Differing Pathogenesis of Perinatal Bilirubinemia in Glucose-6-Phosphate Dehydrogenase-Deficient Versus-Normal Neonates

Kaplan, Michael; Hammerman, Cathy; Renbaum, Paul; Levy-Lahad, Ephrat; Vreman, Hendrik J.; Stevenson, David K.

doi:10.1203/00006450-200110000-00018

Cited by 31 publications

(24 citation statements)

References 26 publications

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“…As expected from previous studies (17,20,21), COHbc values were significantly higher in the G-6-PD-deficient cohort than in the controls. However, despite the increased heme catabolism, PTB concentrations at the time of sampling were similar between the two groups.…”

Section: Discussionsupporting

confidence: 90%

“…In the past, there was some debate as to whether increased hemolysis or diminished conjugation was the primary factor in the pathophysiology of hyperbilirubinemia in G-6-PD deficient neonates (18,19). Recent studies have clarified the situation and shown that, despite increased hemolysis associated with the condition (17,20,21), the icterus appears to be due to a predilection for diminished bilirubin conjugation compared with G-6-PD-normal counterparts (22,23). The diminished bilirubin conjugation is the result of UGT (TA) 7 promoter polymorphism (24).…”

mentioning

confidence: 99%

“…As baseline hemolysis is increased in G-6-PD-deficient neonates (17,20,21), and in light of the increased hemolysis found in G-6-PD-normal neonates who were homozygous for the (TA) 7 promoter polymorphism, we hypothesized that in G-6-PD-deficient newborns, heme catabolism would be increased to an even greater extent than in G-6-PD-normal controls of the identical UGT promoter genotype. Our objective in this study was to further elucidate, in steady state, the respective roles, individually and in combination, of heme catabolism and (TA) 7 UGT promoter polymorphism in determining PTB concentrations in a G-6-PD-deficient male neonatal cohort.…”

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confidence: 99%

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(TA)n UGT 1A1 Promoter Polymorphism: A Crucial Factor in the Pathophysiology of Jaundice in G-6-PD Deficient Neonates

et al. 2007

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Section: Discussionsupporting

confidence: 90%

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confidence: 99%

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confidence: 99%

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(TA)n UGT 1A1 Promoter Polymorphism: A Crucial Factor in the Pathophysiology of Jaundice in G-6-PD Deficient Neonates

et al. 2007

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“…The patient cohort consisted of healthy neonates delivered at Ն37 weeks' gestational age at the Shaare Zedek Medical Center. As glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is common in some subsections of the Israeli population and may be associated with differing rates of bilirubin metabolism, 16 males only were included so as not to encounter female G-6-PD-deficient heterozygotes. Infants with direct Coombs' positive hemolytic conditions, G-6-PD deficiency, sepsis, maternal diabetes, extensive bruising, or Down syndrome were excluded.…”

Section: Methodsmentioning

confidence: 99%

Imbalance Between Production and Conjugation of Bilirubin: A Fundamental Concept in the Mechanism of Neonatal Jaundice

