Agustos 2010

Trombozla iliskili gastrointestinal hastaliklarda protein C yolagi ve antitrombin

Protein C pathway and antithrombin in thrombosis-related gastrointestinal disorders

Yazarlar
Hüseyin ALKIM1, Selime AYAZ2, Canan ALKIM3, Nurgül SASMAZ4
Kurumlar
Bakirköy Dr. Sadi Konuk Egitim ve Arastirma Hastanesi, 1Gastroenteroloji Klinigi, Istanbul

Türkiye Yüksek Ihtisas Hastanesi, 2Hematoloji Bölümü, 4Gastroenteroloji Klinigi, Ankara

Sisli Etfal Egitim ve Arastirma Hastanesi, 3Gastroenteroloji Klinigi, Istanbul
Sayfa Numaraları
48-54
Makale Türü
Özgün Görüntüler
Anahtar Kelimeler
Tromboz, protein C, protein S, antitrombin, aktive protein C direnci, portal ven trombozu, Budd-Chiari sendromu, siroz, inflamatuar barsak hastaligi
Keywords
Thrombosis, protein C, protein S, antithrombin, activated protein C resistance, portal vein thrombosis, Budd-Chiari syndrome, cirrhosis, inflammatory bowel disease

Özet

Giris ve Amaç: Etyolojisinde tromboz olan ve/veya dogal seyrinde trombotik komplikasyonlarla sik karsilasilan gastrointestinal hastaliklarda (portal ven trombozu, Budd-Chiari sendromu, karaciger sirozu, inflamatuar barsak hastaligi ve gastrointestinal malignite) aktive protein C direnci sikligi ile protein C, protein S ve antitrombin eksikliklerini arastirmak üzere bu prospektif çalisma planlandi. Gereç ve Yöntem: Hastalardan fonksiyonel yöntemlerle protein C, protein S, antitrombin aktiviteleri ve koagülasyon faktörü V?den yoksun test plazmasi kullanilarak modifiye yöntemle aktive protein C direnci arastirildi. Bulgular: Protein C eksikligi siroz, malign ve sekonder portal ven trombozu gruplarinda diger gruplardan daha sikti (p<0.05). Primer portal ven trombozu ve Budd-Chiari sendromundaki protein C eksikligi ise kontrolden daha fazlaydi (p<0.05). Protein S eksikligi Budd-Chiari sendromunda diger tüm gruplardan istatistiksel önemde fazlaydi. Inflamatuar barsak hastaligi, malign ve her iki portal ven trombozu grubunda protein S eksikligi orani siroz ve kontrolden yüksekdi (p<0.05). Antitrombin eksikligi sirozda diger tüm gruplardan daha fazlaydi. Aktive protein C direnci varligi orani tüm hasta gruplarinda kontrolden istatistiksel önemde fazlalik gösteriyordu (p<0.05). Budd-Chiari sendromunda aktive protein C direnci bulunma orani ise diger tüm gruplardan fazlaydi (p<0.05). Ayrica sirozlu ve maligniteli hastalarda tromboz varligiyla aktive protein C direnci bulunmasi korelasyon gösteriyordu (p<0.05). Trombofilik faktörlerden iki veya daha fazlasinin birarada bulunmasi tromboz riskinde belirgin artisa neden olmaktaydi. Sonuç: Protein C, protein S ve antitrombin eksikliklerinin ve özellikle aktive protein C direnci varliginin; Budd-Chiari sendromu ve portal ven trombozu etyolojisinde rol oynayabilecegi, sirozlu, inflamatuar barsak hastalikli ve maligniteli hastalarda tromboz gelisme riskini arttirdigi saptandi.

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<0.05). Protein C deficiency in primary portal vein thrombosis and Budd-Chiari syndrome was higher than in the healthy controls (p<0.05). Protein S deficiency in Budd-Chiari syndrome was higher than in all other groups (p<0.05). In addition, protein S deficiency in the inflammatory bowel disease, malignancy and both portal vein thrombosis groups was higher than in the cirrhosis and control groups (p<0.05). Antithrombin deficiency in the cirrhosis group was significantly higher than in all other groups (p<0.05). The presence of activated protein C resistance was significantly higher in all of the disease groups compared to the control group (p<0.05). Furthermore, the presence of activated protein C resistance in patients with Budd-Chiari syndrome was significantly higher than in all the other groups (p<0.05). The presence of activated protein C resistance was correlated with the presence of thrombosis in patients with cirrhosis and malignancy. Co-occurrences of two or more abnormalities among these four studied factors significantly increased the risk of thrombosis. Conclusions: Deficiencies in protein C, protein S and antithrombin and especially the presence of activated protein C resistance are important factors playing a role in the pathogenesis of Budd-Chiari syndrome and portal vein thrombosis, and they increased the risk of thrombosis in the cirrhosis, malignancy and inflammatory bowel disease groups.

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