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2009 | 63 | 5 | 41-49
Article title

Carrier-state of the A allele of – 455G>A polymorphism within the beta fibrinogen gene increases the risk of coronary artery disease in the presence of elevated concentration of serum triacylglycerols

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Title variants
PL
Nosicielstwo allela A polimorfizmu – 455G>A genu fibrynogenu beta zwiększa ryzyko choroby wieńcowej przy jednoczesnym podwyższonym stężeniu triglicerydów w surowicy
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EN
Abstracts
EN
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. 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 Hardy- Weinberg equilibrium. There was no signifi cant diff erences 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 eff ects 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 eff ect between –455G>A polymorphism of FGB gene and elevated concentration of serum triacylglycerols which determine the risk of CAD.
PL
WSTĘP Fibrynogen promuje rozwój zmian miażdżycowych przez przyleganie do zmienionej ściany tętnic gdzie jest przekształcany w fibrynę. Celem niniejszej pracy była ocena związku między polimorfi zmem –455G>A genu kodującego łańcuch beta fibrynogenu (FGB) a ryzykiem choroby wieńcowej (CAD, ang. coronary artery disease) w grupie pacjentów z Górnego Śląska i ustalenie czy istnieją interakcje między tym polimorfi zmem a tradycyjnymi czynnikami ryzyka miażdżycy w determinowaniu ryzyka CAD. MATERIAŁ I METODY Grupę badaną stanowiło: 191 pacjentów z potwierdzoną koronarografi cznie CAD oraz 203 krwiodawców bez obciążeń chorobami sercowo-naczyniowymi. Polimorfi zm –455G>A genu FGB genotypowano metodą RFLP-PCR. Wyniki. Częstości genotypów polimorfi zmu -455G>A genu FGB były zgodne z równowagą Hardy-Weinberg’a. Nie stwierdzono znamiennych różnic w częstości allela A i nosicieli allela A polimorfi zmu genu FGB między pacjentami a grupą kontrolną. Obserwowano tendencję do występowania wyższego poziomu fi brynogenu w osoczu osób z genotypami AA i GA w porównaniu do poziomu fibrynogenu w osoczu osób z genotypem GG. Stwierdzono również silny synergiczny efekt między nosicielstwem allela A a podwyższonym poziomem triglicerydów w determinowaniu ryzyka CAD (indeksy synergii SI=5.97, SIM=2.63). Nosiciele allela A charakteryzujący się podwyższonym poziomem triglicerydów występowali trzykrotnie częściej w grupie chorych niż w kontroli (12.0% vs 3.9%, p=0.003,OR=3.34). WNIOSKI Przedstawione wyniki wskazują na synergiczny związek nosicielstwa allela A polimorfi zmu – 455G>A genu FGB z ponadnormatywnym stężeniem triglicerydów w surowicy krwi w kształtowaniu ryzyka CAD w populacji pacjentów z Górnego Śląska.
Discipline
Publisher

Year
Volume
63
Issue
5
Pages
41-49
Physical description
Contributors
  • 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, beatasarecka@poczta.onet.pl
author
  • Department of Biochemistry and Medical Genetics, School of Health Care, Medical University of Silesia, Katowice, Poland
  • The First Department of Cardiac Surgery, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland
References
  • 1. Chung D.W., Harris J.E., Davie E.W. Nucleotide sequences of the three genes coding for human fibrinogen. Adv. Exp. Med. Biol. 1990; 281: 39-48.
  • 2. Zhang J.Z., Redman C.M. Identifi cation of B beta chain domains involved in human fibrinogen assembly. J. Biol. Chem. 1992; 267: 21727-21732.
  • 3. Bazzano L.A., He J., Muntner P., Vupputuri S., Whelton P.K. Relationship between cigarette smoking and novel risk factors for cardiovascular disease in the United States. Ann. Intern. Med. 2003; 138: 891-897.
  • 4. Thomas A.E., Green F.R., Kelleher C.H. i wsp. Variation in the promoter region of the beta fibrinogen gene is associated with plasma fi brinogen levels in smokers and non-smokers. Thromb. Haemost. 1991; 65:487-490.
