article · Malaria Journal
This study investigated the prevalence of Glucose-6-phosphate dehydrogenase (G6PD) deficiency and its genetic variants among individuals suspected of malaria in Metehara, Eastern Ethiopia. G6PD is an enzyme vital for red blood cell function, and its deficiency can lead to severe anaemia when exposed to oxidative stressors like the anti-malarial drug primaquine. Researchers conducted a cross-sectional study with 498 participants, measuring G6PD enzyme activity using a biosensor and sequencing some deficient samples. The overall prevalence of G6PD deficiency was found to be 3.6%, with a higher rate in females (4.8%) than males (2.9%). The predominant genetic variant identified was G267 + 119C/T. The findings suggest that patients receiving primaquine in this area require careful monitoring.
G6PD deficiency can cause severe anaemia when certain malaria drugs, such as primaquine, are administered. Understanding its prevalence and specific genetic types in a region helps healthcare providers safely treat malaria, preventing harmful side effects and improving patient care. This research provides crucial local data for clinical decision-making.
The findings are directly applicable to public health and clinical practice in Eastern Ethiopia. Healthcare providers and public health organisations can use this information to inform G6PD screening protocols before administering primaquine for malaria treatment, thereby enhancing patient safety. This is applied research, providing data for immediate adjustments to clinical guidelines and patient management strategies.
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BACKGROUND: Glucose-6-phosphate dehydrogenase (G6PD) is cytosolic enzyme, which has a vital role for the integrity and functioning of red blood cells. Lower activity of this enzyme leads to the occurrence of acute haemolytic anaemia after exposure to oxidative stressors like primaquine. Primaquine is an important drug for the radical cure of Plasmodium vivax and blocking transmission of Plasmodium falciparum, and thereby enhancing malaria elimination. However, there is a need to identify G6PD deficient individuals and administer the drug with caution due to its haemolytic side effects. The main objective of this study is to determine the prevalence of G6PD deficiency among malaria-suspected individuals. METHODS: A facility-based cross-sectional study was conducted from September 2020 to September 2021 in Metehara Health Centre, Eastern Ethiopia. A structured questionnaire was used to collect the socio-demographic and clinical information of the study participants. Capillary and venous blood samples were collected based on standard procedures for onsite screening, dried blood spot preparation, and malaria microscopy. The G6PD enzyme activity was measured by careSTART™ G6PD biosensor analyzer. Data was entered and analysed by SPSS. RESULTS: A total of 498 study participants were included in the study, of which 62% (309) were males. The overall prevalence of G6PD deficiency based on the biosensor screening was 3.6% (18/498), of which 2.9% and 4.8% were males and females, respectively. Eleven of the G6PD deficient samples had mutations confirmed by G6PD gene sequencing analysis. Mutations were detected in G267 + 119C/T, A376T, and ChrX:154535443. A significant association was found in sex and history of previous malaria infection with G6PD deficiency. CONCLUSIONS: The study showed that the G6PD deficient phenotype exists in Metehara even if the prevalence is not very high. G267 + 119C/T mutation is the predominant G6PD variant in this area. Therefore, malaria patient treatment using primaquine should be monitored closely for any adverse effects.
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DOI: 10.1186/s12936-022-04269-5
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