Gülay CEYLAN, Canan H. HASANOĞLU, Filiz ÇURLACI KARASU, Mükremin ER

Plazminojen Aktivatör İnhibitörü tip-1 Gen (PAİ-1) Polimorfizmi ve Pulmoner Emboli Arasındaki İlişki

Amaç:Pulmoner tromboemboli (PTE) kalıtsal ve kazanılmış risk faktörlerine bağlı gelişebileceği gibi idiopa-tik olarak ta karşımıza çıkabilir. Plazminojen aktivatör inhibitör-1 (PAİ-1) plazmada plasminojen aktivatörü-nün esas inhibitörüdür. Plasminojenin plazmine dönüşümünde aktivatör görev yapan doku plasminojen aktivatörü ve ürikinaz’ ı inhibe eder. Bu çalışmanın amacı PTE gelişiminde PAİ-1 gen polimorfizminin tek başına ve diğer genetik mutasyonlarla birlikte etkinliğini araştırmaktır.Yöntem: Çalışmaya 64 PTE hastası ve 60 sağlıklı kontrol grubu dahil edildi. Kalıtsal risk faktörlerinden PAİ-1 gen polimorfizmi, Faktör V leiden mutasyonu, Faktör V 1299, Metilen tetrahidrofolat redüktaz C677 ve A1298, Faktör II G20210A (protrombin gen mutasyonu) çalışıldı. Ayrıca hastaların kazanılmış risk faktörle-ri belirlendi. Hasta grubunda HDL, homosistein, D-dimer düzeyleri çalışıldı.Bulgular:Hasta grubunda yaş ortalaması 60,8±15,4 ve kontrol grubunda yaş ortalaması 56,6±16,9 idi. Hasta grubunda PAİ-1 gen polimorfizmi 5G/5G (normal) olan 18 kişi, 4G/5G olan 27 kişi, 4G/4G olan 19 kişi vardı. Kontrol grubunda PAİ-1 gen polimorfizmi 5G/5G (normal) olan 11 kişi, 4G/5G olan 34 kişi, 4G/4G olan 15 kişi vardı. Hasta ve kontrol grubu karşılaştırıldığında fark istatistiksel olarak anlamlı değildi (p>0.05). PAİ-1 gen polimorfizmleri ile diğer genetik risk faktörlerinin ikişerli ve üçerli birlikteliği hasta ve kontrol grubunda karşı-laştırıldığında fark istatistiksel olarak anlamlı değildi. Sonuç olarak çalışmamızda; PAİ-1 gen polimorfizminin diğer mutasyonlarla birlikte veya yalnız olarak pulmoner tromboemboli riskini artırdığına dair veriye ulaşıla-mamıştır. Sonuç:Çalışmamızda, PAİ-1 gen polimorfizminin diğer mutasyonlarla birlikte veya yalnız olarak pulmoner tromboemboli riskini artırdığına dair veriye ulaşılamamıştır.

Association Between Plasminogen Activator Inhibitor type-1 Gene (PAI-1) Polymorphism and Pulmonary Embolism

43Özgün Araştırma / Research Articleİzmir Göğüs Hastanesi Dergisi 2020;34(1):43-9doi:10.5222/İGH.2020.1746ABSTRACTObjective:Pulmonary thromboembolism (TPE) may develop due to hereditary and acquired risk factors but idiopathic cases may face us. Plasminogen activator inhibitor-1 (PAI-1) is the primary inhibitor of the plasminogen activator in plasma. It inhibits tissue plasminogen activator which involves in conversion of plasminıgen to plasmin, and urokinase. The objective of this study is to investigate the effectiveness of PAI-1 gene polymorphism in the development of PTE alone and in combination with other genetic mutations.Method:Sixty-four patients with PTE and a control group of 60 individuals were enrolled in our study. Among hereditary risk factors, PAI-1 gene polymorphisms, Factor V Leiden mutation, Factor V 1299, methylene tetrahydrofolate reductase C677 and A1298, and Factor II G20210A were studied. Besides acquired risk factors of the patients were identified. Levels of HDL, homocysteine, and D-dimer were analyzed. Results:The mean ages of the patient, and the control groups were 60.8±15.4, and 56.6±16.9 years, respectively. In the patient group, PAI-1 gene 5G/5G polymorphism (normal) (n=18), 4G/5G polymorphism (n=27) and 4G/4G polymorphism (n=19) were detected in indicated number of participants. In the control group, PAI-1 5G/5G 11 polymorphism (normal) (n=11), 4G/5G polymorphism (n=34) and 4G/4G polymorphism (n=15) in respective number of patients. There was no statistically significant difference between patients and the control group when comparisons were made in double and triple combinations in terms of PAI-1 gene polymorphisms, and other risk factors (p>0.05). Also, we found a weak association between PAI-1 gene polimorphism and pulmonary embolism.Conclusion:In our study we couldn’t arrive at data suggesting increase in the risk of pulmonary trhromboembolism in the presence of PAI-1 gene polymorphism alone or in combination with other mutations.

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