Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive genetic disorder that can cause severe anemia in affected individuals exposed to oxidative stress. This risk is particularly relevant in patients treated with the antimalarial drug primaquine. In Myanmar, primaquine has been widely administered as a Plasmodium vivax malaria treatment; however, prevalence of G6PD deficiency among the population remains insufficiently characterized. This study investigated the prevalence of G6PD variants among various minority ethnic subgroups residing in Kachin State, Myanmar. Blood samples from 440 participants were analyzed; however, the Mahidol variant (G487A) was identified in 21 individuals (4.8%). A major limitation of this study was the absence of G6PD enzyme activity data to confirm whether the Mahidol variant induces G6PD deficiency.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is caused by X-linked recessive disorderliness. It induces severe anemia when a patient with G6PD deficiency is exposed to oxidative stress that occurs with administration of an antimalarial drug, primaquine. The distribution of G6PD deficiency remains unknown while primaquine has been used for malaria treatment in Myanmar. This study aimed to investigate the prevalence of G6PD deficiency and its variants in Chin State, Myanmar. Among 322 participants, 18 (11 males and 7 females) demonstrated a G6PD deficiency. Orissa variant was dominant in the molecular analysis. This would be related to neighboring Indian and Bangladeshi population, in which Orissa variant was also reported as the main mutation type. The screening test for G6PD deficiency before primaquine treatment appears to be important in Myanmar.
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