Fatih AYDIN, Ercan AKŞİT, Özge TURGAY YILDIRIM, Hanefi Yekta GÜRLERTOP, Yücel KAÇMAZ

Koroner Arter Hastalığında Endotelyal Nitrik Oksit Sentaz Geninin Glu 298-Asp Ve T786-C Polimorfizmlerinin Araştırılması

Amaç: Bu çalışma ile eNOS geninin Glu298-Asp ve T-786C polimorfizmleri ile Koroner arter hastalığı (KAH) arasındaki ilişkisinin araştırılması ve KAH gelişmesinde rol oynayan genetik faktörlerin aydınlatılmasına katkıda bulunulması amaçlandı. Hastalar ve Yöntemler: Çalışmada toplam 200 hasta değerlendirildi. Ciddi KAH, majör koroner arterlerin en az birinde ≥%50 darlık olması olarak tanımlanmış ve bu hastalar KAH grubuna alındı (n=144). Stenozisi olmayan hastalar kontrol grubuna dahil edildi (n=66). Bulgular: T-786C polimorfizminin değerlendirilmesi sonucunda, KAH ve kontrol grupları karşılaştırıldığında TT (p=0,660), TC (p=0,73) ve CC (p=0,634) genotipleri arasında anlamlı fark saptanmamıştır. Her iki grupta da dominant (p=0,439) ve resesif (p=0,622) model karşılaştırmasında anlamlı fark yoktur. Glu 298-Asp polimorfizmi incelendiğinde; gruplar genotip dağılımlarına göre karşılaştırıldığında, GG (p=0,836), GT (p=0,581) ve TT (p=0,767) genotipleri arasında istatistiksel olarak anlamlı fark bulunmamıştır. Gruplar, hem dominant (p=0,697) hem de resesif (p=0,485) model karşılaştırmalarına göre istatistiksel açıdan benzer nulunmuştur. Sonuç: Çalışma sonucunda, T-786 C ve Glu 298-Asp polimorfizmleri ve KAH arasında istatistiksel bir ilişki bulunmamıştır. T-786 C ve Glu 298-Asp polimorfizmlerinin rolünü açıklığa kavuşturmak için daha büyük çalışma popülasyonları ile benzer çalışmalar yapılmalıdır.

Glu 298-Asp And T786-C Polymorphisms Of Endothelial Nitric Oxide Synthase Gene In Coronary Artery Disease Patients

Aim: We aimed to investigate the association of eNOS gene with Glu298-Asp andT-786C polymorphisms with Coronary artery disease (CAD) and to contribute to theelucidation of the genetic factors involved in the development of CAD.Patients and Methods: A total of 200 patients were evaluated. Severe CAD was defined as ≥ 50% stenosis in at least one of major coronary arteries and these patientswere taken into the CAD group (n=144). Patients without stenosis were included inthe control group (n=66).Results: After the evaluation of T-786C polymorphism, there was no significant difference between TT (p=0,660), TC (p=0,73) and CC (p=0,634) genotypes betweenCAD and control groups. There was no significant difference between the groups inboth dominant (p=0,439) and recessive (p=0,622) model comparisons. When Glu298-Asp polymorphism was examined, there was no statistically significantdifference between GG (p=0,836), GT (p=0,581) and TT (p=0,767) genotypes whenthe groups were compared according to genotype distributions. The groups werestatistically similar according to both dominant (p=0,697) and recessive (p=0,485)model com-parisons.Conclusion: There was no statistical correlation between T-786 C and Glu 298-Asppolymorphisms and CAD. Similar studies with larger study populations should beconducted to clarify the role of T-786 C and Glu 298-Asp polymorphisms.

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