Glucose-6-phosphate dehydrogenase deficiency and carboxyhemoglobin concentrations associated with bilirubin-related morbidity and death in Nigerian infants☆,☆☆,★,★★
Section snippets
Patients
The study protocol was approved by the institutional review board at the University of Texas Southwestern Medical Center at Dallas, as well as by the hospital administrator at Eku Baptist Hospital, Eku, Nigeria, and included informed consent from the parents or guardians of the infants who served as subjects of this investigation. Fifty-five clinically jaundiced infants, ≤10 days of age, admitted to Eku Baptist Hospital were enrolled from June to October 1991 and during June and July of 1992,
RESULTS
Infants ranged in age from 1 to 10 days, with a mean of 3.9 ± 1.6 days, (n = 55). Average weight was 2.7 ± 0.8 kg, with a range of 1.1 to 4.2 (n = 54; one not recorded). Twenty-one infants (39%) were > 2.5 kg. There were 39 boys and 15 girls (one not recorded); all infants were black. Twenty-two infants were born in the hospital at Eku and admitted directly from the obstetrics department. Twenty were born in outlying hospitals or clinics and subsequently came to Eku without a documented stay at
DISCUSSION
The COHb level is an accepted index of total bilirubin production in neonatal subjects under various clinical conditions.16, 17 Although COHb concentrations in this study correlated with bilirubin levels, half of the variability cannot be explained by this relationship, most likely because of individual differences in bilirubin elimination from the body during the first several days of life. Except when bilirubin production is extremely high and associated consequently with extremely high
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Cited by (111)
Hyperbilirubinemia in the Term Infant: Re-evaluating What We Think We Know
2021, Clinics in PerinatologyCitation Excerpt :Recently, in a Californian survey, Wickremasinghe and colleagues54 confirmed that black infants were at greater risk than white infants of developing extreme hyperbilirubinemia levels greater than or equal to 30 mg/dL (RR 4.2; 95% CI, 1.33–13.2). Black newborns in the United Kingdom, Ireland,14 and Central and West Africa also have been shown to have a high incidence of severe neonatal hyperbilirubinemia and kernicterus.55,56 The increased risk of extreme hyperbilirubinemia and kernicterus in black newborns may be explained in part by a higher incidence of G6PD deficiency56 and a higher frequency of the UGT1A1∗28 promoter polymorphism in this population group.57
Estimated disease burden and lost economic productivity due to glucose-6-phosphate dehydrogenase deficiency in Nigerian newborns
2021, Seminars in PerinatologyCitation Excerpt :We used a descriptive analytical model from previously reported study4 as a primary template on a REDCap databasae9 with data on the prevalence of G6PD deficiency in Nigeria entered to calculate outcome measures categorized as bilirubin-related morbidities and mortality. The model was then adapted to include additional data extracted from available literature7,10-21 in order to perform a meta-analysis to establish pooled estimates. Quantitative estimations for country-wide populations were derived from pooled estimates to define disease burden in terms of number of life years lost and number of years lived with disability.
Mutations and Polymorphisms of Genes Active in the Formation and Elimination of Bilirubin With the Potential for Modulating Neonatal Hyperbilirubinemia
2017, Fetal and Neonatal Physiology, 2-Volume SetHyperbilirubinemia, hemolysis, and increased bilirubin neurotoxicity
2014, Seminars in PerinatologyCitation Excerpt :In an analysis of 249 newborns admitted to the Cairo University Children׳s Hospital, Egypt, with a STB value ≥ 25 mg/dL, Rh incompatibility, ABO incompatibility, and G-6-PD deficiency dominated the list of identified etiologies for hyperbilirubinemia.24 In a study of 55 clinically jaundiced newborns admitted to a rural hospital in Nigeria, blood carboxyhemoglobin (COHb) values more than the median (reflective of endogenous heme catabolism and indicative of excessive heme catabolism) and G-6-PD deficiency were associated with findings compatible with kernicterus.25 Both increased bilirubin production as evidenced by COHb values and G-6-PD deficiency were associated with increased incidence of death, compared with those with lower COHb values or a normal level of G-6-PD activity, respectively.
Is it accurate to separate glucose-6-phosphate dehydrogenase activity in neonatal hyperbilirubinemia as deficient and normal?
2014, Pediatrics and NeonatologyCitation Excerpt :Previous reports have shown that G6PD deficiency leads to early occurrence of hyperbilirubinemia, which requires phototherapy or exchange transfusion.32,33 In different populations, this could be concomitant with kernicterus or death.34,35 In our study, G6PD activity in the group treated with exchange transfusion was significantly lower.
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From the Departments of Pediatrics, University of Texas Southwestern Medial Center at Dallas, Stanford University School of Medicine, Stanford, California, State University of New York Health Science Center at Brooklyn, Eku Baptist Hospital, Eku, Nigeria, and Children's Medical Center of Dallas, Dallas, Texas.
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Supported in part by National Institute of Child Health and Development grants HD14426 and RR00070, by the Mary L. Johnson Research Fund, and by designated gifts from individuals of Pike County Methodist and Baptist churches.
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Reprint requests: David K. Stevenson, MD, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305-5119.
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0022-3476/95/$3.00 + 0 9/23/59586