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TO THE EDITOR—We have read with great interest the article by Paganotti et al [1], in which evidence is presented about the possible influence of human pharmacogenetics on the development of chloroquine (CQ) resistance by Plasmodium falciparum. This prompted us to hypothesize that such influence would be more visible and significant when considering the structurally related amodiaquine (AQ). In fact, although CYP2C8 is a secondary player in the metabolism of CQ [2], it is essential for the cytochrome P450 (CYP) associated biotransformation of AQ to its therapeutically main active metabolite, desethylamodiaquine (DEAQ)[3]. The in vivo parasite response to AQ therapy is modulated by polymorphisms in the P. falciparum multidrug resistance 1 gene (pfmdr1), particularly those concerning the N86Y [4], Y184F, and D1246Y [5, 6] single-nucleotide polymorphisms (SNPs). Accordingly, we hypothesized that …