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At least 91 records · Page 5Linked to original sources
PubMed2000

Effect of bilirubin UDP glucuronosyltransferase 1 gene TATA box genotypes on serum bilirubin concentrations in chronic liver injuries.

TATA box abnormality in the promoter region of the bilirubin UDP glucuronosyltransferase 1 gene has been reported to cause Gilbert's syndrome in white subjects. It has also been reported that the majority of Japanese patients with Gilbert's syndrome are heterozygous for Gly71Arg in the coding region of this gene. On the other hand, some patients with chronic hepatitis often show signs of unexpected hyperbilirubinemia. The aims of this study were to determine which of the genetic variations, TATA box genotype or codon 71 genotype, is most closely related to serum bilirubin concentrations, and whether the TATA box genotype has an effect on serum bilirubin concentrations in patients with hepatitis C-associated chronic liver diseases. In a sample of 300 individuals selected from among the general Japanese population, mean concentrations of total serum bilirubin differed significantly among TATA box genotypes, but not among codon 71 genotypes. Concentration of total serum bilirubin was significantly correlated with TATA box genotypes. In 211 patients with hepatitis C-associated chronic liver diseases, mean concentrations of total serum bilirubin also differed significantly among TATA box genotypes. In patients with chronic hepatitis C, concentration of total serum bilirubin was significantly correlated with TATA box genotypes. In summary, TATA box genotypes, but not codon 71 genotypes, are closely related to serum bilirubin concentrations. TATA box genotypes should therefore be considered when evaluating hepatic function by serum bilirubin concentrations in cases of hepatitis C-associated chronic liver diseases.

Adult↗
PubMed2001

Bile bilirubin pigment analysis in disorders of bilirubin metabolism in early infancy.

BACKGROUND: Early and accurate diagnosis of Crigler-Najjar syndrome, which causes prolonged unconjugated hyperbilirubinaemia in infancy, is important, as orthotopic liver transplantation is the definitive treatment. AIM: To determine whether bilirubin pigment analysis of bile in infants with prolonged unconjugated hyperbilirubinaemia provides useful diagnostic information in the first 3 months of life. METHODS: Retrospective review of patients with prolonged unconjugated hyperbilirubinaemia referred to the liver unit, Birmingham Children's Hospital, for the diagnosis of Crigler-Najjar syndrome. Bile bilirubin pigment composition was determined by high performance liquid chromatography. Initial diagnoses were made based on the result of bile bilirubin pigment composition. Final diagnoses were made after reviewing the clinical course, response to phenobarbitone, repeat bile bilirubin pigment composition analysis, and genetic studies. RESULTS: Between 1992 and 1999, nine infants aged less than 3 months of age with prolonged hyperbilirubinaemia underwent bile bilirubin pigment analyses. Based on these, two children were diagnosed with Crigler-Najjar syndrome (CNS) type 1, six with CNS type 2, and one with Gilbert's syndrome. Five children whose initial diagnosis was CNS type 2 had resolution of jaundice and normalisation of serum bilirubin after discontinuing phenobarbitone, and these cases were thought to be normal or to have Gilbert's syndrome. One of the initial cases of CNS type 1 responded to phenobarbitone with an 80% reduction in serum bilirubin consistent with CNS type 2. In all, the diagnoses of six cases needed to be reviewed. CONCLUSIONS: Early bile pigment analysis, performed during the first 3 months of life, often shows high levels of unconjugated bilirubin or bilirubin monoconjugates, leading to the incorrect diagnosis of both type 1 and type 2 Crigler-Najjar syndrome.

Bile Pigments↗
PubMed1971

Bilirubin excretion in rats with normal and impaired bilirubin conjugation: effect of phenobarbital.

The effect of phenobarbital on bilirubin excretion was studied in rats with different capacities for bilirubin conjugation. Drug treatment induced substantial increases in bilirubin UDP-glucuronyl transferase activity in the liver of both normal and heterozygous Gunn rats, but not homozygous Gunn rats in which enzyme activity is completely absent. However, enhancement of bilirubin excretion in vivo was observed only in heterozygous Gunn rats. In these animals the maximum capacity to excrete bilirubin into bile (T(max)), like the activity of the conjugating enzyme, was half normal; phenobarbital caused an increase in T(max) to levels characteristic of normal animals, with a twofold rise in the excretion of conjugated pigment. This appeared to be largely unrelated to enhancement of bile flow, and there was no stimulation of alternate pathways of bilirubin excretion. Conjugated bilirubin was consistently recovered from the plasma and urine of both untreated normal and heterozygous Gunn rats infused with unconjugated pigment. The quantities thus recovered comprised a similar fraction of the total pigment conjugated in both types of animal. Moreover, there were linear correlations between T(max) and both the rate of bile flow and the activity of the conjugating enzyme over the range of values represented by control rats of both types. These findings suggest that the process by which conjugated bilirubin is secreted into the bile is closely related to conjugation and limits the final excretory rate at different levels of pigment excretion. The phenobarbital effect uniquely observed in heterozygous Gunn rats appears to be mediated primarily by enhancement of the limited capacity for bilirubin conjugation with an associated rise in functional secretory capacity.

Animals↗
PubMed1984

The role of bilirubin production in breast-fed infants with elevated serum bilirubin concentrations at 2 weeks of life.

