Prevalence of G6PD deficiency and associated haematological parameters in children from Botswana

Past and current biological factors affecting malaria in the low transmission setting of Botswana: A review

“…Early publications from the 1960s and 1970s could only find relatively low G6PD deficiency in the Khoisan peoples they studied (1-5% with a higher percentage in the Northwest), and surprisingly no deficiency in the Bantu (Jenkins et al, 1968). This finding is somewhat congruent with a recent study that discovered the G6PD deficiency rate in a pattern that peaks in the Northwest (3.37%) and decreases steadily with latitude until reaching its minimum in the Southeast of the country (Motshoge et al, 2018). Interestingly, these latter results reflect the distribution of malaria endemicity in Botswana.…”

“…Admixture has occurred between the two ethnic groups to various extents (Schuster et al, 2010). As a consequence, there is a wider spectrum of genotypes and phenotypes when considering genetic characteristics such as Duffy antigen, sickle cell trait, glucose-6-phosphate dehydrogenase (G6PD), and detoxifying liver enzymes (Howes et al, 2011;Motshoge et al, 2018;Tawe et al, 2018aTawe et al, , 2018b. These human genetic factors play a pivotal role in susceptibility to malaria infection and associated morbidity (Haldane, 1949;Sirugo et al, 2014), as well as for metabolism of medications currently on the market (Tawe et al, 2018a(Tawe et al, , 2018b.…”

“…This medication can result in haemolytic toxicity in individuals that are G6PD deficient when administered the WHO recommended dose of 0.25-0.5 mg/kg over the two week period (World Health Organization, 2015b). In a setting such as Botswana, where G6PD deficiency rates are relatively low, phenotyping patients prior to treatment with the two week course of primaquine may be required in order to avoid malpractice and to better align with national guidelines (Motshoge et al, 2018;Republic of Botswana, 2015). Currently, testing for G6PD is not conducted, nor are patients treated with full two week courses of primaquine due to a lack of point of care diagnostics for G6PD and RDTs that effectively identify P. vivax (Republic of Botswana, 2015).…”

“…It is generally accepted that these two populations converged approximately 2000 years ago with the arrival of the Bantu speaking peoples from the North, which contributed to the diversification and admixture between the two ancestral populations (Schlebusch et al, 2016). Since malaria is acknowledged to have applied significant selective pressure to humans (Kwiatkowski, 2005), genetic differences in Duffy status, haemoglobin S frequency and G6PD deficiency have been noted based upon geographic location and ancestral background (Jenkins et al, 1968;Jenkins et al, 1987;Motshoge et al, 2018;Prugnolle et al, 2013). This is especially pertinent since the Bantu originated from a highly endemic malaria setting, whereas the Khoisan were likely only exposed to sporadic outbreaks that did not apply chronic selective pressure and therefore lack of malaria-resistance alleles (Maingard, 1937;Schuster et al, 2010).…”

Molecular characterization of Glucose-6-Phosphate Dehydrogenase: do single nucleotide polymorphisms affect hematological parameters in HIV positive patients?

“…S3). In a study to find the association between G6PD deficiency and hematological parameters in children from Botswana, Motshoge et al made similar observations [36]. The increased MCV due to the 202G → A mutation is also in harmony with a GWAS study by Ding et al [37].…”