| Joon-Sup Yeom | 3 Articles |
Plasmodium vivax exhibits dormant liver-stage parasites, called hypnozoites, which can cause relapse of malaria. The only drug currently used for eliminating hypnozoites is primaquine. The antimalarial properties of primaquine are dependent on the production of oxidized metabolites by the cytochrome P450 isoenzyme 2D6 (CYP2D6). Reduced primaquine metabolism may be related to P. vivax relapses. We describe a case of 4 episodes of recurrence of vivax malaria in a patient with decreased CYP2D6 function. The patient was 52-year-old male with body weight of 52 kg. He received total gastrectomy and splenectomy 7 months before the first episode and was under chemotherapy for the gastric cancer. The first episode occurred in March 2019 and each episode had intervals of 34, 41, and 97 days, respectively. At the first and second episodes, primaquine was administered as 15 mg for 14 days. The primaquine dose was increased with 30 mg for 14 days at the third and fourth episodes. Seven gene sequences of P. vivax were analyzed and revealed totally identical for all the 4 samples. The CYP2D6 genotype was analyzed and intermediate metabolizer phenotype with decreased function was identified.
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Vivax malaria incidence in Korea is now decreased and showing a low plateau. Nowadays, vivax malaria in Korea is expected to be successfully eliminated with anti-malaria chemotherapy, primaquine, and vector control. The glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with potential hemolytic anemia after primaquine administration. This inborn disorder has a pivotal polymorphism with genetic variants and is the most prevalent X-chromosome-linked disorder. The prevalence of G6PD deficiency was previously reported negligible in Korea. As the population of multicultural families pertaining marriage immigrants and their adolescents increases, it is necessary to check G6PD deficiency for them prior to primaquine treatment for vivax malaria. The prevalence of G6PD variants and G6PD deficiency in multicultural families was performed in 7 counties and 2 cities of Jeollanam-do (Province), Gyeonggi-do, and Gangwon-do. A total of 733 blood samples of multicultural family participants were subjected to test the phenotypic and genetic G6PD deficiency status using G6PD enzyme activity quantitation kit and PCR-based G6PD genotyping kit. The G6PD phenotypic deficiency was observed in 7.8% of male adolescent participants and 3.2% of materfamilias population. Based on the PCR-based genotyping, we observed total 35 participants carrying the mutated alleles. It is proposed that primaquine prescription should seriously be considered prior to malaria treatment.
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