Prevalence of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency among Malaria Patients in Southern Thailand: 8 Years Retrospective Study

Khammanee, Thunchanok; Sawangjaroen, Nongyao; Buncherd, Hansuk; Tun, Aung Win; Thanapongpichat, Supinya

doi:10.3347/kjp.2022.60.1.15

Cited by 5 publications

(8 citation statements)

References 45 publications

(58 reference statements)

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“…G6PD Kaiping, G6PD Vanua Lava, and G6PD Coimbra were Class B variants and potentially susceptible to 8-aminoquinoline hemolytic toxicity [ 45 , 46 ]. G6PD Mahidol was previously reported to be the most common variant in southern Thailand, and it is also commonly found in Malaysia [ 29 , 31 , 47 , 48 ]. However, G6PD Viangchan and G6PD Mediterranean (Class B variants), the other two most common variants among Malays, were not found in our study [ 47 , 48 ].…”

Section: Discussionmentioning

confidence: 99%

“…In 88-vivax patients from Yala province, the mutation frequency was 5.68% and Class B G6PD variants with a risk of mild to severe drug-induced hemolysis were identified. A previous study with a larger sample size reported G6PD deficiency in 1.1% (6/562) of the 562 malaria patients in Yala province [ 29 ]. Using DiaplexC G6PD genotyping kit (Asian type), they identified G6PD Mahidol and G6PD Viangchan with the frequency of 0.5% and 0.4% in vivax malaria patients (n = 545).…”

Section: Discussionmentioning

confidence: 99%

“…In Thailand, the prevalence of G6PD deficiency ranges between 5% and 34%, and more than 20 G6PD variants have been identified. A high frequency of G6PD mutations was found in the malaria-endemic areas along the Thai-Myanmar border, and G6PD Mahidol (487 G>A) was the most common variant in this area [22][23][24][25], while G6PD Viangchan (871 G>A) was commonly found in central and southern regions [26][27][28][29][30][31][32]. For CYP2D6, CYP2D6 � 10, which causes a reduction in enzyme activity, is common in the Thai population, accounting for approximately 50% of all allelic variants [33][34][35][36].…”

Section: Introductionmentioning

confidence: 99%

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Cytochrome P450 2D6 (CYP2D6) and glucose-6-phosphate dehydrogenase (G6PD) genetic variations in Thai vivax malaria patients: Implications for 8-aminoquinoline radical cure

et al. 2022

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Background Primaquine and tafenoquine are the only licensed drugs that effectively kill the hypnozoite stage and are used to prevent Plasmodium vivax malaria relapse. However, both primaquine and tafenoquine can cause acute hemolysis in glucose-6-phosphate dehydrogenase (G6PD)-deficient people with varying degrees of severity depending on G6PD variants. Additionally, primaquine efficacy against malaria parasites was decreased in individuals with impaired cytochrome P450 2D6 (CYP2D6) activity due to genetic polymorphisms. This study aimed to characterize G6PD and CYP2D6 genetic variations in vivax malaria patients from Yala province, a malaria-endemic area along the Thai–Malaysian border, and determine the biochemical properties of identified G6PD variants. Methodology/Principle findings Multiplexed high-resolution melting assay and DNA sequencing detected five G6PD variants, including G6PD Kaiping, G6PD Vanua Lava, G6PD Coimbra, G6PD Mahidol, and G6PD Kerala-Kalyan. Biochemical and structural characterization revealed that G6PD Coimbra markedly reduced catalytic activity and structural stability, indicating a high susceptibility to drug-induced hemolysis. While Kerala-Kalyan had minor effects, it is possible to develop mild adverse effects when receiving radical treatment. CYP2D6 genotyping was performed using long-range PCR and DNA sequencing, and the phenotypes were predicted using the combination of allelic variants. Decreased and no-function alleles were detected at frequencies of 53.4% and 14.2%, respectively. The most common alleles were CYP2D*36+*10 (25.6%), *10 (23.9%), and *1 (22.2%). Additionally, 51.1% of the intermediate metabolizers showed CYP2D6*10/*36+*10 as the predominant genotype (15.9%). Conclusions/Significance Our findings provide insights about genetic variations of G6PD and CYP2D6 in 88 vivax malaria patients from Yala, which may influence the safety and effectiveness of radical treatment. Optimization of 8-aminoquinoline administration may be required for safe and effective treatment in the studied population, which could be a significant challenge in achieving the goal of eliminating malaria.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cytochrome P450 2D6 (CYP2D6) and glucose-6-phosphate dehydrogenase (G6PD) genetic variations in Thai vivax malaria patients: Implications for 8-aminoquinoline radical cure

et al. 2022

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“…The prevalence of G6PD deficiency and G6PD variants has been reported in the southern Thai population. However, those reports recruited the samples from one province and five provinces with a high prevalence of malaria ( Pattaranggoon & Yimtiang, 2014 , Khammanee et al, 2022 ) with a retrospective study. The samples from all provinces located in southern Thailand were collected in a cross-sectional study in this study.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of G6PD deficiency and G6PD variants amongst the southern Thai population

