Journals / MN Kardiyoloji / 2004 / Cilt: 11 - Sayı: 1

Repeted deep vein thrombosis developed after minor travma in a young, factor V Leiden heterozigot carier

Faktör V Leiden heterozigot taşıyıcısı olan genç hastada minör travma sonrası gelişen ve tekrarlayan derin ven trombozu

Pages
53–56
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this report we present a repeated DVT case which had developed after a minor trauma in an eighteen years old, male factor V Leiden heterezigot carier.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:G1691A point mutation of factor V gene (Leiden mutation) and active protein C resistance that develops related to this mutation are the most common genetic disorders that increase the risk of thrombosis.
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Key Findings & Data:While the incidence of Deep Vein Thrombosis(DVT) increases especially after major operations and traumas in patients with this gene mutation, there are some DVT cases which, were reported to develop spontaneously and after minor traumas.
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Conclusion & Impact:In this report we present a repeated DVT case which had developed after a minor trauma in an eighteen years old, male factor V Leiden heterezigot carier.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Nokta mutasyonu · Venöz tromboz · Faktör V

Abstract

G1691A point mutation of factor V gene (Leiden mutation) and active protein C resistance that develops related to this mutation are the most common genetic disorders that increase the risk of thrombosis. While the incidence of Deep Vein Thrombosis(DVT) increases especially after major operations and traumas in patients with this gene mutation, there are some DVT cases which, were reported to develop spontaneously and after minor traumas. In this report we present a repeated DVT case which had developed after a minor trauma in an eighteen years old, male factor V Leiden heterezigot carier.

Özet

Faktör V geninin G1691A nokta mutasyonu (Faktör V Leiden) ve buna bağlı gelişen aktive protein C rezistansı tromboza egilim riskini artıran en sık genetik bozukluktur. Bu mutasyona sahip hastalarda özellikle majör cerrahi ve travmalardan sonra derin ven trombozu (DVT) görülme sıklığı artarken, minör travma sonucu veya spontan olarak gelişen DVT vaka bildirileri de bulunmaktadır. Bu yazıda faktör V Leiden heterozigot taşıyıcısı 18 yaşında erkek hastada minör travma sonrası gelişen ve tekrarlayan DVT, olgu bildirisi olarak sunuldu.

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Cite This Article

MUTLU, B., BİTİGEN, A., BAYRAK, F., TÜRKMEN, M., BAŞARAN, Y. (2004). Repeted deep vein thrombosis developed after minor travma in a young, factor V Leiden heterozigot carier. MN Kardiyoloji, Cilt: 11 - Sayı: 1, 53–56. https://ajindex.com/articles/297674

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References (13)

  1. Clogett GP, Reisch JS. Prevention of venous thromboembolism in general surgical patients: Results of a meta-analysis. Ann Surg 1988; 2:227-40. Goldhaber ZS. Pulmonary embolism In: Braunwald E, Zipes DP, Libby P, editors. Heart Disease. Philadelphia: W.B. Saunders company, 2001:1886-907. Rosendal FR. Venous thrombosis: A multicausal disease. Lancet, 1999; 353:1167-73.
  2. Bertina RM, Koeleman BPC, Koster T, et al. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature, 1994; 369:64-7.
  3. De Stefano V, Chiusolo P, Paciaroni K, Leone G Epidemiology of factor V Leiden: clinical implications. Semin Thromb Hemost, 1998; 24:367-79.
  4. Ridker PM, Herinekeıis CH, Lindpaintner K, et al. Mutation in the gene coding for coagulation factor V and risk of future myocardial infaction,stroke,and venous thrombosis in apparently healthy men. N Engl J Med, 1995; 332:912-7.
  5. Sullivan W, Wolk SW, Whitehouse WM Jr. Simultaneous bila teral upper extremity venous thrombosis in a factor V Leiden he terozygote: a case report and review. Vase Surg, 2001; 35:361-8. Giangrande PL. Air travel and thrombosis. Int J Clin Pract 2001; 55:690-3.
  6. Hilberg T, Jeschke D, Gabriel HH. Hereditary thrombophilia in elite athletes. Med Sci Sports Exerc 2002; 34:218-21.
  7. Ridker PM, Hennekens CH, Miletich JP. G20210A mutation in prothrombin gene and risk of myocardial infaction, and venous thrombosis in a large cohort of US men. Circulation, 1999; 99:999-1004.
  8. De Stephano V, Martinelli I, Mannucci PM, et al. The risk of recurrent deep venous thrombosis among heterozygous carries of both Factor V leidenand G20210A prothrombin mutation. N Eng J Med, 1999; 341:801-6.
  9. Turkstra F, Karemaker R, Kuijer PMM, et al. Is the prevalence of the factor V leiden mutation in patients with pulmonary embolism and deep venous thrombosis really different? Thromb Haemost, 1999; 81:345- Simioni P, Prandoni P, Lensing A, et al. The risk of recurrent venous thromboembolism in patients with an Arg506 Gln mutation in the gene for Factor V (Factor V leiden). N Engl J Med, 1997; 336:399-403.
  10. Myers TM, Hull RD, Weg JG. Antithrombotic therapy for venous thromboembolic disease. Chest. 1992; 102:408-25.
  11. Coon WW, Willis PW. Recurrence thromboembolism. Surgery. 1973; 73:823-7.
  12. Hull R, Delmore T, Genton E, et al. Warfarin sodium versus low-dose heparin in the long term treatment of venous thrombosis. N Engl J Med. 1979; 301:855-9.
  13. Hull R, Delmore T, Carter C, et al. Adjusted subcutaneous heparin versus warfa