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33 records – page 1 of 4.

Rare and common mutations in hyperlipidemia and atherosclerosis. With special reference to familial defective apolipoprotein B-100.

https://arctichealth.org/en/permalink/ahliterature52799
Source
Scand J Clin Lab Invest Suppl. 1995;220:57-76
Publication Type
Article
Date
1995
Author
A. Tybjaerg-Hansen
Author Affiliation
Department of Clinical Biochemistry, Rigshospitalet, National University Hospital of Denmark, Copenhagen.
Source
Scand J Clin Lab Invest Suppl. 1995;220:57-76
Date
1995
Language
English
Publication Type
Article
Keywords
Apolipoproteins B - blood - genetics
Arteriosclerosis - genetics
Female
Humans
Hyperlipidemia - genetics
Male
Mutation
Abstract
The aim was to identify genetic determinants for the development of hyperlipidemia and/or atherosclerosis. The present set of studies demonstrates for the first time the clinical expression (phenotype) of a newly discovered monogenic disorder named Familial Defective Apolipoprotein B-100 (FDB). FDB is caused by a G to A mutation in the binding protein (apolipoprotein B-100) for the cholesterol-rich low density lipoprotein (LDL), such that the affinity of LDL to the LDL receptor is severely reduced. In all 135 individuals with FDB from 56 families and 8 different countries, including Denmark, are described. On average, the effect of the FDB mutation was to increase plasma and LDL cholesterol in both men and women by about 3 mmol/l; at age 55 the average plasma cholesterol of men and women with FDB was 9.4 mmol/l and 8.9 mmol/l, respectively. A sharp rise in frequency of coronary artery disease as a function of age in both FDB males and females was comparable to that found in Familial Hypercholesterolemia (FH). At the age of 60, about 70% of both men and women with FDB had coronary artery disease; at the same age approximately 40% had tendon xanthomas, and 35% had arcus corneae, irrespective of gender. Surprisingly, the frequencies of arcus corneae were not strikingly higher than those found in the general population sample from the Copenhagen City Heart Study. Only few patients with FDB had xanthelasmas. Finally, the frequency of this mutation was estimated at 1/500-1/700 in the general population, which is equivalent to that of clinical FH. All in all the results suggest FDB to be a severe genetic disorder with early penetrance, associated with substantial elevations in plasma and LDL cholesterol and with an increased frequency of premature coronary artery disease and of tendon xanthomas. For comparison, a number of common polymorphisms in the 5'-flanking region of the insulin gene, in the apoB gene and in the apoAI-CIII-AIV gene cluster, associated with minor effects on hyperlipidemia and/or cardiovascular disease are also examined.
PubMed ID
7652481 View in PubMed
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Novel mutations in leukotriene C4 synthase and risk of cardiovascular disease based on genotypes from 50,000 individuals.

https://arctichealth.org/en/permalink/ahliterature143676
Source
J Thromb Haemost. 2010 Aug;8(8):1694-701
Publication Type
Article
Date
Aug-2010
Author
J J Freiberg
A. Tybjaerg-Hansen
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Copenhagen, Denmark.
Source
J Thromb Haemost. 2010 Aug;8(8):1694-701
Date
Aug-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Cardiovascular Diseases - genetics
Case-Control Studies
Cross-Sectional Studies
Denmark
Female
Genetic Predisposition to Disease
Genetic Variation
Genotype
Glutathione Transferase - genetics
Heterozygote
Humans
Ischemia - pathology
Male
Middle Aged
Mutation
Odds Ratio
Prospective Studies
Risk factors
Sex Factors
Stroke - pathology
Abstract
Atherosclerosis is an inflammatory condition where cysteinyl leukotrienes have been identified to play an important role. Furthermore, cysteinyl leukotrienes may also affect thrombus formation. Using prospective, cross-sectional and case-control designs, we tested the hypothesis that hitherto unknown genetic variation, likely to affect the function of leukotriene C(4) synthase, is associated with risk of venous thromboembolism, ischemic stroke and myocardial infarction.
Resequencing the gene coding for leukotriene C(4) synthase in an extreme risk population with more than 1500 individuals revealed 17 new mutations, of which four are likely to change protein function (211G>A (minor allele frequency, 0.0001), IVS3 + 1G>A (0.002), 374G>A (0.0006) and 451_453+10del (0.0007)). Based on genotyping 50,000 individuals, age and sex adjusted odds ratios for venous thromboembolism were 2.0 (95% CI, 1.3-3.5) for IVS3+1G>A heterozygotes vs. wild type, and 1.9 (1.5-2.7) for any mutation heterozygote vs. wild type. Corresponding values were 2.0 (1.3-3.2) and 1.5 (1.1-2.1) for ischemic stroke, and 1.0 (0.8-1.3) and 1.2 (1.0-1.4) for myocardial infarction.
Four novel mutations that are likely to change the function of leukotriene C(4) synthase were associated with increased risk of venous thromboembolism and ischemic stroke. These findings need confirmation in other independent studies. In addition, the mechanism behind these findings deserves further investigation.
PubMed ID
20456754 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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DeltaF508 heterozygosity in cystic fibrosis and susceptibility to asthma.

