Pharmacogenomics in clinical practice to prevent risperidone-induced hyperprolactinemia in autism spectrum disorder
Issued Date
2022-06-01
Resource Type
ISSN
14622416
eISSN
17448042
Scopus ID
2-s2.0-85131217314
Pubmed ID
35477330
Journal Title
Pharmacogenomics
Volume
23
Issue
8
Start Page
493
End Page
503
Rights Holder(s)
SCOPUS
Bibliographic Citation
Pharmacogenomics Vol.23 No.8 (2022) , 493-503
Suggested Citation
Biswas M., Vanwong N., Sukasem C. Pharmacogenomics in clinical practice to prevent risperidone-induced hyperprolactinemia in autism spectrum disorder. Pharmacogenomics Vol.23 No.8 (2022) , 493-503. 503. doi:10.2217/pgs-2022-0016 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/83720
Title
Pharmacogenomics in clinical practice to prevent risperidone-induced hyperprolactinemia in autism spectrum disorder
Author(s)
Other Contributor(s)
Abstract
Autism spectrum disorder (ASD) is a global challenge that may disrupts family and social life significantly. There is robust evidence for the association of a pharmacokinetic gene variant (e.g., CYP2D6) with risperidone-induced hyperprolactinemia in ASD. Association of a pharmacodynamic gene variant (e.g., DRD2) with risperidone-induced hyperprolactinemia in ASD is also evident from multiple studies. In addition to genetic factors, dose, duration and drug-drug interactions of risperidone might also increase the serum prolactin level. There are several difficulties, such as reimbursement, knowledge and education of healthcare providers, in implementing risperidone pharmacogenomics into clinical practice. However, preparation of national and international pharmacogenomics-based dosing guidelines of risperidone may advance precision medicine of ASD.