SavedAdd your journal

Journals / Akademik Gastroenteroloji Dergisi / 2010 / Cilt: 9 - Sayı: 2

Protein C pathway and antithrombin in thrombosis-related gastrointestinal disorders

Trombozla ilişkili gastrointestinal hastalıklarda protein C yolağı ve antitrombin

Hüseyin ALKIM
Selime AYAZ
CANAN ALKIM
Nurgül ŞAŞNAZ
Pages
48–54
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

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

Results: Protein C deficiency in the cirrhosis, malignancy and secondary portal vein thrombosis groups was significantly higher than in the other groups (p

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background and Aims: We aimed to determine the frequency of activated protein C resistance and deficiencies of protein C, protein S and antithrombin in different gastrointestinal diseases (portal vein thrombosis, Budd-Chiari syndrome, liver cirrhosis, inflammatory bowel disease and gastrointestinal malignancies), which related with thrombosis etiologically and/or pathogenetically.
📊
Key Findings & Data:Materials and Methods: Protein C, protein S and antithrombin activities were measured by functional methods.
💡
Conclusion & Impact:Results: Protein C deficiency in the cirrhosis, malignancy and secondary portal vein thrombosis groups was significantly higher than in the other groups (p
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Tromboz · protein C · protein S

Abstract

Background and Aims: We aimed to determine the frequency of activated protein C resistance and deficiencies of protein C, protein S and antithrombin in different gastrointestinal diseases (portal vein thrombosis, Budd-Chiari syndrome, liver cirrhosis, inflammatory bowel disease and gastrointestinal malignancies), which related with thrombosis etiologically and/or pathogenetically. Materials and Methods: Protein C, protein S and antithrombin activities were measured by functional methods. Activated protein C resistance was detected by the modified method using factor V-deficient plasma. Results: Protein C deficiency in the cirrhosis, malignancy and secondary portal vein thrombosis groups was significantly higher than in the other groups (p

Özet

Giriş ve Amaç: Etyolojisinde tromboz olan ve/veya doğal seyrinde trombotik komplikasyonlarla sık karşılaşılan gastrointestinal hastalıklarda (portal ven trombozu, Budd-Chiari sendromu, karaciğer sirozu, inflamatuar barsak hastalığı ve gastrointestinal malignite) aktive protein C direnci sıklığı ile protein C, protein S ve antitrombin eksikliklerini araştırmak üzere bu prospektif çalışma planlandı. Gereç ve Yöntem: Hastalardan fonksiyonel yöntemlerle protein C, protein S, antitrombin aktiviteleri ve koagülasyon faktörü V’den yoksun test plazması kullanılarak modifiye yöntemle aktive protein C direnci araştırıldı. Bulgular: Protein C eksikliği siroz, malign ve sekonder portal ven trombozu gruplarında diğer gruplardan daha sıktı (p < 0.05). Primer portal ven trombozu ve Budd-Chiari sendromundaki protein C eksikliği ise kontrolden daha fazlaydı (p < 0.05). Protein S eksikliği Budd-Chiari sendromunda diğer tüm gruplardan istatistiksel önemde fazlaydı. ‹nflamatuar barsak hastalığı, malign ve her iki portal ven trombozu grubunda protein S eksikliği oranı siroz ve kontrolden yüksekdi (p < 0.05). Antitrombin eksikliği sirozda diğer tüm gruplardan daha fazlaydı. Aktive protein C direnci varlığı oranı tüm hasta gruplarında kontrolden istatistiksel önemde fazlalık gösteriyordu (p < 0.05). Budd-Chiari sendromunda aktive protein C direnci bulunma oranı ise diğer tüm gruplardan fazlaydı (p < 0.05). Ayrıca sirozlu ve maligniteli hastalarda tromboz varlığıyla aktive protein C direnci bulunması korelasyon gösteriyordu (p < 0.05). Trombofilik faktörlerden iki veya daha fazlasının birarada bulunması tromboz riskinde belirgin artışa neden olmaktaydı. Sonuç: Protein C, protein S ve antitrombin eksikliklerinin ve özellikle aktive protein C direnci varlığının; Budd-Chiari sendromu ve portal ven trombozu etyolojisinde rol oynayabileceği, sirozlu, inflamatuar barsak hastalıklı ve maligniteli hastalarda tromboz gelişme riskini arttırdığı saptandı.

