Document Type
Article
Publication Date
7-2023
Identifier
DOI: 10.2217/pgs-2023-0091
Abstract
Aim: Antimalarial primaquine (PQ) eliminates liver hypnozoites of Plasmodium vivax. CYP2D6 gene variation contributes to PQ therapeutic failure. Additional gene variation may contribute to PQ efficacy. Information on pharmacogenomic variation in Madagascar, with vivax malaria and a unique population admixture, is scanty. Methods: The authors performed genome-wide genotyping of 55 Malagasy samples and analyzed data with a focus on a set of 28 pharmacogenes most relevant to PQ. Results: Mainly, the study identified 110 coding or splicing variants, including those that, based on previous studies in other populations, may be implicated in PQ response and copy number variation, specifically in chromosomal regions that contain pharmacogenes. Conclusion: With this pilot information, larger genome-wide association analyses with PQ metabolism and response are substantially more feasible.
Journal Title
Pharmacogenomics
Volume
24
Issue
11
First Page
583
Last Page
597
MeSH Keywords
Humans; Antimalarials; Primaquine; DNA Copy Number Variations; Genome-Wide Association Study; Pharmacogenetics; Chloroquine
Keywords
Madagascar; Plasmodium vivax; copy number variation; genome-wide array; malaria treatment; primaquine
Recommended Citation
Cramer EY, Bartlett J, Chan ER, et al. Pharmacogenomic variation in the Malagasy population: implications for the antimalarial drug primaquine metabolism. Pharmacogenomics. 2023;24(11):583-597. doi:10.2217/pgs-2023-0091
Comments
Grant support
This work is licensed under the Attribution-NonCommercial-NoDerivatives 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.
Publisher's Link: https://www.futuremedicine.com/doi/epub/10.2217/pgs-2023-0091