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Pharmacogenetic Association Between Glutamatergic Genes and Sri Treatment Response in Obsessive Compulsive Disorder

Published online by Cambridge University Press:  23 March 2020

T. Shukla ,
R.M.J. Jabeen Taj ,
K. Kulkarni ,
P. Shetty ,
B. Viswanath ,
M. Purushottam ,
Y.C. Reddy  and
S. Jain
T. Shukla
Affiliation:
King George's Medical University, Psychiatry, Lucknow, India
R.M.J. Jabeen Taj
Affiliation:
Centre de Recherche du CHU Sainte-Justine, université de Montréal, Montreal, Canada
K. Kulkarni
Affiliation:
National Institute of Mental Health and Neurosciences, Psychiatry, Bangalore, India
P. Shetty
Affiliation:
Cairns and Hinterland Hospital and Health Service, Psychiatry, Melbourne, Australia
B. Viswanath
Affiliation:
National Institute of Mental Health and Neurosciences, Psychiatry, Bangalore, India
M. Purushottam
Affiliation:
National Institute of Mental Health and Neurosciences, Psychiatry, Bangalore, India
Y.C. Reddy
Affiliation:
National Institute of Mental Health and Neurosciences, Psychiatry, Bangalore, India
S. Jain
Affiliation:
National Institute of Mental Health and Neurosciences, Psychiatry, Bangalore, India

Abstract

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Introduction

Pharmacogenetic studies in obsessive-compulsive disorder (OCD) primarily focussing on serotonergic and dopaminergic polymorphisms, provided inconsistent findings. There is recent evidence for glutamatergic abnormalities in OCD.

Aims

Examine the association glutamatergic genes with serotonin reuptake inhibitor (SRI) response in OCD.

Objectives

To study pharmacogenetic association between SLC1A1 and GRIN2B polymorphisms with SRI response in OCD.

Methods

DSM-IV OCD patients were recruited from a specialty OCD clinic and evaluated using the Yale-Brown obsessive compulsive scale (YBOCS), Mini International Neuropsychiatric Interview (MINI) plus, Clinical Global Impression scale (CGI). They were subsequently reassessed with YBOCS and CGI. To study extreme phenotypes, we included only full responders (> 35% YBOCS improvement and CGI-I score of 1 or 2) to any SRI (n = 191) and non-responders (< 25% YBOCS improvement and CGI-I score ≥ 4) to adequate trial of at least two SRIs (n = 84). Partial responders were excluded. Genotyping was performed using an ABI9700 PCR machine.

Results

Genotype frequencies did not deviate significantly from the values predicted by the Hardy-Weinberg equation. Case-control association analyses revealed no significant association between genotype/allele frequencies with SRI response.

Conclusion

Our data does not show any association between polymorphisms in glutamatergic genes and SRI response in OCD though such associations have been found in other studies. More SNP's in the same gene could be responsible for the pharmacogenetic associations. More homogenous sample considering symptom dimensions and other phenotypic variables may be needed. It may be critical to go beyond “usual suspect” candidate gene research. In this regard, a novel approach to identify SRI response biomarkers is the use of cellular models.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
e-Poster walk: Anxiety disorders and somatoform disorders
Information
European Psychiatry , Volume 41 , Issue S1: Abstract of the 25th European Congress of Psychiatry , April 2017 , pp. S111
Copyright
Copyright © European Psychiatric Association 2017
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