iMedPub Journals ht tp://wwwimedpub.com ARCHIVES OF MEDICINE 2015 Vol. 7 No. 4:2 1 © Copyright iMedPub | This article is available from: www.archivesofmedicine.com Chloroquine Resistance and Host Genetc Factors among Nigerian Children with Uncomplicated P. falciparum Infecton Introducton Malaria remains a signifcant health problem in Nigeria with Plasmodium falciparum being the predominant species. It is responsible for 25% of infant mortality, 30% of childhood mortality and about 50% of outpatent visits [1]. Chloroquine which was once the mainstay of treatment of uncomplicated falciparum malaria is now threatened by resistance. Chloroquine-resistant parasites are present in most areas where malaria is endemic [2]. Consequently, the decline in efcacy of chloroquine has led to the use of alternatve antmalarials, such as antfolates, mefoquine and artemisinin derivatves. However, parasite resistance to these drugs except artemisinin, is also becoming a real problem CM Nneji 1 , ADA Adedapo 1 , PN Okorie 2 , OG Ademowo 1,2* 1 Department of Pharmacology and Therapeutcs, 2 Insttute for Advanced Medical Research and Training, University of Ibadan, Ibadan, Nigeria Corresponding Author: Olusegun George Ademowom Insttute for Advanced Medical Research and Training, University of Ibadan, Ibadan, Nigeria,  bogdandeleanu@yahoo.com Tel Number: +234 802 334 2856 Abstract Chloroquine resistance and host genetc factors among Nigerian children with uncomplicated P.falciparum infecton. Background: Chloroquine resistance is widespread. Host factors play a role in drug resistance. The study aims to determine the associaton between hosts red cell factors namely G6PD status, ABO blood group and haemoglobin genotype with Pfmdr1 mutatons and treatment outcome. Methods: One hundred and twenty patents (aged 1-15years) with acute symptoms of P.falciparum malaria were treated with chloroquine (CQ). Blood sample was obtained for haematological parameters and analysis of parasite DNA. Nested PCR followed by restricton fragment length polymorphism (RFLP) at codon 86 of the Pfmdr1 gene was determined in the 120 isolates. Relatonship between Pfmdr1 alleles, CQ resistance, G6PD defcient, sickle cell trait and parasite diversity was evaluated. Results: Seventy of the 120 patents enrolled into this study completed the 14-day follow-up, aged 7.8 ± 4.6 years, 62 (52%) were females with parasites geometric mean 21,861 (range 1000-354,667) asexual parasites per microlitre of blood. Thirty- seven of the 70 (53%) were cured while 47% failed chloroquine treatment; mean parasite clearance tme (PCT) was 7.1 days, whereas the mean fever clearance tme was 3.4 days. Mutaton revealed wild type N86 (56), mutant type Y86 (50) and mixed genotype N86+Y86 (14). No signifcant correlaton was found between Pfmdr1 mutatons and in-vivo outcome (p=0.21). About 51% (36/70) of the in-vivo pre-treatment samples carried the Pfmdr1 Y86 mutaton and its prevalence varied with age (p=0.017). The Pfmdr1Y86 mutaton was detected in majority (19/33) of patents with clinical failure OR=1.711; 95% CI: 0.517-5.668; p=0.378 and was more in younger OR=1.200; 95% CI: 0.782-1.840 than in older children OR=0.818; 95% CI: 0.507-1.321. Conclusion: There is an associaton between Pfmdr1Y86 mutaton and CQ treatment failure which tends to be stronger in younger children. These suggest the role of age and host immunity in modifying the relatonship between molecular markers and resistance.