🔖

Cite This Article

ALKIM, H., AYAZ, S., ALKIM, C., ŞAŞNAZ, N. (2010). Protein C pathway and antithrombin in thrombosis-related gastrointestinal disorders. Akademik Gastroenteroloji Dergisi, Cilt: 9 - Sayı: 2, 48–54. https://ajindex.com/articles/166901

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Harker LA. Disorders of hemostasis and thrombosis: Pathogenesis of thrombosis. In: Williams WJ, Beutler E, Erslev AJ, Lichtman MA, Eds. Hematology 4thed. New York, McGraw Hill 1991; 1559-69. Handin RI. Bleeding and thrombosis. In: Fauci AS, Braunwald Eeds. Harrison’s Principles of Internal Medicine 14thed. New York, McGraw Hill 1998; 339-45.
  2. Florell SR, Rodgers GM. Inherited thrombotic disorders: an update. Am J Hematol 1997; 54: 53-60.
  3. Martinelli I, Mannuci PM, De Stefano V, et al. Different risks of thrombosis in four coagulation defects associated with inherited thrombophilia: a study of 150 families. Blood 1998; 92: 2353-8.
  4. Murin S, Marelich G, Arroliga A, Matthay R. Hereditary thrombop- hilia and venous thromboembolism. Am J Respir Crit Care Med 1998; 158: 1369-73. Dahlbäck B, Carlsson M, Svensson PJ. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor an- ticoagulant response to activated protein C: prediction of a cofac- tor to activated protein C. Proc Natl Acad Sci USA 1993; 90: 1004- 8. Bertina RM, Koeleman BPC, Koster T, et al. Mutation in blood co- agulation factor V associated with resistance to activated protein C. Nature 1994;369: 64-7.
  5. Gürgey A, Mesci L. The prevalence of factor V Leiden (1691G-A) mutation in Turkey. Turk J Pediatr 1997; 39: 313-5.
  6. Akar N, Akar E, Dalgın G, et al. Frequency of factor V Leiden (1691G-A) mutation in Turkish population. Thromb Haemost 1997; 78: 1527-8.
  7. Özbek U, Tangün Y. Frequency of factor V Leiden in Turkey. Br J Haematol 1997; 97: 504-5.
  8. Aboud MR, Ma DDF. A comparison between two activated prote- in C resistance methods as routine diagnostic tests for factor V Lei- den mutation. Br J Haematol 1997; 97: 798-803.
  9. Tripodi A, Negri B, Bertina RM, Mannuci PM. Screening for the FV:Q506 mutation-evaluation of thirteen plasma-based methods for their diagnostic efficacy in comparison with DNA analysis. Thromb Haemost 1997; 77: 436-9.
  10. Svensson PJ, Zöller B, Dahlbäck B. Evaluation of original and modi- fied APC-resistance tests in unselected outpatients with clinically suspected thrombosis and in healthy controls. Thromb Haemost 1997; 77: 332-5.
  11. Parikh S, Shah R, Kapoor P. Portal vein thrombosis. Am J Med 2010; 123: 111-9.
  12. Kelly DA, Tuddenham EGD. Haemostatic problems in liver disease. Gut 1986; 27: 339-49.
  13. Bick RL, Strauss JF, Frenkel EP. Thrombosis and hemorrhage in on- cology patients. Hematol Oncol Clin North Am 1996; 10: 875-907.
  14. Hudson M, Chitolie A, Hutton RA, et al. Thrombo