Relationship among glucose-6-phosphate dehydrogenase (G-6-PD) activity, G-6-PD variants and reticulocytosis in neonates of northeast Thailand

Kitcharoen, Suttiphan; Dechyotin, Sumalai; Khemtonglang, Noppmats; Kleesuk, Chanudda

doi:10.1016/j.cca.2015.01.017

Cited by 6 publications

(9 citation statements)

References 29 publications

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“…In this region of Thailand, G6PD Viangchan accounts for >50% of the seven common variants. 24 G6PD Viangchan is also the most common variant in Cambodia and PDR Laos, 35 , 36 reflecting the common ancestral origin of populations in northeastern Thailand, Cambodia and PDR Laos. 24 , 37 The other less common variants found in this study were Canton, Chinese-4, Chinese-5, Gaohe, Kaiping and Union (common variants in Chinese population), and Mahidol (the most common variant in Myanmar population), 33 indicating the presence of people originating from these two countries in northeastern Thailand.…”

Section: Discussionmentioning

confidence: 99%

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Prevalence and Molecular Characterization of Glucose-6-Phosphate Dehydrogenase (G6pd) Deficiency in Females From Previously Malaria Endemic Regions in Northeastern Thailand and Identification of a Novel G6pd Variant

Dechyotin¹,

Sakunthai²,

Khemtonglang³

et al. 2021

Mediterr J Hematol Infect Dis

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Introduction: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common X-linked enzymopathy, highly prevalent in areas where malaria is or has been endemic. Prevalence of G6PD deficiency and characterization of G6PD variants in females from previously malaria endemic areas of northeast Thailand remain unstudied. Methods: Prevalence of G6PD deficiency was determined by a fluorescent spot test (FST) and multiplex allele specific (AS)- and restriction fragment length polymorphic (RFLP)-PCR developed for detection of common G6PD variants in the Thai population. Results: Prevalence of G6PD deficiency in female samples (n = 355) was 18% by FST and 27% by PCR-based genotyping. The most common variant was G6PD Viangchan (54%), followed by G6PD Canton (11%) and G6PD Union (11%); in addition, a novel heterozygous variant, G6PD Khon Kaen (c.305T>C, p.F102S located in the coenzyme-binding domain), was identified. The majority (75%) of G6PD activities of heterozygotes were within the intermediate deficiency range (30-80% of median normal enzyme activity). Conclusion: High prevalence of G6PD deficiency was present in females from northeast Thailand, the majority being due to heterozygosity of G6PD variants. The findings will have a bearing on an inclusion of primaquine in antimalarial-based policies for malaria elimination in populations with high prevalence in G6PD deficiency.

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Section: Discussionmentioning

confidence: 99%

“…All samples positive for G6PD variants were confirmed by RFLP-PCR as previously described (data not shown). 24 …”

Section: Methodsmentioning

confidence: 99%

Prevalence and Molecular Characterization of Glucose-6-Phosphate Dehydrogenase (G6pd) Deficiency in Females From Previously Malaria Endemic Regions in Northeastern Thailand and Identification of a Novel G6pd Variant

Dechyotin¹,

Sakunthai²,

Khemtonglang³

et al. 2021

Mediterr J Hematol Infect Dis

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“…G6PDd is considered one of the most common genetic disorders worldwide, but prevalence estimates are highest in Africa, Asia, the Mediterranean, and the Middle East [16,[29][30][31]. One of the main clinical consequences of G6PD deficiency, especially in new-borns is neonatal hyperbilirubinemia, which requires immediate diagnosis and treatment to prevent brain damage induced by irreversible bilirubin, known as kernicterus [32][33][34]. Furthermore, the use of certain anti-malarial drugs, including primaquine increase the risk of haemolysis for G6PD deficient patients [8].…”

Section: Discussionmentioning

confidence: 99%

The prevalence of glucose-6-phosphate dehydrogenase deficiency in the Cape Verdean population in the context of malaria elimination

