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PubMed1981

Effect of exchange transfusion on serum reserve albumin for binding of bilirubin and index of serum bilirubin toxicity.

Seventeen newborn infants, who received their first exchange transfusion due to hyperbilirubinaemia and/or rhesus haemolytic disease, were studied. The exchange transfusions were performed with fresh, citrated blood. During the exchange transfusion a marked increase in the serum reserve albumin concentration for binding of bilirubin measured by the [14C]-MADDS method was observed, followed by a smaller decrease after the transfusion. Plasma pH increased both during and after the exchange transfusion. During the exchange transfusion a drastic fall in index of serum bilirubin toxicity was observed, followed by a smaller increase after the transfusion. Citrate was not found to interfere in the binding of bilirubin to albumin. The results are in agreement with the clinical finding that an exchange transfusion performed with fresh, citrated blood effectively reduced the risk of bilirubin encephalopathy. The ratio in serum of binding albumin, i.e. bilirubin plus reserve albumin, to total albumin failed to be increased by the exchange transfusion, and a decrease occurred after the transfusion. These findings indicate the presence in infant serum of non-binding albumin. Donor albumin with intact binding potential is partly transformed into the non-binding variety in the course of one hour after the transfusion. In the most severely rhesus sensitized infant a drastic decline of the serum albumin binding capacity was seen during the first day of life.

Bilirubin↗
PubMed1988

Toxicity of bilirubin and bilirubin diglucuronide to rat tissue culture fibroblasts.

The effects of obstructive and non-obstructive jaundice on rat tissue culture fibroblasts have been compared. Tissue culture fibroblasts were grown in medium containing unconjugated bilirubin and medium containing conjugated bilirubin (bilirubin diglucuronide). The addition of bilirubin to the culture medium caused morphological changes in the fibroblasts and significantly decreased their rate of multiplication. The addition of bilirubin diglucuronide had no effect. As the fibroblast plays an important role in wound healing, patients with obstructive jaundice (where surgery is most frequently required) may be less likely to undergo wound failure than patients with non-obstructive jaundice.

Animals↗
PubMed1982

Relationship of plasma total bilirubin, apparent unbound bilirubin and total albumin with cerebellar glycogen and abnormal Purkinje cells in the Gunn rat.

Total plasma bilirubin, apparent unbound plasma bilirubin, cerebellar glycogen and Purkinje cells were quantified in heterozygous Gunn rats, homozygous Gunn rats and normal Wistar rats. Our results indicated that, in the Gunn rat, total bilirubin, apparent unbound bilirubin, and the bilirubin/albumin molar ratio are highly correlated with each other and with alterations in cerebellar Purkinje cells and accumulation of cerebellar glycogen. In addition, cerebella of heterozygous Gunn rats contained many abnormal Purkinje cells without intramitochondrial glycogen and cerebella of homozygous Gunn rats showed many Purkinje cells with intramitochondrial glycogen. Our results demonstrate previously unreported differences between heterozygous Gunn rats and controls. We suggest that population of Purkinje cells in the heterozygous Gunn rats may have received a cellular insult from fetal exposure to bilirubin.

Animals↗
PubMed1984

The effect of hematin on bilirubin binding in bilirubin-enriched neonatal cord serum.

It has been suggested that the serum of infants with ABO hemolytic disease contains hematin which might interfere with bilirubin binding to albumin, increasing the risk of kerincterus. Using the horseradish peroxidase assay, we investigated this possibility. Cord serum from healthy term infants was enriched with bilirubin to a bilirubin/albumin molar ratio of 0.6, and then varying amounts of hematin were added. Hematin had a significant adverse effect on bilirubin binding when present in half to equimolar ratios with bilirubin. This high concentration of hematin does not appear to be present in serum from infants with ABO hemolytic disease and no difference was seen when comparing the dilute and the undilute peroxidase assays. These data suggest that hematin can alter bilirubin binding in neonatal serum but is not os physiologic importance for infants with ABO-isoimmune hemolysis.

Bilirubin↗
PubMed1988

The determination of bilirubin with a new enzymatic method (Dri-STAT bilirubin) using the Hitachi 704 selective analyzer.

A new enzymatic method for the determination of bilirubin in serum and plasma by means of a Hitachi 704 selective analyzer was evaluated. This endpoint method (37 degrees C) including a sample blank showed very reliable results. The range of linearity was 0.3 to 437 mumol/l bilirubin. The within-run imprecision of three different bilirubin concentrations (n = 16) was 0.37, 0.44 and 0.76% (coefficient of variation). Between-assay imprecision (n = 15) was 0.51 to 1.76% (coefficient of variation) for five different control materials. Inaccuracy, determined with 5 control sera (assigned values: 19, 23.9, 90.7, 142.0 and 295.6 mumol/l bilirubin), was 0.14 to 4.27%. Recovery rates, determined in two spiked plasma samples, were 97.8% and 99.1%, and in six bilirubin standard solutions between 92 and 99%. The comparison with the routinely used 2.5-dichlorophenyl diazonium salt method as well as with the Jendrassik & Grof [1938) Biochem. Z. 297, 81-89) method as the reference yielded correlation coefficients of r = 0.997 and r = 0.998.

Bilirubin↗
PubMed2004

Noninvasive transcutaneous bilirubin as a screening test to identify the need for serum bilirubin assessment.

