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Full list of author information is available at the end of the articleBackground Prevention and treatment of malaria is mainly based on the use of drugs [1]. Treatment response in Plasmodium falciparum malaria depends on various factors such as parasite resistance, host natural immunity, drug quality and the pharmacokinetics of the administered drug [2]. Various studies have been carried out on molecular mechanisms for resistance in malaria chemotherapy [3]. However limited efforts have been made to determine genetic polymorphisms in cytochrome P450 enzymes, which may be associated with treatment failure (in ex-tensive metabolizers) as a result of subtherapeutic drug concentrations. Cytochrome P450 (CYP) polymorphisms may also cause toxicity (in slow metabolizers) due to high drug concentrations and emergence or spread of drug resistance (in extensive metabolizers) as a result of subtherapeutic drug concentrations. Recent studies have also associated drug resistant selection with poor metabolizer (PM) phenotype. The increasing use of artemisinin-based combinations as an effective treatment of resistant malaria demands deter