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Prevalence and distribution of G6PD deficiency: implication for the use of primaquine in malaria treatment in Ethiopia
Journal article   Open access   Peer reviewed

Prevalence and distribution of G6PD deficiency: implication for the use of primaquine in malaria treatment in Ethiopia

Eugenia Lo, Daibin Zhong, Beka Raya, Kareen Pestana, Cristian Koepfli, Ming-Chieh Lee, Delenasaw Yewhalaw and Guiyun Yan
Malaria journal, v 18(1), 340
07 Oct 2019
DOI: https://doi.org/10.1186/s12936-019-2981-x
PMID: 31590661
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1186/s12936-019-2981-xView
Published, Version of Record (VoR) Open

Abstract

Adolescent Adult Aged Aged, 80 and over Antimalarials - adverse effects Antimalarials - therapeutic use Child Child, Preschool Ethiopia - epidemiology Female Genotype Glucosephosphate Dehydrogenase Deficiency - epidemiology Glucosephosphate Dehydrogenase Deficiency - genetics Humans Infant Infant, Newborn Malaria, Vivax - prevention & control Male Middle Aged Prevalence Primaquine - adverse effects Primaquine - therapeutic use Young Adult Malaria Phenotype
G6PD enzyme deficiency is a common enzymatic X-linked disorder. Deficiency of the G6PD enzyme can cause free radical-mediated oxidative damage to red blood cells, leading to premature haemolysis. Treatment of Plasmodium vivax malaria with primaquine poses a potential risk of mild to severe acute haemolytic anaemia in G6PD deficient people. In this study, the prevalence and distribution of G6PD mutations were investigated across broad areas of Ethiopia, and tested the association between G6PD genotype and phenotype with the goal to provide additional information relevant to the use of primaquine in malaria treatment. This study examined G6PD mutations in exons 3-11 for 344 febrile patient samples collected from seven sites across Ethiopia. In addition, the G6PD enzyme level of 400 febrile patient samples from Southwestern Ethiopia was determined by the CareStart™ biosensor. The association between G6PD phenotype and genotype was examined by Fisher exact test on a subset of 184 samples. Mutations were observed at three positions of the G6PD gene. The most common G6PD mutation across all sites was A376G, which was detected in 21 of 344 (6.1%) febrile patients. Thirteen of them were homozygous and eight were heterozygous for this mutation. The G267+119C/T mutation was found in 4 (1.2%) individuals in South Ethiopia, but absent in other sites. The G1116A mutation was also found in 4 (1.2%) individuals from East and South Ethiopia. For the 400 samples in the south, 17 (4.25%) were shown to be G6PD-deficient. G6PD enzyme level was not significantly different by age or gender. Among a subset of 202 febrile patients who were diagnosed with malaria, 11 (5.45%) were G6PD-deficient. These 11 infected samples were diagnosed with Plasmodium vivax by microscopy. Parasitaemia was not significantly different between the G6PD-deficient and G6PD-normal infections. The prevalence of G6PD deficiency is modest among febrile patients in Ethiopia. G6PD deficiency testing is thus recommended before administrating primaquine for radical cure of P. vivax infected patients. The present study did not indicate a significant association between G6PD gene mutations and enzyme levels.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Infectious Diseases
Parasitology
Tropical Medicine
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