Abnormalities of Hemoglobin and Glucose-6-Phosphate-Dehydrogenase Deficiency in Children with Uncomplicated Malaria and Living in Banfora and Saponé, Two Different Malaria Setting of Burkina Faso

Abstract

Aims: The aim of this study is to assess the prevalence of hemoglobin abnormalities and G6PD deficiency and their respective influence on anemia occurring in less than five years old children with clinical P. falciparum malaria living in Burkina Faso.
 Study Design: The study was a cross-sectional survey with descriptive focus conducted from December 2010 to January 2013 in Saponé health district and from May to October 2011 in Banfora health district. Clinical and laboratory data were collected. Blood smears on slides for malaria diagnosis by microscopy, hemoglobin level and filter paper for the detection of human genetic factors were performed.
 Methodology: A total of 386 subjects from Saponé (131) and Banfora (255) were enrolled. DNA collected from each sample was extracted using chelex-100 method and the human genetic resistance factors background was assessed by RFLP-PCR. Abnormal hemoglobin patients were classified as NonAA while AA was defined the normal hemoglobin.
 Results: In this study, 70.98% (274/386) were classified normal hemoglobin (AA) while 29.02% (112/386) of subjects were carrying at least one abnormal (NonAA) allele: 24.35%AC, 3.63% AS, 0.78%CC and 0.26%SC. G6PD deficiency was 9.59% (37/386) among which, 4.92% for male and 4.66% in female. However, this gender difference was not statistically significant (p=1.00). 319/367 (86.92%) of the patients were anemic (59.4% with moderate anemia and 20.98% with mild anemia). The prevalence of anemia in G6PD deficient subjects was 83.33% (of which 58.33% were moderate anemia and 22.22% mild anemia). The difference between types of hemoglobin (p=0.64) in the occurrence of anemia (AA 87.64% and Non AA 85.18%) was not statistically significant.
 Conclusion: This study showed that the prevalence of these genetic factors was relatively low among children with clinical falciparum malaria with high parasite density. In addition, these factors appear to have no effect on anemia.

Inherited Disorders of Hemoglobin and Plasmodium falciparum Malaria

“…In these surveys, parasite densities were reported in HbAS children as lower [6,62,76,79,80] or similar [27,78,81,82] to those in HbAA children. We can conclude that HbAS does not consistently protect from P. falciparum parasitaemia.…”

“…RBCs of persons with HbAS typically have 40% HbS and 56-58% HbA [24]. The frequency of allele S is up to 0.2 in some parts of sub-Saharan Africa [26][27][28]. In equatorial Africa, where malaria is endemic, the prevalence of HbAS is much higher and can reach over 30% in some populations because of the survival advantage of HbAS heterozygotes from complications of P. falciparum malaria.…”

“…G6PD and a number of other human genetic traits including sickle cell anemia and related haemoglobinopathies are predominantly found in populations living in malaria endemic countries and have been suggested to provide the host protection from severe forms of malaria [30,[43][44][45] and asymptomatic malaria [27].…”

“…Other hand, other authors found that in two populations in Mali, the reduction in risk of severe malaria in male hemizygotes was also 58%, but no reduction in risk in the female heterozygotes [93]. Some authors [27,133] found no protective effect for either male hemizygotes or female heterozygotes. However, a protective effect has been reported on for females that were found to be G6PD deficient.…”