  • 5. Tybjaerg-Hansen A., Agerholm-Larsen B., Humphries S.E., Abildgaard S., Schnohr P., Nordestgaard B.G. A common mutation (G-455--> A) in the beta-fi brinogen promoter is an independent predictor of plasma fi brinogen, but not of ischemic heart disease. A study of 9,127 individuals based on the Copenhagen City Heart Study. J. Clin. Invest. 1997; 99: 3034- 3039.
  • 6. Smith E.B., Keen G.A., Grant A., Stirk C. Fate of fibrinogen in human arterial intima. Arteriosclerosis 1990; 10:263-275.
  • 7. Lindsberg P.J., Grau A.J. Infl ammation and infections as risk factors for ischemic stroke. Stroke 2003; 34: 2518-2532.
  • 8. Behague I., Poirier O., Nicaud V. i wsp. Beta fi brinogen gene polymorphisms are associated with plasma fi brinogen and coronary artery disease in patients with myocardial infarction. The ECTIM Study. Etude Cas-Temoins sur l‘Infarctus du Myocarde. Circulation 1996; 93: 440-449.
  • 9. Hamsten A., Iselius L., de Faire U., Blomback M. Genetic and cultural inheritance of plasma fi brinogen concentration. Lancet 1987; 2: 988-991.
  • 10. Dalmon J., Laurent M., Courtois G. The human beta fibrinogen promoter contains a hepatocyte nuclear factor 1-dependent interleukin-6-responsive element. Mol. Cell Biol. 1993; 13: 1183-1193.
  • 11. Judkin M.P., Gander M.P. Prevention of complications of coronary arteriography. Circulation 1974; 49: 599-602.
  • 12. Alpert J.S., Thygesen K. Myocardial infarction redefi ned – A consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefi nition of Myocardial Infarction. Eur. Heart J. 2000; 21: 1502-1513.
  • 13. Sarecka-Hujar B., Zak I., Krauze J. Interactions between rs5498 polymorphism in the ICAM1 gene and traditional risk factors infl uence susceptibility to coronary artery disease. Clin. Exp. Med. 2009; 9:117-124.
  • 14. Friedewald W.T., Levy R.I., Fredrickson D.S. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without the use of preparative centrifuge. Clin. Chem. 1972; 18: 499- 502.
  • 15. Nishiuma S., Kario K., Yakushijin K. i wsp. Genetic variation in the promoter region of the beta-fibrinogen gene is associated with ischemic stroke in a Japanese population. Blood Coagul. Fibrinolysis 1998; 9:373-379.
  • 16. Rothman K.J. Synergy and antagonism in cause-eff ect relationship. Am. J. Epidemiol. 1974; 99: 385-388.
  • 17. Khoury M.J., Flanders W.D. Nontraditional epidemiologic approaches in the analysis of gene-environment interaction: case-control studies with no controls! Am. J. Epidemiol. 1996; 144: 207-213.
  • 18. Lam K.S., Ma O.C., Wat N.M., Chan L.C., Janus E.D. Beta-fibrinogen gene G/A-455 polymorphism in relation to fi brinogen concentrations and ischaemic heart disease in Chinese patients with type II diabetes. Diabetologia 1999; 42: 1250-1253.
  • 19. de Maat M.P., Kastelein J.J., Jukema J.W. i wsp. -455G/A polymorphism of the beta-fibrinogen gene is associated with the progression of coronary atherosclerosis in symptomatic men: proposed role for an acute-phase reaction pattern of fi brinogen. REGRESS group. Arterioscler. Thromb. Vasc. Biol. 1998; 18: 265-271.
  • 20. Bi S., Wang D., Li G., Wen S., Pan S. Beta-fi brinogen promoter -455 G/A (HaeIII) polymorphism prediction of plasma fi brinogen but not of ischemic cerebrovascular disease. Chin. Med. Sci. J. 2004; 19: 1-5.
  • 21. Ando R., Doi M., Yamauchi K. i wsp. Association of beta-fi brinogen and factor VII polymorphism with plasma fi brinogen and factor VII levels, and no association of PAI-1 polymorphism with plasma PAI-1 levels in hemodialysis patients. Clin. Nephrol. 2002; 58: 25-32.
  • 22. Lee A.J., Fowkes F.G., Lowe G.D., Connor J.M., Rumley A. Fibrinogen, factor VII and PAI-1 genotypes and the risk of coronary and peripheral atherosclerosis: Edinburgh Artery Study. Thromb. Haemost. 1999; 81: 553-560.
