SEVDA KORKMAZ, EBRU ÖNALAN, HÜSEYİN YÜCE, Murad ATMACA

Obsesif kompulsif bozukluk hastalarında triptofanhidroksilaz gen polimorfizmi

Giriş: Triptofanhidroksilaz 1 (TPH1) A218C gen polimorfizminin obsesifkompulsif bozukluk (OKB) etiyolojisindeki etkisi konusunda yapılan çalışmalar sınırlı sayıdadır. Çalışmamızda TPH1 A218C gen polimorfizminin OKB etiyolojisindeki rolünü araştırmayı amaçladık. Yöntem: Çalışmaya, kliniğimize başvuran, çalışma ölçütlerine uyan, 60 OKB hastası alındı. Hasta gruplarıyla yaş ve cinsiyet açısından eşleştirilmiş 60 sağlıklı kontrol grubu oluşturuldu. Tedavinin başlangıcında katılımcılara, DSM-IV Eksen-I Bozuklukları için Yapılandırılmış Klinik Görüşme Ölçeği, Sosyodemografik ve Klinik Veri Formu, Yale-Brown Obsesyon Kompulsiyon Derecelendirme Ölçeği (Y-BCOS) ve Hamilton Depresyon Derecelendirme Ölçeği uygulandı. Hastalar tedavi öyküleri ve Y-BCOS puanlarına göre tedaviye yanıt veren ve tedaviye dirençli olmak üzere iki alt gruba ayrıldı. DNA izolasyonu için, standart yöntemlere göre 300 ?l kan kullanıldı. Kan örneklerinde TPH-1 genindeki A218C polimorfizminin değerlendirilmesinde; Restriksiyon Fragment Uzunluk Polimorfizm yöntemi uygulandı. Sonuç: Hasta ve kontrol grubu arasında TPH1 genotipleri açısından anlamlı bir farklılık saptanmadı. Tedaviye dirençli olan hasta grubunda TPH1 genine ait AA genotip sıklığında tedaviye yanıt veren hasta grubunda ise CC genotip sıklığında istatistiksel olarak anlamlı bir artış gözlendi. Bu polimorfizmdeki genotiptipioranlarının her hasta grubunda farklı olması, tedaviye yanıtla ilişkili olabilir. Çalışmadan elde edilen verilerin doğrulanabilmesi için aynı polimorfizmlerin farklı toplumlardaki OKB'li hastalarda çalışılarak, daha fazla araştırma ile desteklenmesi gerekmektedir.

Tryptophan hydroxylase gene polymorphism in patients with obsessive-compulsive disorder

Objective: There is limited number of studies on the effects of tryptophan hydroxylase1 (TPH1) A218C gene polymorphism on obsessive-compulsive disorder (OCD) etiology. This study aims to scrutinize the role of TPH1A218C gene polymorphism on OCD etiology. Methods: Sixty patients diagnosed with OCD, applied to our clinic and fitting the study criteria were accepted as patient group. A group of 60 healthy individuals matching the patient group in age and gender were selected as the control group. In the study the Clinical Interview Scale Structured for DSM-IV Axis-I Disorders, Socio-demographic and Clinical Data Form, Yale Brown Obsessive Compulsive Rating Scale (Y-BOCS) and Hamilton Depression Rating Scale were applied to participants initially. Consequently, they were classified into two groups of 'responsive to therapy' and 'resistant to therapy' based on their therapy histories and Y-BOCS points. For DNA isolation 300?l blood samples were used in compliance with standard methods. Restriction Fragment Length Polymorphism method was used to evaluate A218C polymorphism in TPH-1 gene within the blood samples. Results: No significant difference was observed between patient and control groups related to TPH-1 genotypes. However, a significant increase was observed in AA genotype frequency for TPH-1 gene in the patient group resistant to therapy and in CC genotype frequency in the patient group responsive to therapy. The difference of the allele type ratios in this polymorphism between each patient group could be related to the response to therapy. To confirm the findings of the study, more research on the same gene polymorphisms is required with OCD patients in different societies.

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