https://arctichealth.org/en/permalink/ahliterature15728
Source
Lancet. 1998 Jun 27;351(9120):1911-3
Publication Type
Article
Date
Jun-27-1998
Author
M. Dahl
A. Tybjaerg-Hansen
P. Lange
B G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev University Hospital, Denmark.
Source
Lancet. 1998 Jun 27;351(9120):1911-3
Date
Jun-27-1998
Language
English
Publication Type
Article
Keywords
Asthma - complications - diagnosis - epidemiology - genetics
Cross-Sectional Studies
Cystic Fibrosis - complications - epidemiology - genetics
Cystic Fibrosis Transmembrane Conductance Regulator - genetics
Denmark - epidemiology
Disease Susceptibility
Female
Heterozygote
Heterozygote Detection
Humans
Male
Middle Aged
Research Support, Non-U.S. Gov't
Spirometry
Abstract
BACKGROUND: Cystic fibrosis is a recessive disorder mainly characterised by lung disease. We tested the hypothesis that individuals heterozygous for the common cystic fibrosis deltaF508 mutation are at risk of obstructive pulmonary disease. METHODS: We studied a cross-sectional sample from the general population of Copenhagen, Denmark, aged 20 years and older. We did spirometry to measure forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), and did genotyping on blood samples of 9141 individuals. We asked all participants whether they had asthma, and asked for information on smoking and other factors that could have contributed to obstructive pulmonary disease. FINDINGS: We identified 250 carriers of the deltaF508 mutation (2.7% [95% CI 2.5-3.1]). 9% of carriers reported having asthma compared with 6% of non-carriers (p=0.04). The odds ratio for asthma in participants heterozygous for deltaF508 mutation was 2.0 (1.2-3.5, p=0.02). Furthermore, among individuals with airway obstruction, the percentage predicted FEV1 and FVC were significantly lower in participants heterozygous for deltaF508 than in non-carriers (49 vs 58%, p=0.004; and 70 vs 82%, p
Notes
Comment In: Lancet. 1998 Sep 19;352(9132):984-5; author reply 986-79752838
Comment In: Lancet. 1998 Sep 19;352(9132):984; author reply 986-79752837
Comment In: Lancet. 1998 Sep 19;352(9132):985-6; author reply 986-79752840
Comment In: Lancet. 1998 Sep 19;352(9132):985; author reply 986-79752839
Comment In: Lancet. 1998 Sep 19;352(9132):9869752841
Erratum In: Lancet 1998 Oct 10;352(9135):1230
PubMed ID
9654257 View in PubMed
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Scavenger receptor AI/II truncation, lung function and COPD: a large population-based study.

