to premature ischemic heart disease and is often caused by mutations in the gene for the low-density lipoprotein receptor. Mutations in the apolipoprotein B gene, which encodes a ligand for this receptor, may also result in this phenotype. METHODS: We studied the genotypes of 9255 women and men from the general population, 948 patients with ischemic heart disease, and 36 patients with familial hypercholesterolemia, all from Denmark, for three mutations in the apolipoprotein B gene: Arg3500Gln, Arg3531Cys, and Arg3500Trp. RESULTS: The prevalence of heterozygotes in the general population was 0.08 percent (95 percent confidence interval, 0.03 to 0.16 percent) for both the Arg3500Gln and the Arg3531Cys mutations, and 0.00 percent (95 percent confidence interval, 0.00 to 0.18 percent) for the Arg3500Trp mutation. Among carriers of the Arg3500Gln mutation, cholesterol levels were significantly higher than among noncarriers in the general population - by 100 mg per deciliter (2.6 mmol per liter) among carriers in the general population, 154 mg per deciliter (4.0 mmol per liter) among patients with ischemic heart disease, and 172 mg per deciliter (4.5 mmol per liter) among patients with familial hypercholesterolemia. Heterozygous carriers of the Arg3500Gln mutation were significantly more common among patients with ischemic heart disease (odds ratio, 7.0; 95 percent confidence interval, 2.2 to 22; P=0.003) and patients with familial hypercholesterolemia (odds ratio, 78; 95 percent confidence interval, 16 to 388; P=0.001) than in the general population. Heterzygous carriers of the Arg3531Cys mutation in the general population did not have higher-than-normal plasma cholesterol levels or an increased risk of ischemic heart disease (odds ratio; 1.4; 95 percent confidence interval, 0.2 to 11; P=0.54). CONCLUSIONS: The Arg3500Gln mutation in the apolipoprotein B gene, which is responsible for familial defective apolipoprotein B-100 and is present in approximately 1 in 1000 persons in Denmark, causes severe hypercholesterolemia and increases the risk of ischemic heart disease.
Notes
Comment In: N Engl J Med. 1998 Nov 26;339(22):1640-1; author reply 1641-29867529
Comment In: N Engl J Med. 1998 Nov 26;339(22):1641-29867530
PubMed ID
9603795 View in PubMed
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Common cholesteryl ester transfer protein mutations, decreased HDL cholesterol, and possible decreased risk of ischemic heart disease: The Copenhagen City Heart Study.

https://arctichealth.org/en/permalink/ahliterature54019
Source
Circulation. 2000 Oct 31;102(18):2197-203
Publication Type
Article
Date
Oct-31-2000
Author
B. Agerholm-Larsen
A. Tybjaerg-Hansen
P. Schnohr
R. Steffensen
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev University Hospital, University of Copenhagen, Copenhagen, Denmark.
Source
Circulation. 2000 Oct 31;102(18):2197-203
Date
Oct-31-2000
Language
English
Publication Type
Article
Keywords
Alleles
Amino Acid Substitution - genetics
Apolipoproteins - blood
Carrier Proteins - genetics
Case-Control Studies
DNA Mutational Analysis
Denmark - epidemiology
Female
Genetic Screening
Glycoproteins
Heterozygote
Homozygote
Humans
Lipids - blood
Lipoproteins - blood
Lipoproteins, HDL Cholesterol - blood
Logistic Models
Male
Middle Aged
Mutation - genetics
Myocardial Ischemia - blood - epidemiology - genetics
Polymorphism, Genetic
Research Support, Non-U.S. Gov't
Risk assessment
Risk factors
Sex Distribution
Abstract
BACKGROUND: Cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl ester from HDL in exchange for triglycerides in apolipoprotein B-containing lipoproteins. METHODS AND RESULTS: We studied 2 common mutations in CETP, A373P and R451Q, in 8467 healthy women and men from the Danish general population and in 1636 Danish women and men with ischemic heart disease. The prevalence of 373P and 451Q was 0.10 and 0.07, respectively, for heterozygous carriers and 0.003 and 0.002, respectively, for homozygous carriers. All carriers of the 451Q allele also carried the 373P allele. HDL cholesterol in female noncarriers, heterozygotes, and homozygotes of 373P was 1.74+/-0.01 (mean+/-SE), 1.62+/-0.02, and 1.38+/-0.09 mmol/L, respectively (ANOVA, P:
PubMed ID
11056092 View in PubMed
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A common mutation in lipoprotein lipase confers a 2-fold increase in risk of ischemic cerebrovascular disease in women but not in men.

https://arctichealth.org/en/permalink/ahliterature54092
Source
Circulation. 2000 May 23;101(20):2393-7
Publication Type
Article
Date
May-23-2000
Author
H H Wittrup
B G Nordestgaard
H. Sillesen
P. Schnohr
A. Tybjaerg-Hansen
Author Affiliation
Department of Clinical Biochemistry, Herlev and Glostrup University Hospitals, the Copenhagen City Heart Study, Bispebjerg University Hospital, Copenhagen, Denmark.
Source
Circulation. 2000 May 23;101(20):2393-7
Date
May-23-2000
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Amino Acid Substitution
Brain Ischemia - complications - genetics
Carotid Stenosis - complications
Female
Genotype
Humans
Lipids - blood
Lipoprotein Lipase - genetics
Lipoproteins - blood
Male
Middle Aged
Mutation - genetics - physiology
Odds Ratio
Research Support, Non-U.S. Gov't
Risk factors
Sex Characteristics
Abstract
BACKGROUND: We previously showed that the common Asn291Ser substitution in lipoprotein lipase is associated with elevated plasma triglyceride levels and a 2-fold increase in the risk of ischemic heart disease in women but not men. In this study, we tested the hypothesis that this substitution is also associated with an increased risk of ischemic cerebrovascular disease (ICVD). METHODS AND RESULTS: We compared 260 patients who had nonfatal ICVD and carotid stenosis >/=50% with 1560 age-matched controls and also compared 205 Copenhagen City Heart Study cases who had nonfatal ICVD with 1210 age-matched controls. All subjects were white and from Denmark. Overall, no significant difference was observed between carrier frequencies among those with and without ICVD; however, sex interacted with genotype in predicting ICVD in the ICVD and carotid stenosis cases (P=0.02). In Copenhagen City Heart Study cases, sex was not significant (P=0.18). Odds ratios for ICVD in female mutation carriers were 2.9 (95% confidence interval [CI], 1.3 to 6. 4) and 1.9 (95% CI, 0.8 to 4.6) in ICVD plus carotid stenosis cases and Copenhagen City Heart Study cases, respectively. Equivalent values in male mutation carriers were 0.8 (95% CI, 0.3 to 1.8) and 0.8 (95% CI, 0.3 to 2.0), respectively. These results were similar in analyses that also allowed for other conventional cardiovascular risk factors. CONCLUSIONS: These results suggest that the Asn291Ser substitution in lipoprotein lipase is not associated with nonfatal ICVD in men but that it possibly confers a 2-fold risk in women.
PubMed ID
10821816 View in PubMed
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33 records – page 1 of 4.