ArticleFrontiers in pediatrics2023
Etiology analysis and G6PD deficiency for term infants with jaundice in Yangjiang of western Guangdong.
Article in Frontiers in pediatrics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- Prevalence, aetiology, and treatment needs of neonates with G6PD deficiency in Central Peninsular Malaysia.Scientific reports · 2026Article
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with elevated mean corpuscular volume (MCV) and bilirubin.BMC genomic data · 2026Article
- The influencing factors of amplitude-integrated electroencephalography and bilirubin-induced neurological dysfunction scores in neonates with hyperbilirubinemia: a cross-sectional study.BMC pediatrics · 2026Article
- Establishment of reference interval (RI) for G6PD/6PGD ratio in adults from Yangjiang, China.Annals of hematology · 2025Article
- The medium-fluorescence reticulocyte ratio is an independent predictor of G6PD deficiency neonates.International journal of hematology · 2025Article
- Rate of glucose-6-phosphate dehydrogenase deficiency in neonatal indirect hyperbilirubinemia at a private tertiary centre.Saudi medical journal · 2024Article
- Evaluation of Glucose 6-Phosphate Dehydrogenase, Pyruvate Kinase, and New Generation Inflammation Biomarkers in Prolonged Neonatal Jaundice.Medicina (Kaunas, Lithuania) · 2024Article
- Molecular epidemiological investigation of G6PD deficiency in Yangjiang region, western Guangdong province.Frontiers in genetics · 2023Article
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12 authors at 3 institutions in 1 country.
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Abstract
Objective: Glucose 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. Methods: The 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. Results: Out 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 ( Conclusion: In 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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