Abstract
Background The use of single-dose primaquine to block transmission of Plasmodium falciparum malaria is complicated by variation in glucose-6-phosphate-dehydrogenase (G6PD) activity and potentially cytochrome P450 2D6 (CYP2D6). G6PD deficiency determines primaquine safety while the CYP2D6 metabolizer phenotype may determine primaquine efficacy by influencing metabolism into active metabolite(s). While there is evidence that the CYP2D6 metabolizer phenotype influences primaquine efficacy against P. vivax hypnozoites, there is currently no evidence for CYP2D6 in relation to its gametocytocidal activity in P. falciparum.
Highlights
cytochrome P450 2D6 (CYP2D6) intermediate metabolizer status could slow down Plasmodium falciparum gametocyte clearance after single-dose primaquine
The use of single-dose primaquine to block transmission of Plasmodium falciparum malaria is complicated by variation in glucose-6-phosphate-dehydrogenase (G6PD) activity and potentially cytochrome P450 2D6 (CYP2D6)
The number of poor metabolizers (PM) is low in our study population and does not allow a firm conclusion on its impact on gametocyte clearance following primaquine
Summary
The use of single-dose primaquine to block transmission of Plasmodium falciparum malaria is complicated by variation in glucose-6-phosphate-dehydrogenase (G6PD) activity and potentially cytochrome P450 2D6 (CYP2D6). G6PD deficiency determines primaquine safety while the CYP2D6 metabolizer phenotype may determine primaquine efficacy by influencing metabolism into active metabolite(s). While there is evidence that the CYP2D6 metabolizer phenotype influences primaquine efficacy against P. vivax hypnozoites, there is currently no evidence for CYP2D6 in relation to its gametocytocidal activity in P. falciparum
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