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Nosicielstwo allela A polimorfizmu – 455G>A genu fibrynogenu beta zwiększa ryzyko choroby wieńcowej przy jednoczesnym podwyższonym stężeniu triglicerydów w surowicy
| 1 | Department of Biochemistry and Medical Genetics, School of Health Care, Medical University of Silesia, Katowice, Poland |
| 2 | The First Department of Cardiac Surgery, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland |
CORRESPONDING AUTHOR
Beata Sarecka-Hujar
Department of Biochemistry and Medical Genetics, School of Health Care Medical University of Silesia, Kasztanowa Str. 3, 41-200 Sosnowiec, Poland; phone: (+48 32) 269 98 20
Department of Biochemistry and Medical Genetics, School of Health Care Medical University of Silesia, Kasztanowa Str. 3, 41-200 Sosnowiec, Poland; phone: (+48 32) 269 98 20
Ann. Acad. Med. Siles. 2009;63:41–49
KEYWORDS
ABSTRACT
Background:
Fibrinogen promotes development of atherosclerosis by directed integration in atherosclerotic lesions where it is converted into fi brin. The aim of the study was to assess a relationship between –455G>A polymorphism of beta fi brinogen (FGB) gene and coronary artery disease (CAD) in the Polish patients from Upper Silesia region and to establish whether there are any interactions between this polymorphism and traditional risk factors that infl uence the risk of CAD.
Material and Methods:
We analyzed 191 patients with angiographically documented CAD and 203 blood donors. Genetic analysis was performed using PCR-RFLP method.
Results:
The frequency of FGB -455G>A genotypes was compatible with HardyWeinberg equilibrium. There was no significant differences in the distribution of A allele and A allele carriers of FGB polymorphism between cases and controls. We observed a tendency to higher level of plasma fibrinogen in subjects with AA or GA genotypes than in GG homozygotes. We also found strong synergistic effects between A allele carrier-state and increased level of triacylglycerols (TG) in determining the risk of CAD (SI=5.97, SIM=2.63). Carriers of A allele with elevated level of TG were 3-fold more frequent among cases than in control group (12.0% vs 3.9%, p=0.003,OR=3.34).
Conclusions:
There is a synergistic effect between –455G>A polymorphism of FGB gene and elevated concentration of serum triacylglycerols which determine the risk of CAD.
Fibrinogen promotes development of atherosclerosis by directed integration in atherosclerotic lesions where it is converted into fi brin. The aim of the study was to assess a relationship between –455G>A polymorphism of beta fi brinogen (FGB) gene and coronary artery disease (CAD) in the Polish patients from Upper Silesia region and to establish whether there are any interactions between this polymorphism and traditional risk factors that infl uence the risk of CAD.
Material and Methods:
We analyzed 191 patients with angiographically documented CAD and 203 blood donors. Genetic analysis was performed using PCR-RFLP method.
Results:
The frequency of FGB -455G>A genotypes was compatible with HardyWeinberg equilibrium. There was no significant differences in the distribution of A allele and A allele carriers of FGB polymorphism between cases and controls. We observed a tendency to higher level of plasma fibrinogen in subjects with AA or GA genotypes than in GG homozygotes. We also found strong synergistic effects between A allele carrier-state and increased level of triacylglycerols (TG) in determining the risk of CAD (SI=5.97, SIM=2.63). Carriers of A allele with elevated level of TG were 3-fold more frequent among cases than in control group (12.0% vs 3.9%, p=0.003,OR=3.34).
Conclusions:
There is a synergistic effect between –455G>A polymorphism of FGB gene and elevated concentration of serum triacylglycerols which determine the risk of CAD.
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