Nuinoon

Krithong

Pramtong

et al. 2022

PeerJ

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Background Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme essential for NADPH production and protecting cells, especially red blood cells, from free radicals. The oxidative stress from drugs, chemicals, and infections can induce red blood cell hemolysis in G6PD deficiency patients, causing a genetic disorder. Objectives This study aims to provide more information on G6PD deficiency prevalence and the G6PD variants in the southern Thai population. Methods Five hundred and twenty healthy subjects in 14 provinces in the southern part of Thailand participated in the study. EDTA-blood samples were collected for a hematological parameters study, G6PD deficiency screening, and a molecular study for G6PD mutation. G6PD deficiency screening was tested using a fluorescent spot test. The types of G6PD mutation were identified by the allele-specific PCR method. Results The prevalence of G6PD deficiency in southern Thailand was 6.1% (14/228) in males and 9.6% (28/292) in females. Two homozygous and 26 heterozygous G6PD deficiencies were found in females. G6PD Viangchan (871G>A) was the most common variant with 43%, followed by G6PD Mahidol (487G>A), 24% with an allele frequency of 0.025 and 0.012, respectively. Uncharacterized mutations existed in three samples. The study volunteers had anemia in 36.6% (107/292) females and 7.5% (17/228) males. Among G6PD deficiency subjects, only ten partial G6PD deficiency females had mild anemia. Conclusions This study suggests that the prevalence of G6PD deficiency in southern Thailand aligns with that of other parts of Thailand. Newborn screening for G6PD deficiency is recommended for personal information and medical reference to prevent acute hemolysis from oxidative stressors.

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“…In persons with G6PD deficiency, both drugs, PQ and TQ can hemolyze red blood cells, resulting in anemia [ 98 ]. PQ's hemolytic activity has long been thought to be caused by intraerythrocytic oxidative stress mediated by redox-active metabolites rather than the parent drug.…”

Section: Control Challengesmentioning

confidence: 99%

Plasmodium vivax: the potential obstacles it presents to malaria elimination and eradication

Habtamu

Petros

Yan

2022

Trop Dis Travel Med Vaccines

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Initiatives to eradicate malaria have a good impact on P. falciparum malaria worldwide. P. vivax, however, still presents significant difficulties. This is due to its unique biological traits, which, in comparison to P. falciparum, pose serious challenges for malaria elimination approaches. P. vivax's numerous distinctive characteristics and its ability to live for weeks to years in liver cells in its hypnozoite form, which may elude the human immune system and blood-stage therapy and offer protection during mosquito-free seasons. Many malaria patients are not fully treated because of contraindications to primaquine use in pregnant and nursing women and are still vulnerable to P. vivax relapses, although there are medications that could radical cure P. vivax. Additionally, due to CYP2D6's highly variable genetic polymorphism, the pharmacokinetics of primaquine may be impacted. Due to their inability to metabolize PQ, some CYP2D6 polymorphism alleles can cause patients to not respond to treatment. Tafenoquine offers a radical treatment in a single dose that overcomes the potentially serious problem of poor adherence to daily primaquine. Despite this benefit, hemolysis of the early erythrocytes continues in individuals with G6PD deficiency until all susceptible cells have been eliminated. Field techniques such as microscopy or rapid diagnostic tests (RDTs) miss the large number of submicroscopic and/or asymptomatic infections brought on by reticulocyte tropism and the low parasitemia levels that accompany it. Moreover, P. vivax gametocytes grow more quickly and are much more prevalent in the bloodstream. P. vivax populations also have a great deal of genetic variation throughout their genome, which ensures evolutionary fitness and boosts adaptation potential. Furthermore, P. vivax fully develops in the mosquito faster than P. falciparum. These characteristics contribute to parasite reservoirs in the human population and facilitate faster transmission. Overall, no genuine chance of eradication is predicted in the next few years unless new tools for lowering malaria transmission are developed (i.e., malaria elimination and eradication). The challenging characteristics of P. vivax that impede the elimination and eradication of malaria are thus discussed in this article.

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Prevalence of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency among Malaria Patients in Southern Thailand: 8 Years Retrospective Study

Cited by 5 publications

References 45 publications

Cytochrome P450 2D6 (CYP2D6) and glucose-6-phosphate dehydrogenase (G6PD) genetic variations in Thai vivax malaria patients: Implications for 8-aminoquinoline radical cure

Cytochrome P450 2D6 (CYP2D6) and glucose-6-phosphate dehydrogenase (G6PD) genetic variations in Thai vivax malaria patients: Implications for 8-aminoquinoline radical cure

Prevalence of G6PD deficiency and G6PD variants amongst the southern Thai population

Plasmodium vivax: the potential obstacles it presents to malaria elimination and eradication

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