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Impact of DRD2 polymorphisms on prolactin level in risperidone-treated Thai children and adolescent with autism spectrum disorders

Published online by Cambridge University Press:  23 March 2020

Y. Hongkaew
Affiliation:
Faculty of Medicine Ramathibodi hospital, Pathology, Bangkok, Thailand

Abstract

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Introduction

A large number of studies have reported that the prolactin concentration was significantly increased in the Taq1A A1 allele carriers because several reports revealed that individuals with the DRD2 Taq1A A1 allele have a reduced density of brain D2 receptors.

Objective

The main aim of this study was to identify the impact of pharmacogenetic markers associated with prolactin concentration in risperidone-treated children and adolescents with autism spectrum disorders.

Methods

One hundred and forty-seven children and adolescents with autism, aged 3 to 19, received risperidone. The clinical data of patients were recorded from medical records. Prolactin levels were measured by chemiluminescence immunoassay. Three CYP2D6 single nucleotide polymorphisms (SNPs), CYP2D6*4 (1846G>A), *10 (100C>T), and *41 (2988G>A), one gene deletion (*5), and DRD2 Taq1A (rs1800497) polymorphism were genotyped by TaqMan real-time PCR.

Results

The three common allelic frequencies were CYP2D6*10 (55.10%), *1 (32.65%) and *5 (6.12%), respectively. Patients were grouped according to their CYP2D6 genotypes. The DRD2 genotype frequencies were Taq1A A2A2 (38.77%), A1A2 (41.50%), and A1A1 (19.73%), respectively. There were statistically significant differences in prolactin level of patients among the three groups (P = 0.033). The median prolactin level in patients with DRD2 Taq1A A2A2 (17.80 ng/mL) was significantly higher than A1A2 (17.10 ng/mL) and A1A1 (12.70 ng/mL).

Conclusion

DRD2 Taq1A A2A2 polymorphisms may be a critical role in an influence prolactin elevation during risperidone treatment in ASD.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
FC56
Copyright
Copyright © European Psychiatric Association 2016
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