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Journal of Thrombosis and Thrombolysis

, Volume 19, Issue 1, pp 61–63 | Cite as

Is Tissue-Plasminogen Activator Gene Polymorphism a Risk Factor for Venous Thromboembolism in Every Population?

  • I. Kivilcim OguzulgenEmail author
  • Numan Ekim
  • Ferda Oner Erkekol
  • Buket Altinok
  • Nejat Akar
Article

Abstract

Background: Tissue-plasminogen activator is a key protein of fibrinolytic system. In recent years the relation between t-PA, its genetic polymorphisms and arterial or venous thrombosis were investigated in different populations. The aim of this study is to investigate the role of t-PA gene polymorphism in Turkish venous thromboembolism (VTE) patients.

Methods: A case-control study was performed. We investigated the t-PA insertion/deletion (I/D) polymorphism in 93 VTE patients and 146 controls without VTE. Recurrent cases and documented risk factors for PTE were recorded.

Results: Cases and controls did not differ with respect to the different t-PA genotypes. The prevalence of I allele was 44.1%, 44.5% in cases and controls respectively (OR = 0.95, 95% CI: 0.78–1.24, p > 0.05). Different t-PA genotypes had no effect on recurrent disease. No gender difference was observed with respect to the different t-PA genotypes. There was no significant difference for genotype frequency between PTE patients with documented risk factors and unprovoked cases.

Conclusions: In conclusion there was no association between t-PA genotype and VTE in this group of Turkish population. It was also found that genotype frequencies for t-PA in both VTE and control subjects seems different from those reported from western part of the world.

Abbreviated Abstract. The aim of this study is to investigate the role of t-PA gene polymorphism in Turkish VTE patients. We investigated 93 VTE patients and 146 controls without VTE. Cases and controls did not differ with respect to the different t-PA genotypes. The prevalence of I allele was 44.1%, 44.5% in cases and controls respectively (OR = 0.95, 95% CI: 0.78–1.24, p > 0.05). Different t-PA genotypes had no effect on recurrent disease. No gender difference was observed with respect to the different t-PA genotypes. There was no significant difference for genotype frequency between PTE patients with documented risk factors and unprovoked cases. In conclusion there was no association between t-PA genotype and VTE in this group of Turkish population. It was also found that genotype frequencies for t-PA in both VTE and control subjects seems different from those reported from western part of the world.

venous thromboembolism pulmonary embolism t-PA gene genetics 

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References

  1. 1.
    Lane DA, Grant PJ. Role of haemostatic gene polymorphisms in venous and arterial thrombotic disease. Blood 2000;95:1517–1532.PubMedGoogle Scholar
  2. 2.
    Hooper WC, El-Jamil M, Dilley A, et al. The relation between the tissue plasminogen activator Alu I/D polymorphism and venous thromboembolism during pregnancy. Thromb Res 2001;102:33–37.CrossRefPubMedGoogle Scholar
  3. 3.
    Walker ID, Davidson JF, Hutton I, Lawrie TDV. Disordered “fibrinolytic potential” in coronary artery disease. Thromb Res 1977;10:509–520.CrossRefPubMedGoogle Scholar
  4. 4.
    Ridker PM, Vaughan DE, Stampfer MJ, Manson JE, Hennekens CH. Endogenous tissue-type plasminogen activator and risk of myocardial infarction. Lancet 1993;341:1165–1168.CrossRefPubMedGoogle Scholar
  5. 5.
    van der Bom JG, Knijff P, Haverkate F, et al. Tissue Plasminogen Activator and the Risk of Myocardial Infarction. The Rotterdam Study. Circulation 1997;95:2623–2627.PubMedGoogle Scholar
  6. 6.
    Jansson JH, Olofsson BO, Nilsson TK. Predictive value of tissue plasminogen activator mass concentration on long term mortality in patients with coronary artery disease. Circulation 1993;88:2030–2034.PubMedGoogle Scholar
  7. 7.
    Thompson SG, Kienast J, Pyke SDN, Haverkate F, van de Loo JCW. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995;332:635–641.CrossRefPubMedGoogle Scholar
  8. 8.
    Degen SJF, Rajput B, Reich E. The human tissue-type plasminogen activator gene. J Biol Chem 1986;261:6972–6985.PubMedGoogle Scholar
  9. 9.
    Yang-Feng TL, Opdenakker G, Volckaert G, Francke U. Human tissue-type plasminogen activator gene located near chromosomal breakpoint in myeloproliferative disorders. Am J Human Genet 1986;39:79–87.Google Scholar
  10. 10.
    Ludwig M, Wohn KD, Schleuning WD, Olek K. Allelic dimorphism in the human tissue-type plasminogen activator (t-PA) gene as a result of Alu insertion/deletion event. Hum Genet 1992;88:388–392.PubMedGoogle Scholar
  11. 11.
    Carter AM, Catto AJ, Grant PJ. Determinants of tPA antigen and associations with coronary artery disease and acute cerebrovascular disease. Thromb Haemost 1998;80:632–636.PubMedGoogle Scholar
  12. 12.
    Ridker PM, Baker MT, Hennekens CH, Stampfer MJ, Vaughan DE. Alu-repeat polymorphism in the gene coding for tissue-type plasminogen activator (t-PA) and risks of myocardial infarction among middle-aged men. Arterioscler Thromb Vasc Biol 1997;17:1687–1690.PubMedGoogle Scholar
  13. 13.
    Juhan-Vauge I, Valadier J, Alessi MC, et al. Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis. Thromb Haemost 1987;57:67–72.PubMedGoogle Scholar
  14. 14.
    Schulman S, Wiman B and the Duration of Anticoagulation (DURAC) Trial Study Group. The significance of hypofibrinolysis for the risk of recurrence of venous thromboembolism. Thromb Haemost 1996;75:607–611.PubMedGoogle Scholar
  15. 15.
    Hooper WC, Lally C, Austin H, Renshaw M, Dilley A. The role of the t-PA I/D and PAI-1 4G/5G polymorphisms in African-American adults with a diagnosis of myocardial infarction or venous thromboembolism. Thromb Res 2000;99:223–230.CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science + Business Media, Inc. 2005

Authors and Affiliations

  • I. Kivilcim Oguzulgen
    • 1
    Email author
  • Numan Ekim
    • 1
  • Ferda Oner Erkekol
    • 2
  • Buket Altinok
    • 3
  • Nejat Akar
    • 4
  1. 1.Department of Pulmonary MedicineGazi University School of MedicineAnkaraTurkey
  2. 2.Department of Pulmonary MedicineAnkara University School of MedicineAnkaraTurkey
  3. 3.Ankara University Biotechnology InstituteAnkaraTurkey
  4. 4.Department of Pediatric Molecular GeneticsAnkara University School of MedicineAnkaraTurkey

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