Studies in hemolysis in glucose-6-phosphate dehydrogenase-deficient African American neonates

Michael Kaplan, Marguerite Herschel, Cathy Hammerman, Theodore Karrison, James Hoyer, David K. Stevenson

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background: The role of hemolysis in the mechanism and prediction of hyperbilirubinemia was contrasted between glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and -normal African American neonates. Methods: Corrected end tidal carbon monoxide (ETCOc) values from the subset of male neonates born to non-smoking African American mothers, drawn from a previously published study, were analyzed. The relationship between ETCOc and bilirubin values, the latter represented as percentiles on the hour of life specific bilirubin nomogram, was determined. Hyperbilirubinemia was defined as any bilirubin value ≥95th percentile for hour of life. Results: 18.6% of 59 G-6-PD-deficient neonates developed hyperbilirubinemia, compared with 7.5% of 362 controls (relative risk 2.50, 95% confidence interval 1.31 to 4.76). As reported, ETCOc values (median, interquartile range) were significantly higher among G-6-PD-deficient neonates than controls (2.4 [2.0-2.9] vs. 2.1 [1.7-2.5] ppm, p < 0.001. However, higher ETCOc values were limited to those G-6-PD-deficient neonates with lower bilirubin percentiles: among those whose bilirubin value did not exceed the 95th percentile ETCOc was 2.30 [2.00-2.85] vs. 2.00 [1.70-2.40] ppm in controls, p = 0.001. In contrast, among the hyperbilirubinemic neonates ETCOc values were similar between G-6-PD-deficient neonates and controls: 2.7 [2.03-3.33] vs. 2.6 [2.33-3.45] ppm, p = 0.9. In the G-6-PD-deficient neonates ETCOc ≥75th percentile contributed no additional predictive value for hyperbilirubinemia (likelihood ratio 1.8). Conclusions: G-6-PD-deficient African American neonates have increased hemolysis and increased rate of hyperbilirubinemia, but the hemolysis is neither a predominant factor in the pathogenesis of hyperbilirubinemia nor is it predictive of hyperbilirubinemia, over and above the already increased risk conferred by G-6-PD deficiency.

Original languageEnglish (US)
Pages (from-to)177-182
Number of pages6
JournalClinica Chimica Acta
Volume365
Issue number1-2
DOIs
StatePublished - Mar 1 2006

Fingerprint

Glucosephosphate Dehydrogenase
Hemolysis
African Americans
Hyperbilirubinemia
Newborn Infant
Bilirubin
Nomograms
Glucosephosphate Dehydrogenase Deficiency
Carbon Monoxide
Mothers
Confidence Intervals

Keywords

  • African American
  • End tidal carbon monoxide
  • Glucose-6-phosphate dehydrogenase deficiency
  • Hemolysis
  • Neonatal hyperbilirubinemia
  • Prediction
  • Receiver Operating Characteristic curves

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Studies in hemolysis in glucose-6-phosphate dehydrogenase-deficient African American neonates. / Kaplan, Michael; Herschel, Marguerite; Hammerman, Cathy; Karrison, Theodore; Hoyer, James; Stevenson, David K.

In: Clinica Chimica Acta, Vol. 365, No. 1-2, 01.03.2006, p. 177-182.