https://arctichealth.org/en/permalink/ahliterature100065
Source
J Intern Med. 2010 Oct 25;
Publication Type
Article
Date
Oct-25-2010
Author
M. Thomsen
B G Nordestgaard
A. Tybjaerg-Hansen
M. Dahl
Author Affiliation
From the 1Department of Clinical Biochemistry The Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital The Copenhagen City Heart Study, Bispebjerg Hospital, Copenhagen University Hospital Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
Source
J Intern Med. 2010 Oct 25;
Date
Oct-25-2010
Language
English
Publication Type
Article
Abstract
Abstract. Thomsen M, Nordestgaard BG, Tybjaerg-Hansen A, Dahl M (Department of Clinical and The Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital; The Copenhagen City Heart Study, Bispebjerg Hospital, Copenhagen University Hospital; Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark) Scavenger receptor AI/II truncation, lung function and COPD: a large population-based study. J Intern Med 2010; doi: 10.1111/j.1365-2796.2010.02308.x. Objectives. The scavenger receptor A-I/II (SRA-I/II) on alveolar macrophages is involved in recognition and clearance of modified lipids and inhaled particulates. A rare variant of the SRA-I/II gene, Arg293X, truncates the distal collagen-like domain, which is essential for ligand recognition. We tested whether the Arg293X variant is associated with reduced lung function and risk of chronic obstructive pulmonary disease (COPD) in the general population. Methods. We genotyped 48 741 individuals from the adult Danish general population for Arg293X, and recorded lung function and spirometry-defined COPD. Results. Arg293X homozygotes (n = 5) and heterozygotes (n = 587), compared with noncarriers (n = 48 149), had a 6% and 1% reduction in predicted percentage of forced vital capacity (FVC % predicted) (P = 0.05) and a nonsignificant 7% and 1% reduction in predicted percentage of forced expiratory volume in one second (FEV(1) % predicted) (P = 0.06), respectively. The Arg293X genotype interacted with gender (P = 0.004) and a(1) -antitrypsin MZ heterozygosity (P = 0.049), but not with superoxide dismutase-3 E1I1 heterozygosity (P = 0.11) in determining FEV(1) % predicted. Amongst men, FEV(1) % predicted and FVC % predicted were both reduced by 4% (P = 0.0004 and P = 0.0003, respectively) in Arg293X heterozygotes compared with noncarriers. Corresponding values were 14% (P = 0.03) and 11% (P = 0.04) amongst MZ heterozygotes, and 9% (P = 0.03) and 8% (P = 0.04) amongst E1I1 heterozygotes, compared with noncarriers. Lung function did not differ between Arg293X heterozygotes and noncarriers amongst females or individuals without MZ and E1I1. Arg293X heterozygosity was associated with spirometry-defined COPD amongst men [odds ratio (95% confidence interval): 1.7 (1.1-2.4)], but not with COPD in the whole cohort or in any other subgroup. Conclusions. SRAI/II Arg293X heterozygotes have reduced lung function and increased COPD risk amongst men. They also have reduced lung function amongst individuals heterozygous for the a(1) -antitrypsin MZ and superoxide dismutase-3 E1I1 genotypes.
PubMed ID
21077973 View in PubMed
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Fifteen-year follow-up of pulmonary function in individuals heterozygous for the cystic fibrosis phenylalanine-508 deletion.

https://arctichealth.org/en/permalink/ahliterature15494
Source
J Allergy Clin Immunol. 2001 May;107(5):818-23
Publication Type
Article
Date
May-2001
Author
M. Dahl
B G Nordestgaard
P. Lange
A. Tybjaerg-Hansen
Author Affiliation
Department of Clinical Biochemistry, Glostrup, Herlev, and Copenhagen University Hospital, Copenhagen, Denmark.
Source
J Allergy Clin Immunol. 2001 May;107(5):818-23
Date
May-2001
Language
English
Publication Type
Article
Keywords
Adult
Aged
Asthma - epidemiology - genetics
Codon - genetics
Cystic Fibrosis - genetics
Cystic Fibrosis Transmembrane Conductance Regulator - genetics
DNA Mutational Analysis
Denmark - epidemiology
Female
Follow-Up Studies
Forced expiratory volume
Gene Frequency
Genetic Predisposition to Disease
Heterozygote
Humans
Lung Diseases, Obstructive - epidemiology - genetics
Male
Middle Aged
Odds Ratio
Polymerase Chain Reaction
Research Support, Non-U.S. Gov't
Respiratory Function Tests
Risk factors
Sequence Deletion
Smoking - epidemiology
Vital Capacity
Abstract
BACKGROUND: In a cross-sectional study, we previously showed that cystic fibrosis phenylalanine-508 deletion (DeltaF508) heterozygosity may be overrepresented among individuals with asthma. OBJECTIVE: Using 15-year follow-up data from the Copenhagen City Heart Study, we now further explore this relationship. METHODS: As part of 3 surveys in 1976 to 1978, 1981 to 1983, and 1991 to 1994, we measured pulmonary function and asked all participants about asthma and pulmonary risk factors. RESULTS: There was no difference in annual decline in lung function between DeltaF508 heterozygotes and noncarriers overall; however, among individuals with familial asthma, the annual declines in FEV(1) and forced vital capacity (FVC) were 49 and 36 mL in DeltaF508 heterozygotes versus 24 and 17 mL in noncarriers (P =.01 and P =.12, respectively). Cross-sectionally based on triple measurements, FEV(1) and FVC in individuals aged 20 to 70 years were lower in heterozygous participants versus noncarriers (P =.02 and P =.004, respectively). The average reduction of FEV(1) and FVC in DeltaF508 heterozygotes versus noncarriers was 70 mL (P =.06) and 136 mL (P =.008). Finally, 10% of carriers reported asthma versus 7% of noncarriers (P =.02), resulting in an odds ratio of 2.0 (1.3-3.2) for asthma in DeltaF508 heterozygotes. CONCLUSION: Cystic fibrosis DeltaF508 heterozygotes may be overrepresented among individuals with asthma and may have poorer lung function than noncarriers. Furthermore, DeltaF508 heterozygosity in context with familial predisposition to asthma may be associated with a greater annual FEV(1) decline.
PubMed ID
11344348 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 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

