Donor Blood Glucose 6-Phosphate Dehydrogenase Deficiency Reduces the Efficacy of Exchange Transfusion in Neonatal Hyperbilirubinemia

Samanta, Sujay; Kumar, Praveen; Kishore, Sunil; Garewal, G.; Narang, Anil

doi:10.1542/peds.2008-2021

Cited by 30 publications

(27 citation statements)

References 11 publications

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“…This is especially in neonates (preterm). Transfusion of G6PD deficient red cells to the premature infants has been associated with hemolytic and severe hyperbilirubinemia requiring exchange transfusion [5]. In our study also one neonate developed suspected hemolytic transfusion reaction following transfusion of G6PD deficient blood.…”

supporting

confidence: 52%

Screening for G6PD Deficiency in Blood Donor Population

Devi

Helen

Alwar

et al. 2010

Indian J Hematol Blood Transfus

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supporting

confidence: 52%

Screening for G6PD Deficiency in Blood Donor Population

Devi

Helen

Alwar

et al. 2010

Indian J Hematol Blood Transfus

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“…Although genetic interactions are alleged to induce NH in G6PD deficiency, 8,9 destruction of red blood cells has still been observed in some circumstances. 6,13,14 For instance, G6PD-deficient infants who were born outside medical centers were more susceptible to hemolysis. 15,16 Moreover, our study identified that infants with G6PD deficiency tended to have extreme NH, defined as a peak TSB value Z25 mg/dL.…”

Section: Discussionmentioning

confidence: 99%

Clinical Characteristics of G6PD Deficiency in Infants With Marked Hyperbilirubinemia

Weng

Chiu

2010

Journal of Pediatric Hematology/Oncology

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This study analyzes the clinical features of glucose-6-phosphate dehydrogenase (G6PD) deficiency in infants with marked hyperbilirubinemia. We retrospectively assessed a cohort of 413 infants with peak total serum bilirubin (TSB) level >or=20 mg/dL from 1995 to 2007. The prevalence of G6PD deficiency was proportional to the level of peak TSB: 21.1% (81/383) in 20 mg/dL to 29.9 mg/dL, 45.5% (10/22) in 30 mg/dL to 39.9 mg/dL, and 100% (8/8) in >or=40 mg/dL. Male sex was more common in G6PD deficiency (75.8%). When compared with G6PD-normal infants, those with G6PD deficiency tended to have extreme hyperbilirubinemia (peak TSB level >or=25 mg/dL) and hemoglobin value<13 g/dL (P<0.001). Furthermore, mortality rate was significantly higher in G6PD-deficient infants (3.0%) than in the G6PD-normal counterparts (0.0%). Among 58 of the G6PD-deficient infants who were followed for more than 12 months, 4 developed the classic neurologic manifestations of kernicterus (6.6%). These findings show that G6PD deficiency is an important risk factor of extreme hyperbilirubinemia, death, and kernicterus.

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“…Infants with G6PD deficiency are at higher risk of mortality secondary to bilirubin encephalopathy if total serum bilirubin (TSB) is ≥40 mg/dL3). While spectrums of G6PD-deficient infants in relation to severe NIH have been evaluated in many countries234910111213), to our knowledge it has not been evaluated in Bahrain.…”

Section: Introductionmentioning

confidence: 99%

Neonatal indirect hyperbilirubinemia and glucose-6-phosphate dehydrogenase deficiency

Isa

Mohamed

et al. 2017

Korean J Pediatr

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PurposeThis study aimed to determine the prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency among infants with neonatal indirect hyperbilirubinemia (NIH); compare G6PD-deficient and G6PD-normal patients regarding hyperbilirubinemia and need for exchange transfusions (ET); and assess risk factors for ET and kernicterus.MethodsThis is a case-control retrospective study. Medical records of NIH patients admitted to the Pediatric Department, Salmaniya Medical Complex, Bahrain, between January 2007 and June 2010 were reviewed. Data on sex, age at presentation, hospitalization duration, need for ET, hemoglobin (Hb) level, reticulocyte count, direct Coombs test, serum total and indirect bilirubin levels, thyroid function, blood and urine cultures, G6PD status, and blood groups were collected and compared between the G6PD-deficent and G6PD-normal patients.ResultsOf 1,159 NIH patients admitted, 1,129 were included, of whom 646 (57%) were male. Among 1,046 patients tested, 442 (42%) were G6PD deficient, 49 (4%) needed ET, and 11 (1%) had suspected Kernicterus. The G6PD-deficient patients were mainly male (P<0.0001), and had lower Hb levels (P<0.0001) and higher maximum bilirubin levels (P=0.001). More G6PD-deficient patients needed ET (P<0.0001). G6PD deficiency (P=0.006), lower Hb level (P=0.002), lower hematocrit count (P=0.02), higher bilirubin level (P<0.0001), higher maximal bilirubin level (P<0.0001), and positive blood culture result (P<0.0001) were significant risk factors for ET. Maximal bilirubin level was a significant risk factor for kernicterus (P=0.021) and independently related to ET (P=0.03).ConclusionG6PD deficiency is an important risk factor for severe NIH. In G6PD-deficent neonates, management of NIH should be hastened to avoid irreversible neurological complications.

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Donor Blood Glucose 6-Phosphate Dehydrogenase Deficiency Reduces the Efficacy of Exchange Transfusion in Neonatal Hyperbilirubinemia

Abstract: Exchange transfusion with glucose 6-phosphate dehydrogenase-deficient donor blood leads to a lesser drop in postexchange total serum bilirubin. It prolongs the duration of phototherapy and increases the need for repeat exchange transfusions.

Cited by 30 publications

References 11 publications

Screening for G6PD Deficiency in Blood Donor Population

Screening for G6PD Deficiency in Blood Donor Population

Clinical Characteristics of G6PD Deficiency in Infants With Marked Hyperbilirubinemia

Neonatal indirect hyperbilirubinemia and glucose-6-phosphate dehydrogenase deficiency

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