et al. 2002

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ABSTRACT. Objective. The objective of this study was to evaluate the roles of production and conjugation of bilirubin, individually and in combination, in the mechanism of neonatal jaundice.Methods. A cohort of healthy, term male newborns was sampled on the third day of life, coincident with routine metabolic screening, for blood carboxyhemoglobin determination, a reflection of heme catabolism, and for serum unconjugated and conjugated bilirubin fractions, reflecting bilirubin conjugation. The former was determined by gas chromatography, corrected for inspired CO (COHbc), and expressed as percentage of total hemoglobin. Serum bilirubin fractions were quantified by alkaline methanolysis and reverse phase high performance liquid chromatography. The sum of all bilirubin fractions comprised serum total bilirubin (STB). Conclusions. Within the range of STB concentrations encountered, both increasing bilirubin production and diminishing bilirubin conjugation contributed to STB. The production/conjugation index confirmed that imbalance between production and conjugation of bilirubin plays an important role in the mechanism of neonatal bilirubinemia. Pediatrics 2002;110(4). URL: http://www. pediatrics.org/cgi/content/full/110/4/e47; alkaline methanolysis, bilirubin, bilirubin conjugation, carbon monoxide, carboxyhemoglobin, gas chromatography, hemolysis, high performance liquid chromatography, physiologic jaundice. Total conjugated bilirubin (TCB) was comprised of the sum of the conjugated fractions and was expressed as percentage of STB (TCB[%]). A "bilirubin production/conjugation index" (COHbc/[TCB(%)]ABBREVIATIONS. STB, serum total bilirubin; CO, carbon monoxide; COHb, carboxyhemoglobin; COHbc, COHb corrected for inspired CO; UGT, uridine diphosphoglucuronate glucuronosyltransferase 1A1; G-6-PD, glucose-6-phosphate dehydrogenase; TCB, serum total conjugated bilirubin. J aundice is common during the first days of postnatal life and affects almost two thirds of human newborns. The mechanism of this bilirubinemia is multifactorial, as recently summarized, and comprises primarily processes contributing to increased bilirubin load, or diminished bilirubin clearance. 1,2 The former may be the result of factors that augment bilirubin production and the enterohepatic circulation, whereas the latter is primarily the result of immature conjugative capacity, although impaired hepatic uptake or excretion may also play a part. It has been suggested that serum total bilirubin (STB) concentrations that remain within the physiologic range result from equilibrium between bilirubin production and elimination. In contrast, in some neonates, imbalance between these processes may occur, with bilirubin production being relatively higher than conjugation. This imbalance is thought to result in hyperbilirubinemia. 3 Assessment of the role of hemolysis may be accomplished through assessment of endogenous carbon monoxide (CO) production by accurately measuring blood carboxyhemoglobin (COHb), or end tidal CO, both with correction for ambient ...

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“…Carboxihemoglobin concentrations, for example, have been used in the evaluation of hemolysis associated to ABO incompatibility and glucose-6-phosphate dehydrogenase deficient in newborns. 29,30 HPT could also potentially be used in the evaluation of neonatal hemolysis. Our results indicate the need for a more thorough analysis of neonatal HPT concentrations using ELISA.…”

Section: 'Haptoglobin In Newborns'mentioning

confidence: 99%

‘Haptoglobin concentrations in preterm and term newborns’

et al. 2011

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Objective: To measure systemic haptoglobin (HPT) concentrations from birth in preterm (PT) and T newborns. To compare HPT in newborns without hemolysis or infection with values in bacteremic newborns.Study Design: HPT was measured using enzyme-linked immunosorbent assay in 30 PT and 28 T newborns without hemolysis or infection at birth (cord blood), on days of life 2 to 4, and at 1 to 2 weeks of life. Concentrations were measured in eight additional newborns with bacteremia. Wilcoxon-Mann-Whitney test was used for comparisons.Result: HPT concentrations were consistently measurable from birth in PT and T neonates. Values were significantly greater in 2-to 4-day-old PT and T newborns than in newborns at birth (P<0.01). Bacteremic newborns had higher HPT concentrations than newborns without infection (P ¼ 0.033). Conclusion:HPT is detectable from birth in PT and T newborns. HPT concentrations increase in bacteremic newborns. HPT levels may have clinical utility in the evaluation of neonatal sepsis.

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Differing Pathogenesis of Perinatal Bilirubinemia in Glucose-6-Phosphate Dehydrogenase-Deficient Versus-Normal Neonates

Cited by 31 publications

References 26 publications

(TA)n UGT 1A1 Promoter Polymorphism: A Crucial Factor in the Pathophysiology of Jaundice in G-6-PD Deficient Neonates

(TA)n UGT 1A1 Promoter Polymorphism: A Crucial Factor in the Pathophysiology of Jaundice in G-6-PD Deficient Neonates

Imbalance Between Production and Conjugation of Bilirubin: A Fundamental Concept in the Mechanism of Neonatal Jaundice

‘Haptoglobin concentrations in preterm and term newborns’

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