Haemochromatosis genotype and iron overload: association with hypertension and left ventricular hypertrophy.

https://arctichealth.org/en/permalink/ahliterature97578
Source
J Intern Med. 2010 Jan 29;
Publication Type
Article
Date
Jan-29-2010
Author
C. Ellervik
A. Tybjærg-Hansen
M. Appleyard
H. Ibsen
B G Nordestgaard
Author Affiliation
From theDepartment of Clinical Biochemistry and the Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, Herlev.
Source
J Intern Med. 2010 Jan 29;
Date
Jan-29-2010
Language
English
Publication Type
Article
Abstract
Abstract. Ellervik C, Tybjaerg-Hansen A, Appleyard M, Ibsen H, Nordestgaard BG (Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, Herlev; Naestved Hospital, University of Copenhagen, Naestved; Copenhagen University Hospital, University of Copenhagen, Copenhagen East; Bispebjerg Hospital, Copenhagen University Hospital, University of Copenhagen, Bispebjerg; and Holbaek Hospital, Holbaek; Denmark). Haemochromatosis genotype and iron overload: association with hypertension and left ventricular hypertrophy. J Intern Med 2010; doi: 10.1111/j.1365-2796.2010.02217.x. Objective. We hypothesized that there is an association between haemochromatosis genotype C282Y/C282Y and/or iron overload and risk of hypertension and/or left ventricular hypertrophy (LVH). Methods. We analysed data from a cross-sectional study of the general population including 8992 individuals from the Copenhagen City Heart Study (CCHS), a follow-up study of 36 480 individuals from the Copenhagen General Population Study (CGPS), and a case-only study of 3815 Scandinavians from the Losartan Intervention For End-point Reduction in Hypertension Genetic Substudy (LIFEGEN) with LVH and hypertension. Results. In the CCHS, individuals with C282Y/C282Y versus wild type/wild type had an odds ratio for antihypertensive medication use of 4.8 (1.8-13; P = 0.003). In the CGPS, the corresponding hazard ratio was 1.7 (1.0-2.3; P = 0.003). Also, hazard ratios for antihypertensive medication use in the CGPS were 1.6 (1.0-2.6; P = 0.05) for transferrin saturation >/=80% vs. /=80% vs. wild type/wild type + transferrin saturation
PubMed ID
20337854 View in PubMed
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Variation of apolipoprotein B gene is associated with myocardial infarction and lipoprotein levels in Danes.

https://arctichealth.org/en/permalink/ahliterature55241
Source
Atherosclerosis. 1991 Jul;89(1):69-81
Publication Type
Article
Date
Jul-1991
Author
A. Tybjaerg-Hansen
B G Nordestgaard
L U Gerdes
S E Humphries
Author Affiliation
Charing Cross Sunley Research Centre, London, U.K.
Source
Atherosclerosis. 1991 Jul;89(1):69-81
Date
Jul-1991
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alleles
Apolipoproteins B - genetics
Arteriosclerosis - blood - genetics
Carotid Stenosis - blood - genetics
DNA - genetics
Denmark
Female
Genetic markers
Humans
Lipoproteins - blood
Male
Middle Aged
Myocardial Infarction - blood - genetics
Polymorphism, Restriction Fragment Length
Research Support, Non-U.S. Gov't
Risk factors
Abstract
Three DNA polymorphisms (XbaI, EcoRI, MspI) in the 3'-end of the apolipoprotein B gene were studied in relation to atherosclerosis, lipoprotein levels and age in three groups of atherosclerotic individuals and in nonatherosclerotic controls. The atherosclerotic groups comprised a postmyocardial infarction group with a mean age of 48 years, a group of individuals operated on for carotid stenosis with a mean age of 62 years, and a group of 85-year-olds with clinical coronary artery disease, peripheral arterial disease, or both. All 311 individuals were unrelated Caucasians of Danish ancestry. For the XbaI polymorphism, the X- allele was an independent predictor for myocardial infarction on multivariate analysis, but did not distinguish between patients and controls on univariate analysis. Additionally, this polymorphism was associated with variation in lipoprotein levels, but there was no clear evidence of a gene dosage effect. For the EcoRI polymorphism, the E- allele was associated with elevated levels of VLDL cholesterol, plasma triglycerides and VLDL triglycerides. Similar, but weaker associations were found for the MspI polymorphism. There were no significant differences in allele frequencies as a function of age for any of the DNA polymorphisms. In conclusion, while variation associated with the EcoRI polymorphism appears to be involved in the regulation of VLDL metabolism, variation associated with the XbaI polymorphism may determine susceptibility to coronary artery disease independent of other conventional risk factors, but it also appears to affect variation in lipoprotein levels.
PubMed ID
1685318 View in PubMed
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33 records – page 1 of 4.