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ORIGINAL ARTICLE
Year : 2017  |  Volume : 38  |  Issue : 1  |  Page : 41-48

Early-onset versus late-onset obsessive–compulsive disorder: an immunological comparative study


1 Department of Psychiatry, Faculty of Medicine, Mansoura University, Mansoura, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt

Correspondence Address:
Sahar El Emam Gad
Psychiatry, Lecturer of Psychiatry Mansoura University, Postal code: 35744
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-1105.200719

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Objectives This study was conducted to investigate the possible role of streptococcal infection in obsessive–compulsive disorder (OCD) and to clarify whether the age of onset could affect its clinical presentation and immunological results. Participants and methods The study was carried on 96 participants. They were divided into 46 OCD patients with a mean age of 30.76 years and 50 healthy controls with a mean age of 28.94 years. The patients group was subdivided according to the age of onset into the early-onset group include 21 patients with onset age of 18 years or less and the late-onset group include 25 patients with onset age above 18 years. All participants were subjected to psychometric and serological assessments of serum antibasal ganglia autoantibodies (ABGA) and antistreptolysin O titer (ASOT). Results Rates of ABGA positivity were 26.1% in the OCD group compared with 30% in the control group, with no significant difference (P=0.670). ASOT positivity were 6.5% in the OCD group, whereas none of the controls had positive ASOT (P=0.160). Positivity for ASOT and ABGA was not associated with the age of onset as 95.2 and 71.4% of the early-onset group had positive ASOT and ABGA results against 92 and 76% in the late-onset group, respectively, with no significant differences (P≥0.05) or clinical variables. Positivity for ASOT was not associated with ABGA positivity. Conclusion The negative results of this study do not exclude the role of autoimmunity in OCD pathogenesis. Further investigations are needed to establish this role.


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