Şebnem ÖZKAN, Fatoş ÖNEN, Bülent ÜNDAR, Faize YÜKSEL, Fatih DEMİRKAN, İnci ALACACIOĞLU, Güner Hayri ÖZSAN, Mehmet Ali ÖZCAN, Özden PİŞKİN, Oğuz GÜRLER, Nurullah AKKOÇ, Servet AKAR

Plasma thrombin activatable fibrinolysis inhibitor levels in Behçet’s disease

Amaç: Behçet hastalığında görülen trombotik komplikasyonların patogenetik mekanizmaları henüz net değildir. Patogenezi endotel disfonksiyonu, koagulasyon ve fibrinolitik sistemlerindeki bozukluklar ile açıklayabilmek için pek çok hemostatik parametre çalışılöıştır. Trombin ile active edilebilen fibrinoliz inhibitörü (TAFİ) plazmin oluflumunu ve fibrinolizi inhibe eden, trombotik bozukluklarda etkisi son yıllarda keşfedilmiş bir risk faktörüdür. Bu çalışmada Behçet hastalığında ve kontrol grubunda TAFİ plazma seviyeleri araştırılmıştır. Yöntem ve Gereç: Erkek kadın oranı 5/18, ortalama yaşları 38.3 ± 10.83 olan 23 Behçet hastası (Uluslararası çalışma kriterlerine göre tanı almış) ile, erkek kadın oranı 9/11 ortalama yaşları 38.05 ± 6.29 olan sağlıklı kontroller çalışmaya alındı. Karaciğer, böbrek hastalığı, diyabeti, koroner hastalığı, antifosfolipid antikor pozitifliği olan, oral kontraseptif kullanan hastalar çalışma dışı bırakıldı. Plazma TAFİ seviyesi ELİZA testi kullanılarak ölçüldü. Bulgular: TAFİ antijen plazma seviyeleri Behçet hastalarInda 8.40 ± 1.81μg/ml, sağlığı gönüllülerde 7.30 ± 0.64 μg/ml olarak bulundu. iki grup arasında TAFİ seviyeleri açısından istatistiksel anlamlı fark mevcuttu (P = 0.01). Sonuç: Trombotik olay varlığından bağımsız olarak Behçet hastalığında TAFİ antijen seviyesi yüksekti. Ancak hastalığın etiyolojisinde TAFİ’nin yerinin daha net anlaşılabilmesi için trombotik komplikasyonu olan grubun da bulunduğu, daha fazla sayıda olgu içeren çalışmalara gerek vardır.

Behçet hastalığında plazma trombin ile aktive edilebilen fibrinoliz inhibitör (TAFİ) seviyesi

Aim: The precise pathogenetic mechanisms causing thrombotic complications in Behçet’s disease (BD) are still not known. To explain the pathogenesis with coagulation induction or a defective fibrinolysis superimposed on endothelial dysfunction, various hemostatic parameters were studied. Thrombin activatable fibrinolysis inhibitor (TAFI), downregulating plasmin generation and fibrinolysis, is a novel risk factor for thrombotic disorders. We studied plasma TAFI levels in BD in comparison with healthy controls. Materials and Methods: Twenty-three patients with BD (mean age: 38.3 ± 10.83, M/F: 5/18) diagnosed according to the criteria of the International Study Group and 20 healthy volunteers (mean age: 38.05 ± 6.29, M/F: 9/11) were enrolled in this study. Patients with liver or renal disease, diabetes mellitus, coronary artery disease, hemophilia, antiphospholipid antibody positivity or using oral contraceptive drugs were excluded from the study. Plasma TAFI levels were determined by using an ELISA test. Results: The mean TAFI antigen levels were 8.40 ± 1.81μg/ml in BD patients and 7.30 ± 0.64 μg/ml in healthy volunteers. A statistically significant difference was found between TAFI antigen levels of these two groups (P = 0.01). Conclusions: TAFI antigen levels were found to be increased in BD, regardless of thrombotic events. To clarify the exact role of TAFI in thrombotic complications of the disease, future studies including more patients with and without thrombosis are needed.

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