Research output: Contribution to journalArticle

Kaplan, M, Herschel, M, Hammerman, C, Karrison, T, Hoyer, J & Stevenson, DK 2006, 'Studies in hemolysis in glucose-6-phosphate dehydrogenase-deficient African American neonates', Clinica Chimica Acta, vol. 365, no. 1-2, pp. 177-182. https://doi.org/10.1016/j.cca.2005.08.015
Kaplan, Michael ; Herschel, Marguerite ; Hammerman, Cathy ; Karrison, Theodore ; Hoyer, James ; Stevenson, David K. / Studies in hemolysis in glucose-6-phosphate dehydrogenase-deficient African American neonates. In: Clinica Chimica Acta. 2006 ; Vol. 365, No. 1-2. pp. 177-182.
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abstract = "Background: The role of hemolysis in the mechanism and prediction of hyperbilirubinemia was contrasted between glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and -normal African American neonates. Methods: Corrected end tidal carbon monoxide (ETCOc) values from the subset of male neonates born to non-smoking African American mothers, drawn from a previously published study, were analyzed. The relationship between ETCOc and bilirubin values, the latter represented as percentiles on the hour of life specific bilirubin nomogram, was determined. Hyperbilirubinemia was defined as any bilirubin value ≥95th percentile for hour of life. Results: 18.6{\%} of 59 G-6-PD-deficient neonates developed hyperbilirubinemia, compared with 7.5{\%} of 362 controls (relative risk 2.50, 95{\%} confidence interval 1.31 to 4.76). As reported, ETCOc values (median, interquartile range) were significantly higher among G-6-PD-deficient neonates than controls (2.4 [2.0-2.9] vs. 2.1 [1.7-2.5] ppm, p < 0.001. However, higher ETCOc values were limited to those G-6-PD-deficient neonates with lower bilirubin percentiles: among those whose bilirubin value did not exceed the 95th percentile ETCOc was 2.30 [2.00-2.85] vs. 2.00 [1.70-2.40] ppm in controls, p = 0.001. In contrast, among the hyperbilirubinemic neonates ETCOc values were similar between G-6-PD-deficient neonates and controls: 2.7 [2.03-3.33] vs. 2.6 [2.33-3.45] ppm, p = 0.9. In the G-6-PD-deficient neonates ETCOc ≥75th percentile contributed no additional predictive value for hyperbilirubinemia (likelihood ratio 1.8). Conclusions: G-6-PD-deficient African American neonates have increased hemolysis and increased rate of hyperbilirubinemia, but the hemolysis is neither a predominant factor in the pathogenesis of hyperbilirubinemia nor is it predictive of hyperbilirubinemia, over and above the already increased risk conferred by G-6-PD deficiency.",
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AU - Kaplan, Michael

AU - Herschel, Marguerite

AU - Hammerman, Cathy

AU - Karrison, Theodore

AU - Hoyer, James

AU - Stevenson, David K.

PY - 2006/3/1

Y1 - 2006/3/1

N2 - Background: The role of hemolysis in the mechanism and prediction of hyperbilirubinemia was contrasted between glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and -normal African American neonates. Methods: Corrected end tidal carbon monoxide (ETCOc) values from the subset of male neonates born to non-smoking African American mothers, drawn from a previously published study, were analyzed. The relationship between ETCOc and bilirubin values, the latter represented as percentiles on the hour of life specific bilirubin nomogram, was determined. Hyperbilirubinemia was defined as any bilirubin value ≥95th percentile for hour of life. Results: 18.6% of 59 G-6-PD-deficient neonates developed hyperbilirubinemia, compared with 7.5% of 362 controls (relative risk 2.50, 95% confidence interval 1.31 to 4.76). As reported, ETCOc values (median, interquartile range) were significantly higher among G-6-PD-deficient neonates than controls (2.4 [2.0-2.9] vs. 2.1 [1.7-2.5] ppm, p < 0.001. However, higher ETCOc values were limited to those G-6-PD-deficient neonates with lower bilirubin percentiles: among those whose bilirubin value did not exceed the 95th percentile ETCOc was 2.30 [2.00-2.85] vs. 2.00 [1.70-2.40] ppm in controls, p = 0.001. In contrast, among the hyperbilirubinemic neonates ETCOc values were similar between G-6-PD-deficient neonates and controls: 2.7 [2.03-3.33] vs. 2.6 [2.33-3.45] ppm, p = 0.9. In the G-6-PD-deficient neonates ETCOc ≥75th percentile contributed no additional predictive value for hyperbilirubinemia (likelihood ratio 1.8). Conclusions: G-6-PD-deficient African American neonates have increased hemolysis and increased rate of hyperbilirubinemia, but the hemolysis is neither a predominant factor in the pathogenesis of hyperbilirubinemia nor is it predictive of hyperbilirubinemia, over and above the already increased risk conferred by G-6-PD deficiency.

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KW - End tidal carbon monoxide

KW - Glucose-6-phosphate dehydrogenase deficiency

KW - Hemolysis

KW - Neonatal hyperbilirubinemia

KW - Prediction

KW - Receiver Operating Characteristic curves

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