
ASSOCIATION BETWEEN OBSESSIVE COMPULSIVE
DISORDER AND TUMOR NECROSIS FACTOR-α GENE
–308 (G>A) AND –850 (C>T) POLYMORPHISMS
IN TURKISH CHILDREN Lüleyap HU1, Onatoğlu D1, Tahiroğlu AY2, Alptekin D1,*,
Yılmaz MB1, Çetiner S3, Pazarbaşı A1, Ünal İ4, Avcı A2 *Corresponding Author: Professor Dr. Davut Alptekin, Department of Medical Biology and Genetics, Medical
Faculty, Çukurova University, 01330 Adana, Turkey; Tel.: +90-322-3386060/3498; Fax: +90-322-3386572;
E-mail: alptekin@cu.edu.tr page: 61
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INTRODUCTION
Obsessive compulsive disorder (OCD), attention-
deficit hyperactivity disorder (ADHD) and tic
disorders are prepubertal symptom onset autoimmune
neuropsychiatric disorders associated with
basal ganglia abnormalities in which antibodies
produced against Group A β hemolytic streptococcus
(GABHS) infections cross react against neuron
epitopes. These disorders are referred to as post streptococcal movement disorders [1,2]. Obsessive
compulsive disorder may be triggered by stress, anxiety
and infections (for example; GABHS infections)
[3]. Comor-bidities, GABHS infections, obsessions
and compulsions are characteristic features in the
etiology of OCD [4,5]. Due to the damage of basal
ganglia after a period following a GABHS infection,
tics and obsessive compulsive symptoms occur in
patients. Exacerbations of OCD are accompanied
by unstable emotions, motoric hyperactivity and
symptoms of anxiety [4]. The association between
Sydenham’s chorea and streptococcus infections
was first mentioned by Taranta and Stollerman in
1956 [6] but association between OCD and Sydenham’s
chorea was discovered by Snider and Swedo
[4] and Swedo et al. [7]. In the late 1980s, the National
Institute of Mental Health reported increased
obsessive-compulsive symptoms in Sydenham’s chorea
patients [8]. In the following decades, clinicians
and researchers continued to make studies for neuropsychiatric
disorders [9]. Recent studies suggest that
50.0-80.0% of OCD cases have a childhood onset
[10]. Childhood onset OCD patients usually have a
positive history of childhood tonsillitis, tic disorders
and more antistrep-tolysin O (ASO) titers than adult
onset OCD patients [11]. In addition, obsessions and
compulsions are common symptoms for both of them
[12,13]. According to Walitza et al. [14], 1.0-3.0% of
the general population suffers from OCD. Prevalence
of OCD in adolescents is 0.4% [7]. Clinical studies
indicated that males frequently have earlier age onset
of OCD than girls [15]. It was indicated that boys
are much more affected than girls (3:2 ratio) [10].
However, epidemiological studies have shown that
the incidence of many prepubertal boys diagnosed
with OCD is three times that of girls. In addition,
it was detected that incidence of OCD in females
increases after puberty [15]. The immune system of
patients is affected in OCD. In the patient’s immune
system, the B lymphocyte susceptible to the M group
of antigens, kills them. After B lymphocyte activation,
some of the susceptible B lymphocytes pass
through the blood-brain barrier and associates with
the cell membrane of neuron cells because of epitope
similarity [16-19]. Neurons are destroyed by the patient’s
autoimmunity apoptosis mechanism. The loss
of neurons, especially in basal ganglia, leads to neuropshychiatric
signs such as obsessions, compulsions
or tics because the basal ganglia is part of the brain
which is responsible for cognition controlling, movement
coordination and voluntary movements. Tumor
necrosis factor (TNF) is an important cytokine and
also has an important role in the apoptosis mechanism
of autoimmune diseases. It is expressed by the
TNF-α gene. The aim of our study was to identify
the influence of the TNF-α gene –308 (G>A) and
–850 (C>T) polymorphisms on OCD. Despite other
research studies, the relationship between neuropsychiatric
disorders and GABHS infections are not yet
completely clear. One reason for this uncertainty is
due to the triggering of other existing factors [20].
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