TY - JOUR
T1 - Prevalence of G6PD deficiency and associated haematological parameters in children from Botswana
AU - Motshoge, Thato
AU - Ababio, Grace
AU - Aleksenko, Larysa
AU - Souda, Sajini
AU - Muthoga, Charles Waithaka
AU - Mutukwa, Naledi
AU - Tawe, Leabaneng
AU - Ramatlho, Pleasure
AU - Gabaitiri, Lesego
AU - Chihanga, Simon
AU - Mosweunyane, Tjantilili
AU - Hamda, Shimeles
AU - Moakofhi, Kentse
AU - Ntebela, Davies
AU - Peloewetse, Elias
AU - Mazhani, Loeto
AU - Pernica, Jeffrey M.
AU - Read, John
AU - Quaye, Isaac Kweku
AU - Paganotti, Giacomo Maria
N1 - Funding Information:
The authors acknowledge the study participants for their willingness to participate. Funding for the project was obtained from a grant from the Government of Botswana through the National Malaria Programme and with the support of the Botswana-University of Pennsylvania Partnership (Penn Center for AIDS Research, grant P30 AI 045008 ). Support was also provided from the Sub-Saharan African Network for TB/HIV Research Excellence (SANTHE), a DELTAS Africa Initiative [grant # DEL-15-006]. We thank Dr. Gaseitsiwe S. from Botswana-Harvard Partnership (Gaborone, Botswana) for sequencing the control genotypes for the 202 and 376 polymorphisms. We particularly thank Lucio Luzzatto, Giorgio Sirugo, Federica Verra Ghyslaine Bruna Djeunang Dongho and the two anonymous reviewers for a critical review of this paper. Finally, we express our gratitude to Ms. Talitah Eyman (at University of Botswana) for procurement of the reagents.
Publisher Copyright:
© 2018 Elsevier B.V.
PY - 2018/9
Y1 - 2018/9
N2 - Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is commonly seen in malaria endemic areas as it is known to confer a selective advantage against malaria. Recently, we reported a high proportion of asymptomatic reservoir of Plasmodium vivax in Botswana, that calls for intervention with primaquine to achieve radical cure of vivax malaria. Considering that individuals with this enzyme deficiency are at risk of haemolysis following primaquine treatment, assessment of the population for the relative frequency of G6PD deficiency is imperative. Samples from 3019 children from all the districts of Botswana were successfully genotyped for polymorphisms at positions 202 and 376 of the G6PD gene. Haematological parameters were also measured. The overall population allele frequency (based on the hemizygous male frequency) was 2.30% (95% CI, 1.77–2.83), while the overall frequency of G6PD-deficient genotypes A- (hemizygote and homozygote genotypes only) was 1.26% (95% CI, 0.86–1.66). G6PD deficiency is spread in Botswana according to the historical prevalence of malaria with a North-West to South-East decreasing gradient trend. There was no association between G6PD status and P. vivax infection. G6PD A- form was found to be associated with decreased RBC count and haemoglobin levels without a known cause or illness. In conclusion, we report for the first time the prevalence of G6PD deficiency in Botswana which is relevant for strategies in the malaria elimination campaign. Further work to examine the activities of the enzyme in the Botswana population at risk for malaria is warranted.
AB - Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is commonly seen in malaria endemic areas as it is known to confer a selective advantage against malaria. Recently, we reported a high proportion of asymptomatic reservoir of Plasmodium vivax in Botswana, that calls for intervention with primaquine to achieve radical cure of vivax malaria. Considering that individuals with this enzyme deficiency are at risk of haemolysis following primaquine treatment, assessment of the population for the relative frequency of G6PD deficiency is imperative. Samples from 3019 children from all the districts of Botswana were successfully genotyped for polymorphisms at positions 202 and 376 of the G6PD gene. Haematological parameters were also measured. The overall population allele frequency (based on the hemizygous male frequency) was 2.30% (95% CI, 1.77–2.83), while the overall frequency of G6PD-deficient genotypes A- (hemizygote and homozygote genotypes only) was 1.26% (95% CI, 0.86–1.66). G6PD deficiency is spread in Botswana according to the historical prevalence of malaria with a North-West to South-East decreasing gradient trend. There was no association between G6PD status and P. vivax infection. G6PD A- form was found to be associated with decreased RBC count and haemoglobin levels without a known cause or illness. In conclusion, we report for the first time the prevalence of G6PD deficiency in Botswana which is relevant for strategies in the malaria elimination campaign. Further work to examine the activities of the enzyme in the Botswana population at risk for malaria is warranted.
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M3 - Article
C2 - 29778768
AN - SCOPUS:85047237496
SN - 1567-1348
VL - 63
SP - 73
EP - 78
JO - Infection, Genetics and Evolution
JF - Infection, Genetics and Evolution
ER -