Inter individual differences in the metabolism of antimalarials could be due to polymorphism of NAT2 gene. The authors determined the genotypic frequencies of single nucleotide polymorphism （SNP） of NAT2 gene and it...Inter individual differences in the metabolism of antimalarials could be due to polymorphism of NAT2 gene. The authors determined the genotypic frequencies of single nucleotide polymorphism （SNP） of NAT2 gene and it＇s implication in antimalarial treatment during a vitamin A and zinc supplementation intervention in children aged 6 to 24 months. Children were deparasitized with artesunate-amodiaquine （ASAQ）-toddler 50/135 mg. Pharmacovigilance was done for 40 days, adverse events recorded and blood was spotted on filter paper for DNA extraction by chelex method. PCR-RFLP was performed with restriction enzymes KpnI, TaqI, and BamHl for detection of SNPs of NAT2. Allelic frequencies and phenotypes were compared between participants with or without adverse drug events. The prevalence of fast, slow and intermediate acetylators was 55%, 30% and 11% respectively. There was a significant association （P = 0.035） between NAT2 slow acetylators （and susceptibility to develop skin rash. No significant difference was observed between fast and slow acetylators and susceptibility to develop fever, anorexia, cough and common cold. Slow acetylators were more susceptible, （P = 0.011） to develop any adverse event The NAT2 slow acetylator phenotype was the most predominant and individuals with this phenotype were more significantly susceptible to develop adverse events to ASAQ.展开更多
文摘Inter individual differences in the metabolism of antimalarials could be due to polymorphism of NAT2 gene. The authors determined the genotypic frequencies of single nucleotide polymorphism （SNP） of NAT2 gene and it＇s implication in antimalarial treatment during a vitamin A and zinc supplementation intervention in children aged 6 to 24 months. Children were deparasitized with artesunate-amodiaquine （ASAQ）-toddler 50/135 mg. Pharmacovigilance was done for 40 days, adverse events recorded and blood was spotted on filter paper for DNA extraction by chelex method. PCR-RFLP was performed with restriction enzymes KpnI, TaqI, and BamHl for detection of SNPs of NAT2. Allelic frequencies and phenotypes were compared between participants with or without adverse drug events. The prevalence of fast, slow and intermediate acetylators was 55%, 30% and 11% respectively. There was a significant association （P = 0.035） between NAT2 slow acetylators （and susceptibility to develop skin rash. No significant difference was observed between fast and slow acetylators and susceptibility to develop fever, anorexia, cough and common cold. Slow acetylators were more susceptible, （P = 0.011） to develop any adverse event The NAT2 slow acetylator phenotype was the most predominant and individuals with this phenotype were more significantly susceptible to develop adverse events to ASAQ.