The carboxyhemoglobin level (COHb), an accepted qualitative index of bilirubin production, was measured in normal, full-term, breast-fed (n = 9) or formula-fed (n = 11) infants at 2 days and 2 weeks of life. The mean COHb did not differ significantly at 2 days and 2 weeks in either of the groups, nor did the mean COHb differ between the groups at 2 weeks. The mean serum bilirubin concentration was lower in the formula-fed infants compared to the breast-fed infants at 2 weeks (p less than 0.05). The mean serum bilirubin concentration decreased by only 14 percent among the breast-fed infants, and actually increased in three infants by 2 weeks. In comparison, the mean serum bilirubin concentration of the formula-fed infants decreased by 61 percent (p less than 0.05), with the serum bilirubin concentration decreasing in each infant by 2 weeks. These findings are consistent with the generally held belief that bilirubin production is not the primary etiology of elevated serum bilirubin concentrations associated with breast-feeding in the second week of life. However, continued high bilirubin production at 2 weeks may contribute to the potential for significant jaundice in some infants with impaired hepatic function or increased enterohepatic circulation of bilirubin.

Bilirubin↗
PubMed2000

Bilirubin adsorption therapy and subsequent liver transplantation cured severe bilirubin encephalopathy in a long-term survival patient with Crigler-Najjar disease type I.

Crigler-Najjar disease (CN) type I is characterized by persistent unconjugated hyperbilirubinemia from birth. The male patient here was diagnosed with this disease as a neonate and had been treated by phototherapy. At age 16 he suddenly developed generalized convulsions, followed by impaired cognitive function. The serum level of bilirubin was extremely high (total bilirubin: 41.7 mg/dl) and there were no other detectable causes responsible for the metabolic encephalopathy. He received bilirubin adsorption therapy several times, and the bilirubin encephalopathy improved in response to the fall in the serum level of bilirubin. After this he underwent a successful liver transplantation in Australia, and recovery of his mental faculties was satisfactory. Within the subsequent 3 years epileptic abnormal discharges on the electroencephalogram disappeared. Phototherapy alone can not prevent the rise in the serum level of bilirubin in adolescent or adult patients with CN type I, therefore such patients tend to experience life-threatening bilirubin encephalopathy. To save patients with the acute onset type of bilirubin encephalopathy, sufficient bilirubin adsorption followed by liver transplantation appears to be the most recommended therapeutic approach.

Adsorption↗
PubMed1990

Total and direct-reacting bilirubin values by automated methods compared with liquid chromatography and with manual methods for determining delta bilirubin.

This study compares total and direct-reacting bilirubin values in 40 serum samples from patients with various diagnoses, as measured by automated methods (Beckman Synchron CX-5, Beckman Astra 8, Kodak Ektachem 700) and HPLC and by a manual method for delta bilirubin. For total bilirubin, within-run CVs were less than 6%. The Ektachem 700 method underestimated bilirubin with serum samples from patients with Crigler-Najjar syndrome and from newborns in whom unconjugated bilirubin concentrations were increased but conjugated bilirubins were not present or were present only in small amounts. The Astra 8 and Synchron CX-5 methods were inaccurate with cholestatic serum samples, in which conjugated bilirubin concentrations were increased and other compounds such as bile acids could be expected to interfere. We conclude that each automated method examined provides reasonable estimates for total and direct-reacting bilirubin values for routine clinical use. The need for each laboratory to select the appropriate bilirubin method for its particular situation is obvious.

Autoanalysis↗
PubMedDate not supplied

Conjugated bilirubin: a better indicator of impaired hepatobiliary excretion than direct bilirubin.

A prototype KODAK EKTACHEM Clinical Chemistry Slide (BuBc) provided a measurement of serum conjugated bilirubin which was at least as sensitive to developing conjugated hyperbilirubinemia as values provided by a direct (diazo) bilirubin assay. Under conditions where the impairment of hepatobiliary excretion was relieved in patients being treated for various hepatobiliary diseases, conjugated bilirubin was cleared from serum more rapidly than alkaline phosphatase, the delta bilirubin fraction, and bilirubin measured by the direct and total bilirubin assays. It is concluded that the conjugated bilirubin measurement provided by the BuBc Slide appears to be an earlier indicator of relief from hepatobiliary cholestasis, or conversely of residual impairment, than direct bilirubin, total bilirubin, or alkaline phosphatase.

Alkaline Phosphatase↗
PubMed1979

Bilirubin excretion pattern in manganese-bilirubin cholestasis.

Impaired bilirubin excretion has been investigated as the possible mechanism for the cholestasis observed following the injection of manganese and bilirubin in rats. We studied the biliary excretion pattern of bilirubin in bile under both cholestatic (manganese plus bilirubin) and noncholestatic (manganese or bilirubin alone; manganese plus bilirubin plus sulfobromophthalein) conditions using a diazotization reaction and this layer chromatography. The accumulation of non-C-1-glucuronides or of nonglucuronoconjugates of bilirubin in bile does not seem to be responsible for the cholestasis. The altered biliary bilirubin metabolic pattern of the azodipyrollic fractions observed during manganese-bilirubin cholestasis appeared to be the result of the cholestasis, rather than its cause.

Animals↗