DePina¹,

Pires²,

Andrade³

et al. 2020

PLoS ONE

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Cabo Verde aims to eliminate malaria by 2020. In the country, Plasmodium falciparum had been the main parasite responsible for indigenous cases and primaquine is the first line treatment of cases and for radical cure. However, the lack of knowledge of the national prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency may be one of the constraints to the malaria elimination process. Hence, this first study determines the prevalence of G6PD deficiency (G6PDd) in the archipelago. Blood samples were collected from patients who voluntarily agreed to participate in the study, in the health facilities of eight municipalities on four islands, tested with G6PD CareStart ™ deficiency Rapid Diagnosis Test (RDT). All subjects found to be G6PDd by RDT then underwent enzyme quantification by spectrophotometry. Descriptive statistics and inferences were done using SPSS 22.0 software. A total of 5.062 blood samples were collected, in majority from female patients (78.0%) and in Praia (35.6%). The RDT revealed the prevalence of G6PD deficiency in 2.5% (125/5062) of the general population, being higher in males (5.6%) than in females (1,6%). The highest G6PDd prevalence was recorded in São Filipe, Fogo, (5.4%), while in Boavista no case was detected. The G6PDd activity quantification shown a higher number of partially deficient and deficient males (respectively n = 26 and n = 22) compared to females (respectively n = 18 and n = 7), but more normal females (n = 35) than males (n = 11). According to the WHO classification, most of the G6PDd cases belongs to the class V (34.5%), while the Classes II and I were the less represented with respectively 5.8% and zero cases. This study in Cabo Verde determined the G6PDd prevalence in the population, relatively low compared to other

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“…There is no evidence of hemolysis or exposure to hemolysis trigger agents in most cases of G6PD deficiency-associated hyperbilirubinemia. 10,25,[29][30][31][32][33][34][35] Hyperbilirubinemic G6PD-deficient neonates have been found to have higher hemoglobin and hematocrit and lower reticulocyte counts than nonhyperbilirubinemic G6PD-deficient neonates. 4,17,18,31,36 Blood carboxyhemoglobin corrected for inspired carbon monoxide (COHbc) and end-tidal carbon monoxide corrected for ambient carbon monoxide (ETCOc) have been found to be the same in hyperbilirubinemic G6PD-deficient neonates and their nonhyperbilirubinemic counterparts.…”

Section: Hemolysis Is Absent In Hyperbilirubinemic G6pd-deficient Neomentioning

confidence: 99%

“…10,25,[29][30][31][32][33][34][35] Hyperbilirubinemic G6PD-deficient neonates have been found to have higher hemoglobin and hematocrit and lower reticulocyte counts than nonhyperbilirubinemic G6PD-deficient neonates. 4,17,18,31,36 Blood carboxyhemoglobin corrected for inspired carbon monoxide (COHbc) and end-tidal carbon monoxide corrected for ambient carbon monoxide (ETCOc) have been found to be the same in hyperbilirubinemic G6PD-deficient neonates and their nonhyperbilirubinemic counterparts. 25,29,30,33,34 Correlation between COHbc and total serum bilirubin (TSB) levels has been evident among G6PD-normal neonates only, but not among G6PD-deficient neonates.…”

Section: Hemolysis Is Absent In Hyperbilirubinemic G6pd-deficient Neomentioning

confidence: 99%

Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review

Al-Abdi

2016

Amer J Perinatol

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Classically, genetically decreased bilirubin conjugation and/or hemolysis account for the mechanisms contributing to neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency. However, these mechanisms are not involved in most cases of this hyperbilirubinemia. Additional plausible mechanisms for G6PD deficiency-associated hyperbilirubinemia need to be considered. Glutathione S-transferases (GST) activity depends on a steady quantity of reduced form of glutathione (GSH). If GSH is oxidized, it is reduced back by glutathione reductase, which requires the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH). The main source of NADPH is the pentose phosphate pathway, in which G6PD is the first enzyme. Rat kidney GSH, rat liver GST, and human red blood cell GST levels have been found to positively correlate with G6PD levels in their respective tissues. As G6PD is expressed in hepatocytes, it is expected that GST levels would be significantly decreased in hepatocytes of G6PD-deficient neonates. As hepatic GST binds bilirubin and prevents their reflux into circulation, hypothesis that decreased GST levels in hepatocytes is an additional mechanism contributing to G6PD deficiency-associated hyperbilirubinemia seems plausible. Evidence for and against this hypothesis are discussed in this article hoping to stimulate further research on the role of GST in G6PD deficiency-associated hyperbilirubinemia.

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Relationship among glucose-6-phosphate dehydrogenase (G-6-PD) activity, G-6-PD variants and reticulocytosis in neonates of northeast Thailand

Cited by 6 publications

References 29 publications

Prevalence and Molecular Characterization of Glucose-6-Phosphate Dehydrogenase (G6pd) Deficiency in Females From Previously Malaria Endemic Regions in Northeastern Thailand and Identification of a Novel G6pd Variant

Prevalence and Molecular Characterization of Glucose-6-Phosphate Dehydrogenase (G6pd) Deficiency in Females From Previously Malaria Endemic Regions in Northeastern Thailand and Identification of a Novel G6pd Variant

The prevalence of glucose-6-phosphate dehydrogenase deficiency in the Cape Verdean population in the context of malaria elimination

Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review

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