Evidence for Pharmacogenomic Effects on Risperidone Outcomes in Pediatrics.
Katelyn M Rossow, Kazeem A Oshikoya, Ida T Aka and 3 others
PMID 33759847WHAT IT FOUND
Children with poor or intermediate CYP2D6 metabolism had significantly more adverse events on risperidone than normal metabolizers.
A specific HTR2A variant was linked to fewer events. Other tested genes showed no clear association with adverse outcomes in this retrospective pediatric cohort.
Key findings
01Poor and intermediate CYP2D6 metabolizers experienced adverse events more frequently than normal, rapid, or ultrarapid metabolizers.
02Individuals homozygous for the HTR2A rs6311 variant had a lower odds of experiencing adverse events.
03Variants in ABCB1, ABCG2, CYP3A4, CYP3A5, DRD2, DRD3, and HTR2C did not show an association with overall risperidone adverse events.
STILL TO COME
How it was doneWhat they found
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What it does not show
The study was conducted at a single tertiary care center, which may limit generalizability to other populations. Adverse events were identified retrospectively through chart review, so documentation errors or omissions could have affected the results. Medication adherence could not be determined from the electronic health records. The study did not assess drug efficacy or response, only adverse events. No formal causality assessment was performed to confirm that reported events were directly caused by risperidone, as is standard in retrospective designs.
Declared interests
The study was supported by the National Institutes of Health (Extramural). No specific conflicts of interest regarding commercial pharmacogenomic laboratories or drug manufacturers were declared in the provided text.
The easy way to misread this
Do not change prescribing practices based on these findings alone. The authors state that clinical guidelines for genotype-guided risperidone dosing do not currently exist, and changes in practice are not warranted at this time due to the retrospective nature of the data and the need for further prospective study.