Studies of bilirubin kinetics in normal adults

Berk, Paul D.; Howe, Robert B.; Bloomer, Joseph R.; Berlin, Nathaniel I.

doi:10.1172/jci106184

Cited by 225 publications

(158 citation statements)

References 39 publications

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“…We illustrate this using the UCB steady-state kinetics models reported for healthy adults (20 ) and a child with Crigler-Najjar I disease (21 ), which is an inherited absence of hepatic UCB conjugation resulting in severe, lifelong UCB retention characterized by marked jaundice, unconjugated hyperbilirubinemia, and increased risk of ABE (22 ). Dashed lines indicate intramolecular hydrogen bonds, which make the 4Z,15Z isomer lipophilic and neurotoxic.…”

Section: Abe B T and B F : The Rationale For Measuring B F In Jaunmentioning

confidence: 99%

Unbound (Free) Bilirubin: Improving the Paradigm for Evaluating Neonatal Jaundice

et al. 2009

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Background: The serum or plasma total bilirubin concentration (BT) has long been the standard clinical laboratory test for evaluating neonatal jaundice, despite studies showing that BT correlates poorly with acute bilirubin encephalopathy (ABE) and its sequelae including death, classical kernicterus, or bilirubin-induced neurological dysfunction (BIND). The poor correlation between BT and ABE is commonly attributed to the confounding effects of comorbidities such as hemolytic diseases, prematurity, asphyxia, or infection. Mounting evidence suggests, however, that BT inherently performs poorly because it is the plasma non–protein-bound (unbound or free) bilirubin concentration (Bf), rather than BT, that is more closely associated with central nervous system bilirubin concentrations and therefore ABE and its sequelae. Content: This article reviews (a) the complex relationship between serum or plasma bilirubin measurements and ABE, (b) the history underlying the limited use of Bf in the clinical setting, (c) the peroxidase method for measuring Bf and technical and other issues involved in adapting the measurement to routine clinical use, (d) clinical experience using Bf in the management of newborn jaundice, and (e) the value of Bf measurements in research investigating bilirubin pathochemistry. Summary: Increasing evidence from clinical studies, clinical experience, and basic research investigating bilirubin neurotoxicity supports efforts to incorporate Bf expeditiously into the routine evaluation of newborn jaundice. .

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Section: Abe B T and B F : The Rationale For Measuring B F In Jaunmentioning

confidence: 99%

Unbound (Free) Bilirubin: Improving the Paradigm for Evaluating Neonatal Jaundice

et al. 2009

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“…Total bilirubin value of neonates in the unconjugated hyperbilirubinemia group was high (95%) while the value in the control group was less than 40% according to the percentile-based hour specific bilirubin nomogram (Berk et al, 1969).…”

Section: Research Subjectsmentioning

confidence: 89%

Analysis of uridine diphosphate glucuronosyl transferase 1A1 gene mutations in neonates with unconjugated hyperbilirubinemia

Sun

Cui

et al. 2016

Genet. Mol. Res.

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ABSTRACT. This study was carried out to analyze uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) gene mutations in neonates with unconjugated hyperbilirubinemia, from two different ethnic groups. Polymerase chain reaction and gene sequencing were used to analyze the differences in genotypes and allele frequencies of different gene mutations among the ethnic groups; this was followed by checking their correlation with the serum bilirubin level and the occurrence of unconjugated hyperbilirubinemia in neonates. Our results reveal that the UGT1A1 mutant genotype, 211G>A, is distributed differently in the case vs control groups, as well as in the Zhuang vs Han ethnic groups. Moreover, this difference is statistically significant (P < 0.05); the total serum bilirubin (TSB) and unconjugated bilirubin (UCB) levels in patients carrying the single homozygous mutation, 211G>A, were markedly higher than that in patients without the mutation (P < 0.05). Furthermore, the TSB and UCB levels were significantly different between patients carrying single or compound 211G>A heterozygous mutation, (TA)6/7, and 1941C>G/2042C>G heterozygous mutation, and patients without mutation (P > 0.05). Our findings suggest that the 211G>A mutation in the first exon may be a risk factor for unconjugated hyperbilirubinemia in Zhuang and Han neonates. The serum bilirubin levels seem to be affected by the homozygosity or heterozygosity of the UGT1A1 gene mutation; 211G>A homozygous mutation is an important factor that causes a rise in bilirubin in neonates with unconjugated hyperbilirubinemia.

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“…Daily production of bilirubin IXα in a man amounts to ca. 400 mg, and about 75% of which are accounted for by the degradation of hemoglobin heme [47,48].…”

Section: Intracellular Heme Catabolismmentioning

confidence: 99%

Biological Implications of Heme Metabolism

Sassa

2006

J. Clin. Biochem. Nutr.

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Studies of bilirubin kinetics in normal adults

Cited by 225 publications

References 39 publications

Unbound (Free) Bilirubin: Improving the Paradigm for Evaluating Neonatal Jaundice

Unbound (Free) Bilirubin: Improving the Paradigm for Evaluating Neonatal Jaundice

Analysis of uridine diphosphate glucuronosyl transferase 1A1 gene mutations in neonates with unconjugated hyperbilirubinemia

Biological Implications of Heme Metabolism

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