Abstract
BackgroundRed blood cell (RBC) polymorphisms are common in malaria endemic regions and are known to protect against severe forms of the disease. Therefore, it is important to screen for these polymorphisms in drugs or vaccines efficacy trials. This study was undertaken to evaluate associations between clinical malaria and RBC polymorphisms to assess biological interactions that may be necessary for consideration when designing clinical trials.MethodIn a cross-sectional study of 341 febrile children less than five years of age, associations between clinical malaria and common RBC polymorphisms including the sickle cell gene and G6PD deficiency was evaluated between November 2008 and June 2009 in the middle belt of Ghana, Kintampo. G6PD deficiency was determined by quantitative methods whiles haemoglobin variants were determined by haemoglobin titan gel electrophoresis. Blood smears were stained with Giemsa and parasite densities were determined microscopically.ResultsThe prevalence of clinical malarial among the enrolled children was 31.9%. The frequency of G6PD deficiency was 19.0% and that for the haemoglobin variants were 74.7%, 14.7%, 9.1%, 0.9% respectively for HbAA, HbAC, HbAS and HbSS. In Multivariate regression analysis, children with the HbAS genotype had 79% lower risk of malaria infection compared to those with the HbAA genotypes (OR = 0.21, 95% CI: 0.06–0.73, p = 0.01). HbAC genotype was not significantly associated with malaria infection relative to the HbAA genotype (OR = 0.70, 95% CI: 0.35–1.42, p = 0.33). G6PD deficient subgroup had a marginally increased risk of malaria infection compared to the G6PD normal subgroup (OR = 1.76, 95% CI: 0.98–3.16, p = 0.06).ConclusionThese results confirm previous findings showing a protective effect of sickle cell trait on clinical malaria infection. However, G6PD deficiency was associated with a marginal increase in susceptibility to clinical malaria compared to children without G6PD deficiency.
Highlights
It is estimated that there are about 216 million cases of malaria each year and about 655, 000 deaths worldwide [1]
A Cross Sectional Study in Malaria Endemic Region. These results confirm previous findings showing a protective effect of sickle cell trait on clinical malaria infection
Glucose-6-phosphate dehydrogenase (G6PD) deficiency was associated with a marginal increase in susceptibility to clinical malaria compared to children without G6PD deficiency
Summary
It is estimated that there are about 216 million cases of malaria each year and about 655, 000 deaths worldwide [1]. Glucose-6-phosphate dehydrogenase (G6PD) deficiency and haemoglobins S (HbS) are common genetic disorders in sub-Sahara Africa [7]. Sickle cell trait (HbAS) which is clinically silent occurs when an individual inherits one gene copy of mutated haemoglobin (S) gene and one gene copy of the normal haemoglobin (A) gene. Red blood cell (RBC) polymorphisms are common in malaria endemic regions and are known to protect against severe forms of the disease. Method: In a cross-sectional study of 341 febrile children less than five years of age, associations between clinical malaria and common RBC polymorphisms including the sickle cell gene and G6PD deficiency was evaluated between November 2008 and June 2009 in the middle belt of Ghana, Kintampo. G6PD deficient subgroup had a marginally increased risk of malaria infection compared to the G6PD normal subgroup (OR51.76, 95% CI: 0.98–3.16, p50.06)
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