Glucose-6-phosphate dehydrogenase is dispensable for human erythroid cell differentiation in vitro

Boonpeng, Kanyarat; Ketprasit, Nutpakal; Palasuwan, Attakorn; Kulkeaw, Kasem; Palasuwan, Duangdao

doi:10.1016/j.exphem.2023.02.002

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…In our cohort of infants with hyperbilirubinemia, the hemoglobin levels in the G6PD-deficient group were significantly lower than those in the normal G6PD group ( P < 0.001), and slightly higher than those in the ABO hemolysis group (134.33 ± 24.18 g/L) ( P = 0.014). Since fetal erythropoiesis in infants with G6PD deficiency was the same as that in controls, and G6PD was dispensable for human erythroid cell differentiation ( 22 , 23 ). Our findings suggest that decreased hemoglobin levels may be due to hemolytic factors in jaundiced infants with G6PD deficiency.…”

Section: Discussionmentioning

confidence: 99%

Etiology analysis and G6PD deficiency for term infants with jaundice in Yangjiang of western Guangdong

Yang

Lin

et al. 2023

Front. Pediatr.

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ObjectiveGlucose 6-phosphate dehydrogenase (G6PD) deficiency increases the risk of neonatal hyperbilirubinemia. The aim of this study is to evaluate the risk factors associated with hyperbilirubinemia in infants from the western part of Guangdong Province, and to assess the contribution of G6PD deficiency to neonatal jaundice.MethodsThe term infants with neonatal hyperbilirubinemia in People's Hospital of Yangjiang from June 2018 to July 2022 were recruited for the retrospective analysis. All the infants underwent quantitative detection of the G6PD enzyme. The etiology was determined through laboratory tests and clinical manifestations.ResultsOut of 1,119 term infants, 435 cases presented with jaundice. For the etiology analysis, infection was responsible for 16.09% (70/435), G6PD deficiency accounted for 9.66% (42/435), of which 3 were complicated with acute bilirubin encephalopathy), bleeding accounted for 8.05% (35/435), hemolytic diseases accounted for 3.45% (15/435), and breast milk jaundice accounted for 2.53% (11/435). One case (0.23%) was attributed to congenital hypothyroidism, multiple etiologies accounted for 22.3% (97/435), and 35.63% (155/435) were of unknown etiology. Of the jaundiced infants, 19.54% (85/435) had G6PD deficiency, while only 10.23% (70/684) of non-jaundiced infants had G6PD deficiency; this difference was found to be statistically significant (P < 0.001). Furthermore, the hemoglobin levels in the jaundiced infants with G6PD deficiency (146.85 ± 24.88 g/L) were lower than those without G6PD deficiency (156.30 ± 22.07 g/L) (P = 0.001). 65 jaundiced infants with G6PD deficiency underwent G6PD mutation testing, and six different genotypes were identified, including c.95A > G, c.392G > T, c.1024C > T, c.1311C > T, c.1376G > T, c.1388G > A, c.871G > A/c.1311C > T, c.392G > T/c.1388G > A, and c.1376G > T/c.1311C > T.65iciencyConclusionIn newborns in Yangjiang, G6PD deficiency, infection, and neonatal hemolytic disease were identified as the main causes of hyperbilirubinemia and acute bilirubin encephalopathy. Specifically, Hemolytic factors in infants with G6PD deficiency may lead to reduced hemoglobin and increased bilirubin levels in jaundiced infants.

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Section: Discussionmentioning

confidence: 99%

Etiology analysis and G6PD deficiency for term infants with jaundice in Yangjiang of western Guangdong

Yang

Lin

et al. 2023

Front. Pediatr.

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“…In our cohort of infants with hyperbilirubinemia, the hemoglobin levels in the G6PD-deficient group were significantly lower than those in the normal G6PD group (p<0.001), and slightly higher than those in the ABO hemolysis group (134.33±24.18 g/L) (P = 0.014). Since fetal erythropoiesis in infants with G6PD deficiency was the same as that in controls, and G6PD was dispensable for human erythroid cell differentiation [18,19] . Our findings suggest that decreased hemoglobin levels may be due to hemolytic factors in jaundiced infants with G6PD deficiency.…”

Section: Discussionmentioning

confidence: 95%

Etiology analysis and G6PD deficiency for term infants with jaundice

Ahmed,

Abdulsada,

Hussein

2024

Int. J. Paediatrics Geriatrics

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Background: Neonatal jaundice, characterized by yellow skin, sclera and conjunctiva due to hyperbilirubinemia. Bilirubin can cross the blood-brain barrier, leading to severe hyperbilirubinemia, acute bilirubin encephalopathy, nuclear jaundice, and even permanent brain damage. This study aims to analyses risk factors for baby hyperbilirubinemia and assess the role of G6PD deficiency in neonatal jaundice. Method:The term infants with neonatal hyperbilirubinemia in Al elwyia teaching hospital for children and in Iraq from June 2018 to July 2022 were recruited for the retrospective analysis. All the infants underwent quantitative detection of the G6PD enzyme. The etiology was determined through laboratory tests and clinical manifestations. Results: In a study of 1,119 term newborns, 435 had jaundice, with infection and G6PD deficiency being the main identifiable causes. Jaundiced newborns showed a significantly higher incidence of G6PD deficiency than non-jaundiced ones (19.54% vs. 10.23%, p<0.001), and those with G6PD deficiency had significantly lower hemoglobin levels. Among the jaundiced group, 35.63% had unknown causes, and six G6PD deficiency-related genotypes were identified. Conclusion:In newborns with G6PD deficiency, infection, and neonatal hemolytic disease were identified as the main causes of hyperbilirubinemia and acute bilirubin encephalopathy. Specifically, Hemolytic factors in infants with G6PD deficiency may lead to reduced hemoglobin and increased bilirubin levels in jaundiced infants.

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“…Finally, as G6PD alters several cellular processes under oxidative stress and is frequently associated with anemia, it could be expected a deficient RBC maturation. However, in vitro differentiation of CD34 + hematopoietic progenitor cells isolated from patients with different G6PD severity did not show any alteration in progenitor proliferation, nor differentiation or enucleation [ 175 ].…”

Section: Oxidative Stress In Red Blood Cell Diseasesmentioning

confidence: 99%

Oxidative Stress in Healthy and Pathological Red Blood Cells

Orrico,

Laurance,

Lopez

et al. 2023

Biomolecules

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Red cell diseases encompass a group of inherited or acquired erythrocyte disorders that affect the structure, function, or production of red blood cells (RBCs). These disorders can lead to various clinical manifestations, including anemia, hemolysis, inflammation, and impaired oxygen-carrying capacity. Oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense mechanisms, plays a significant role in the pathophysiology of red cell diseases. In this review, we discuss the most relevant oxidant species involved in RBC damage, the enzymatic and low molecular weight antioxidant systems that protect RBCs against oxidative injury, and finally, the role of oxidative stress in different red cell diseases, including sickle cell disease, glucose 6-phosphate dehydrogenase deficiency, and pyruvate kinase deficiency, highlighting the underlying mechanisms leading to pathological RBC phenotypes.

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Glucose-6-phosphate dehydrogenase is dispensable for human erythroid cell differentiation in vitro

Cited by 4 publications

References 31 publications

Etiology analysis and G6PD deficiency for term infants with jaundice in Yangjiang of western Guangdong

Etiology analysis and G6PD deficiency for term infants with jaundice in Yangjiang of western Guangdong

Etiology analysis and G6PD deficiency for term infants with jaundice

Oxidative Stress in Healthy and Pathological Red Blood Cells

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