Abstract
A large subgroup of around 25% of schizophrenia patients suffers from obsessive-compulsive symptoms (OCS) and about 12% fulfill the diagnostic criteria of an obsessive-compulsive disorder (OCD). The additional occurrence of OCS is associated with high subjective burden of disease, additional neurocognitive impairment, poorer social and vocational functioning, greater service utilization and high levels of anxiety and depression. Comorbid patients can be assigned to heterogeneous subgroups. One hypothesis assumes that second generation antipsychotics (SGAs), most importantly clozapine, might aggravate or even induce second-onset OCS. Several arguments support this assumption, most importantly the observed chronological order of first psychotic manifestation, start of treatment with clozapine and onset of OCS. In addition, correlations between OCS-severity and dose and serum levels and duration of clozapine treatment hint toward a dose-dependent side effect. It has been hypothesized that genetic risk-factors dispose patients with schizophrenia to develop OCS. One study in a South Korean sample reported associations with polymorphisms in the gene SLC1A1 (solute carrier family 1A1) and SGA-induced OCS. However, this finding could not be replicated in European patients. Preliminary results also suggest an involvement of polymorphisms in the BDNF gene (brain-derived neurotrophic factor) and an interaction between markers of SLC1A1 and the gene DLGAP3 (disc large associated protein 3) as well as GRIN2B (N-methyl-D-aspartate receptor subunit 2B). Further research of well-defined samples, in particular studies investigating possible interactions of genetic risk-constellations and pharmacodynamic properties, are needed to clarify the assumed development of SGA-induced OCS. Results might improve pathogenic concepts and facilitate the definition of at risk populations, early detection and monitoring of OCS as well as multimodal therapeutic interventions.
Highlights
Reported data show strong associations between comorbid obsessive-compulsive symptoms (OCS) in schizophrenia and mainly antiserotonergic second generation antipsychotics (SGA), most importantly CLZ
The same group further described a genetic interaction of the solute carrier family gene 1A1 (SLC1A1) polymorphism with variants in the gene disks large associated protein 3 (DLGAP3) and a link to SGAinduced OCS (Ryu et al, 2011)
Because no genetic associations between SLC1A1 polymorphisms and OCS were found within the power limits of this study, much larger samples seem necessary to untangle the interplay of pharmacological and genetic risk factors for OCS in schizophrenia (Schirmbeck et al, 2012a)
Summary
One study in a South Korean sample reported associations with polymorphisms in the gene SLC1A1 (solute carrier family 1A1) and SGA-induced OCS This finding could not be replicated in European patients. Similar concepts were suggested regarding depression (Keers and Uher, 2012), anxiety disorders (Gregory et al, 2008; Nugent et al, 2011) and obsessive-compulsive disorder (OCD) Primary OCD-patients carry a relatively low risk (1.7%) to develop comorbid psychotic symptoms (de Haan et al, 2009)
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