Pharmacogenomics in clinical practice to prevent risperidone-induced hyperprolactinemia in autism spectrum disorder

Pharmacogenomics. 2022 Jun;23(8):493-503. doi: 10.2217/pgs-2022-0016. Epub 2022 Apr 28.

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.

Keywords: CYP2D6 and DRD2 genetic polymorphisms; autism spectrum disorder; hyperprolactinemia; pharmacogenomics; precision medicine; risperidone.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antipsychotic Agents* / therapeutic use
  • Autism Spectrum Disorder* / drug therapy
  • Autism Spectrum Disorder* / genetics
  • Humans
  • Hyperprolactinemia* / chemically induced
  • Hyperprolactinemia* / drug therapy
  • Hyperprolactinemia* / genetics
  • Pharmacogenetics
  • Prolactin
  • Risperidone / adverse effects

Substances

  • Antipsychotic Agents
  • Prolactin
  • Risperidone