  • 23. de Maat M.P., de Knijff P., Green F.R., Thomas A.E., Jespersen J., Kluft C. Genderrelated association between beta-fi brinogen genotype and plasma fi brinogen levels and linkage disequilibrium at the fi brinogen locus in Greenland Inuit. Arterioscler. Thromb. Vasc. Biol. 1995; 15: 856-860.
  • 24. Thomas A., Lamlum H., Humphries S., Green F. Linkage disequilibrium across the fibrinogen locus as shown by fi ve genetic polymorphisms, G/A-455 (HaeIII), C/T- 148 (HindIII/AluI), T/G+1689 (AvaII), and BclI (beta-fi brinogen) and TaqI (alphafi brinogen), and their detection by PCR. Hum. Mutat. 1994; 3: 79-81.
  • 25. Mannila M.N., Lovely R.S., Kazmierczak S.C. i wsp. Elevated plasma fibrinogen gamma‘ concentration is associated with myocardial infarction: eff ects of variation in fi - brinogen genes and environmental factors. J. Thromb. Haemost. 2007; 5: 766-773.
  • 26. Leander K., Wiman B., Hallqvist J., Falk G., De Faire U. The G-455A polymorphism of the fibrinogen Bbeta-gene relates to plasma fi brinogen in male cases, but does not interact with environmental factors in causing myocardial infarction in either men or women. J. Intern. Med. 2002; 252: 332-341.
  • 27. Bots M.L., Elwood P.C., Salonen J.T. i wsp. Level of fi brinogen and risk of fatal and non-fatal stroke. EUROSTROKE: a collaborative study among research centres in Europe. J. Epidemiol. Community Health 2002; 56 Suppl 1: i14-8.
  • 28. Mills J.D., Ariens R.A., Mansfi eld M.W., Grant P.J. Altered fi brin clot structure in the healthy relatives of patients with premature coronary artery disease. Circulation 2002; 106: 1938-1942.
  • 29. Weng X., Cloutier G., Genest J. Jr. Contribution of the -455G/A polymorphism at the betafi brinogen gene to erythrocyte aggregation in patients with coronary artery disease. Thromb. Haemost. 1999; 82:1406- 1411.
  • 30. Scarabin P.Y., Aillaud M.F., Amouyel P. i wsp. Associations of fi brinogen, factor VII and PAI-1 with baseline fi ndings among 10,500 male participants in a prospective study of myocardial infarction--the PRIME Study. Prospective Epidemiological Study of Myocardial Infarction. Thromb. Haemost. 1998; 80: 749-756.
  • 31. Boekholdt S.M., Bijsterveld N.R., Moons A.H., Levi M., Buller H.R., Peters R.J. Genetic variation in coagulation and fi brinolytic proteins and their relation with acute myocardial infarction: a systematic review. Circulation 2001; 104: 3063-3068.
  • 32. Koch W., Hoppmann P., Biele J., Mueller J.C., Schömig A., Kastrati A. Fibrinogen genes and myocardial infarction: a haplotype analysis. Arterioscler. Thromb. Vasc. Biol. 2008; 28: 758-763.
  • 33. Choumerianou D.M., Maumus S., Skoumas J. et all. Polymorphisms associated with apolipoprotein B levels in Greek patients with familial hypercholesterolemia. Clin. Chem. Lab. Med. 2006; 44: 799- 806.
  • 34. Zak I., Sarecka-Hujar B., Krauze J. Cigarette smoking, carrier state of A or G allele of 46A>G and 79C > G polymorphisms of beta2-adrenergic receptor gene, and the risk of coronary artery disease. Kardiol. Pol. 2008; 66: 380-386.
  • 35. Zak I., Sarecka-Hujar B., Krauze J. Relationships between traditional risk factors and carrier-state of C allele of 1059G>C polymorphism in the C-reactive protein gene and the risk of coronary artery disease. Ann. Acad. Med. Siles. 2008; 62: 27- 33.
  • 36. Zak I., Sarecka B., Krauze J. Synergistic eff ects between 561A > C and 98G > T polymorphisms of E-selectin gene and hypercholesterolemia in determining the susceptibility to coronary artery disease. Heart Vessels 2008; 23: 257-263.
Document Type
article
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YADDA identifier
bwmeta1.element.psjd-795ae232-4c60-49a6-8107-6219fa3183dc
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