Assessment of Glucose-6-Phosphate Dehydrogenase Enzyme among Malaria Patients in Sudan

Background: Malaria and glucose-6-phosphate dehydrogenase (G6PD) deficiency are significant health issues in areas where malaria is common, such as Sudan. Malaria, mainly caused by Plasmodium falciparum, is a major contributor to illness and death. The treatment of malaria with antimalarial medications like primaquine and tafenoquine is complicated for those with G6PD deficiency due to the risk of hemolysis. G6PD deficiency is a genetic disorder that affects red blood cells and is prevalent with considerable genetic variation.

Aim: This review aims to evaluate the activity of the G6PD enzyme in malaria patients in Sudan, with an emphasis on the genetic connections between G6PD deficiency and malaria. The research compiles information on the prevalence, molecular features, and clinical significance of G6PD variants to guide malaria treatment approaches and public health strategies.

Materials and Methods: A systematic literature review was performed using databases like PubMed, Scopus, Web of Science, and Google Scholar. The review included studies published from 2000 to 2024 that focused on populations in Sudan. Search terms used were "G6PD deficiency," "malaria," "Sudan," and "antimalarial drug safety." Additionally, relevant reports from the World Health Organization (WHO) and Sudanese health authorities were examined. The chosen studies were assessed based on prevalence rates, genetic variants, diagnostic techniques, and treatment results.

Results: In Sudan, the rate of G6PD deficiency among malaria patients ranges from 10% to 20%, with notable differences based on region and ethnicity. The most frequently found genetic variants are G6PD A- and G6PD Mediterranean, which affect enzyme activity and the likelihood of hemolysis. Research suggests that having G6PD deficiency may offer some degree of protection against malaria by hindering the replication of the parasite. However, individuals with this deficiency face a high risk of hemolysis triggered by certain medications, particularly primaquine and tafenoquine. Current diagnostic methods, such as rapid diagnostic tests (RDTs) and spectrophotometry, have limitations in accurately identifying all instances of G6PD deficiency, especially in heterozygous females.

Conclusion: The high prevalence of G6PD deficiency in Sudan presents a major obstacle for treating malaria. Regular testing for G6PD deficiency is crucial to avoid hemolytic issues and improve antimalarial treatment. Additional studies are necessary to enhance diagnostic techniques, investigate uncommon G6PD variants, and create safer treatment guidelines for patients with G6PD deficiency in areas where malaria is common.