Association between Obsessive Compulsive Disorder and Tumor Necrosis Factor-α Gene −308 (G>A) and −850 (C>T) Polymorphisms in Turkish Children

Obsessive compulsive disorder (OCD) is a neurobiological disease characterized with obsessions and compulsions. Obsessive compulsive disorder occurs with an autoimmune mechanism after Group A β hemolytic streptococcus (GABHS) infection. Tumor necrosis factor (TNF) is an important cytokine, as well as having an important role in the apoptosis mechanism of autoimmune diseases. It is expressed by the TNF-α gene. The aim of this study was to examine the relationship between the TNF-α gene promoter region −308 (G>A) and −850 (C>T) polymorphisms and OCD. In this study, ages of the OCD patients and the control group ranged between 4 and 12 years. We studied two patient groups, one included childhood onset OCD patients (n = 49) and the control group was composed of healthy children (n = 58). Patients were diagnosed according to the Diagnostic and Statistical Manual of Mental Disorder (DSM-IV) criteria and with Kiddie Schedule for Affective Disorders and Schizophrenia-Present and Lifetime (KSAD-S-PL) version. For identifying the polymorphisms, polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP) and polyacrylamide gel electrophoresis (PAGE) methods were used. For the −308 polymorphism, 45 of 49 OCD patients’ results were completed, and for the −850 polymorphism, 47 of 49 OCD patients’ results were completed. According to our statistical results, there is a positive relationship between OCD and the −308 polymorphism (p <0.001) but no association between OCD and the −850 polymorphism (p = 0.053). There is no positive relationship between antistreptolysin O (ASO) titers and the −308 polymorphism (p = 0.953) but there is an important significance between the −850 polymorphism and ASO (p = 0.010). There is no positive relationship between gender of patients and OCD (p = 0.180) and no positive association between ASO and gender (p = 0.467). According to our results, we hypothesize that we can propose the mutant AA genotype for the −308 polymorphism, and that the mutant CT genotype for the −850 polymorphism may be used as molecular indicators for OCD.