Serum bilirubin levels and glucose-6-phosphate dehydrogenase deficiency in newborn American Negroes

O'Flynn, Margaret E.; Hsia, David Yi‐Yung

doi:10.1016/s0022-3476(63)80314-5

Cited by 38 publications

(9 citation statements)

References 5 publications

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“…One possible reason for the apparent contrast between the current data and those of the earlier studies 11,33,34 may be that, in the older studies, bilirubin values were analyzed by using mean values during a particular 24-hour period. In contrast, we plotted bilirubin values on the hour-of-life nomogram 17 and defined hyperbilirubinemia according to the highest noted bilirubin percentile for the hour of life, which is a much more sensitive approach.…”

Section: Discussioncontrasting

confidence: 59%

“…11,33,34 More recent statements suggested that, with AϪ G-6-PD deficiency, spontaneous hemolysis may occur among premature but not term infants. 35 Furthermore, as a group, black neonates in the United States (the majority of whom are not G-6-PD-deficient) have a lower incidence of hyperbilirubinemia than do their Data Relating to Phototherapy for the G-6-PD-Deficient and G-6-PD-Normal Neonatal Groups e216 G-6-PD DEFICIENCY white or Asian counterparts.…”

Section: Discussionmentioning

confidence: 99%

“…Absorbance measurements were performed with a Technicon RA 1000 spectrophotometer (Technicon Instruments, Tarrytown, NY), and enzyme activity was expressed as units per gram of hemoglobin (Hb). For reference, normal values for African American neonates have been reported as 287 Ϯ 63 U/100 mL erythrocytes, 11 which correspond to ϳ8.0 Ϯ 1.5 U/g of Hb. 20 TcB determinations were performed by using Bilichek (Respironics, Norcross, GA).…”

Section: Laboratory Methodsmentioning

confidence: 99%

“…African Americans, of whom 11% to 13% are known to be G-6-PD-deficient (G-6-PD AϪ), represent the largest subgroup affected in North America. [9][10][11] Traditionally, these newborns have not been regarded as being at high risk for G-6-PD deficiency-associated hyperbilirubinemia; Maisels and Newman 12,13 stated that many American pediatricians do not take G-6-PD deficiency into consideration when evaluating likely causes of severe neonatal hyperbilirubinemia. This view was supported by the finding of Brown et al 14 that few neonates readmitted for treatment of hyperbilirubinemia in the greater New York City area had been tested for G-6-PD deficiency.…”

mentioning

confidence: 99%

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Hyperbilirubinemia Among African American, Glucose-6-Phosphate Dehydrogenase-Deficient Neonates

et al. 2004

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ABSTRACT. Background. Although glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is prevalent in African Americans, their risk of associated neonatal hyperbilirubinemia has not been prospectively studied.Objective. To compare hemolysis and the risk of hyperbilirubinemia among African American, G-6-PD-deficient neonates (study group) and G-6-PD-normal control subjects.Methods. Consecutive, healthy, term and near-term, male neonates born to African American mothers comprised the patient cohort. G-6-PD testing was performed with umbilical cord blood samples. Routine management included measurement of the end tidal carbon monoxide level corrected for ambient carbon monoxide level (ETCOc) within 4 hours after delivery (assessment of hemolysis), >1 predischarge bilirubin determination, and additional bilirubin testing as clinically indicated. Indications for phototherapy were identical for study patients and control subjects. Neonates were monitored for the first 1 week of life. ETCOc results, the incidence of hyperbilirubinemia (defined as a transcutaneous or plasma total bilirubin concentration of >95th percentile for the hour of life), and the need for phototherapy were compared between the G-6-PD-deficient and G-6-PDnormal groups.Results. Five hundred male patients were enrolled, of whom 64 (12.8%) were G-6-PD-deficient. ETCOc values (median and interquartile range) were higher among G-6-PD-deficient neonates than among control neonates (2.4 ppm [2.0 -2.9 ppm] vs 2.1 ppm [1.7-2.5 ppm]). More G-6-PD-deficient neonates developed hyperbilirubinemia than did control subjects (14 of 64, 21.9%, vs 29 of 436, 6.7%; relative risk: 3.27; 95% confidence interval: 1.83-5.86), whereas 13 (20.3%) met the criteria for phototherapy, compared with 25 control subjects (5.7%) (relative risk: 3.53; 95% confidence interval: 1.91-6.56). No cases of kernicterus were observed.Conclusions. Within the African American neonatal population, there is a subgroup of G-6-PD-deficient infants with elevated rates of hemolysis, a higher incidence of hyperbilirubinemia, and a greater requirement for phototherapy, compared with G-6-PD-normal control subjects. These newborns should be monitored vigilantly for the development of hyperbilirubinemia. ABBREVIATIONS. ETCOc, end tidal carbon monoxide level corrected for ambient carbon monoxide level; G-6-PD, glucose-6-phosphate dehydrogenase; PTB, plasma total bilirubin; TcB, transcutaneous bilirubin; Hb, hemoglobin. D espite increasing awareness of neonatal hyperbilirubinemia and American Academy of Pediatrics guidelines for the management of this condition, kernicterus continues to be encountered in North America. [1][2][3][4][5][6][7][8] Because many of the reported neonates were also deficient in glucose-6-phosphate dehydrogenase (G-6-PD), a condition associated with hyperbilirubinemia and kernicterus, an etiologic factor linking these 2 conditions is likely. African Americans, of whom 11% to 13% are known to be G-6-PD-deficient (G-6-PD AϪ), represent the largest subgroup affected in North America....

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Section: Discussioncontrasting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Laboratory Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Hyperbilirubinemia Among African American, Glucose-6-Phosphate Dehydrogenase-Deficient Neonates

et al. 2004

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“…Surveys of newborns in Northern Thailand [15], in Israel [29], and in American Negroes [22,37,39] have failed to demonstrate this association.…”

Section: Discussionmentioning

confidence: 99%

Incidence and Mechanism of Neonatal Jaundice Related to Glucose-6-Phosphate Dehydrogenase Deficiency

et al. 1969

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Neonatal Serum Bilirubin and Glucose-6-Phosphate Dehydrogenase

Wolff¹,

Grossman²,

Paya³

1967

Am J Dis Child

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to determine their relationship to otherwise unexplained instances of neonatal jaundice. Materials and MethodsEight hundred and forty-four newborn infants at the Columbia-Presbyterian Medical Center, weighing more than 1,900 gm, were included in the study. Babies were excluded if the mother's blood type was Group O and the baby's was Group A, B, or AB. This was done to eliminate the possibility of including infants whose hemolytic disease might be due to bl ood\x=req-\ group incompatibility. Rh-positive babies of Rh-negative mothers and infants with other possible causes of hyperbilirubinemia, such as infection or congenital anomalies, were also excluded. The following information was obtained about each mother: age, race, place of birth, method of delivery, complications of pregnancy and labor, medication during labor, blood type, serology, and antibiotics given. The following information was obtained about each infant: sex, race, Apgar score, weight, degree of clinical icterus, blood type, transfusions, drugs given, and G-6-PD activity. Serum bilirubin levels were determined for all infants who were clini¬ cally jaundiced. Semiquantitative screening of G-6-PD determinations were performed for all infants, usually within the first 48 hours of life. Quantitative G-6-PD tests were peformed only on subjects with abnormal screening determin¬ ations and on the mothers of such babies.Screening G-6-PD determinations were per¬ formed by a modification of a procedure1 in which the time necessary to reduce triphospho-pyridine nucleotide, (TPN) to its reduced form (TPNH) by G-6-PD is indicated by the color change of brilliant cresyl blue. The time re¬ quired is inversely related to the hemoglobin concentration. If the hemoglobin level exceeds 12.0 gm the time will be less than 45 minutes.

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Serum bilirubin levels and glucose-6-phosphate dehydrogenase deficiency in newborn American Negroes

Cited by 38 publications

References 5 publications

Hyperbilirubinemia Among African American, Glucose-6-Phosphate Dehydrogenase-Deficient Neonates

Hyperbilirubinemia Among African American, Glucose-6-Phosphate Dehydrogenase-Deficient Neonates

Incidence and Mechanism of Neonatal Jaundice Related to Glucose-6-Phosphate Dehydrogenase Deficiency

Neonatal Serum Bilirubin and Glucose-6-Phosphate Dehydrogenase

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