Hyperbilirubinemia is a common problem in the newborn infant. It can progress to develop kernicterus unless intervention is initiated. Severity and decision for management are usually based on serum bilirubin (TsB) which needs blood sampling. Transcutaneous bilirubin measurement is a noninvasive technique and the result correlates closely with TsB. A new transcutaneous bilirubinometer, Minolta AirShields Jaundice Meter, JM103, has been introduced The objectives of this study were: 1) To evaluate the accuracy of transcutaneous bilirubin (TcB) measured by JM 103, when compared to TsB, used clinically in a hospital setting (Leica Unistat Bilirubinometer) and 2) To develop a cut-off point of TcB level which indicated the need for serum bilirubin assessment. Three hundred and eighty eight term and near-term newborn infants with 460 paired TcB-TsB specimens were studied from August to November 2003. Birth weight was 3117.57 +/- 424.82 grams. TsB ranged from 4 to 19.6 mg/dL (x 10.5, SD 2.46). The correlation coefficient between TcB and TsB was significant (r 0.8, p < 0.001). TcB showed a tendency to underestimate TsB, with mean difference of 0.7 mg/dL, SD 1.6 mg/dL, and 95% confidence interval 0.85 and 0.55 mg/dL. TcB values of 8, 9, 10, 12 mg/dL were chosen as cut-off points that indicated the need for blood sampling for TsB (corresponded to hour-specific levels of 10, 12, 13 and 15 mg/dL, respectively when phototherapy should be initiated). In conclusion, noninvasive TcB assessment demonstrates significant accuracy, compared to TsB. It can be used as a screening test to identify the need for blood sampling for serum bilirubin level.

Bilirubin↗
PubMed1995

Evaluation of bilirubin displacing effect of indomethacin by determination of erythrocyte-bound bilirubin.

The effect of indomethacin on bilirubin binding to human erythrocytes at different bilirubin/albumin molar ratios varying from 0.5-3.0 was studied. Progressive addition of indomethacin produced a linear increase in erythrocyte-bound bilirubin. This increase was more pronounced up to 280 microM drug concentration at all molar ratios being maximum at higher bilirubin/albumin molar ratio. On the other hand, percent increase in erythrocyte-bound bilirubin produced by the drug was found to be maximum at lowest bilirubin/albumin molar ratio and decreased on increasing bilirubin/albumin molar ratio. From these results we conclude that indomethacin induces displacement of bilirubin from albumin, thus increases bilirubin binding to human erythrocytes to a significant degree even at lower concentrations.

Bilirubin↗
PubMed1976

Characteristics of a photoproduct of bilirubin found in vitro and in vivo, and its effect on the bilirubin binding affinity of serum.

The 430 pigment isolated from bilirubin-albumin solutions illuminated in vitro, decreased the bilirubin binding affinity of serum. This effect was demonstrated for both tightly and loosely bound bilirubin in serum, but in albumin solutions pretreated with charcoal only the binding of loosely bound bilirubin was decreased. This finding is of importance because a similar pigment has been isolated from the body fluids of an infant with Crigler-Najjar syndrome. The production and accumulation of 430 pigment during phototherapy might decrease the binding of bilirubin to albumin in the circulation.

Albumins↗
PubMed1994

Retinopathy of prematurity and bilirubin--no clinical evidence for a beneficial role of bilirubin as a physiological anti-oxidant.

The prevention of retinopathy of prematurity (ROP) remains a persistent problem. A previous report has focused on the possible protective effect of bilirubin on the development of ROP. These results still await clinical confirmation by other research groups. Therefore, we undertook a retrospective clinical study trying to confirm this attractive hypothesis. Twelve premature newborns under 32 weeks of gestation with ROP stage 3-4 were matched for gestational age with 12 infants without ROP. Data were collected about the infant's characteristics, medical illnesses, ventilatory settings and treatments. The total serum bilirubin concentrations between the 1st and 8th postnatal day were also gathered. The two matched groups were comparable as to their basic data, clinical characteristics and treatment, except for a slight, but significant longer duration of phototherapy for group ROP 0 (mean, 50.2 h; SD 48,6 vs 31.6 h; SD 42.7 in ROP 3-4; P = 0.02). No statistical difference relative to bilirubin was found between the two groups, neither when expressed as daily mean concentrations, nor as area under the curve (AUC) (mean, ROP 0: 17876.7; SD 6077.3 vs 18888.4; SD 55552.7 in ROP 3-4; P = 0.404) or AUC/h (mean, ROP 0: 135.1; SD 36.3 vs 144.1; SD 23.2 in ROP 3-4; P = 0.515). Our findings do not confirm the hypothesis of a clinically measurable, beneficial role of bilirubin on the development of ROP.

Antioxidants↗
PubMed1970

Bilirubin conjugates of human bile. The excretion of bilirubin as the acyl glycosides of aldobiouronic acid, pseudoaldobiouronic acid and hexuronosylhexuronic acid, with a branched-chain hexuronic acid as one of the components of the hexuronosylhexuronide.

Structure elucidations have been performed on the bilirubin conjugates isolated from human hepatic bile as the phenylazo derivatives. The major bilirubin conjugates are excreted, not as was formerly thought in the form of glucuronides, but as the acyl glycosides of aldobiouronic acid, pseudoaldobiouronic acid and hexuronosylhexuronic acid. The isolated aldobiouronides are proposed to have the structures of an acyl 6-O-hexopyranosyluronic acid-hexopyranoside, an acyl 4-O-hexofuranosyluronic acid-d-glucopyranoside, and an acyl 4-O-beta-d-glucofuranosyluronic acid-d-glucopyranoside respectively, with the acyl radicals being those of the phenylazo derivative of bilirubin. The pseudoaldobiouronide is suggested to be the acyl 4-O-alpha-d-glucofuranosyl-beta-d -glucopyranosiduronic acid, with the acyl radical being that of the phenylazo derivative of vinylneoxanthobilirubinic acid. The hexuronosylhexuronide presumably is the acyl 4-O-(3-C-hydroxymethylribofuranosyluronic acid)-beta-d-glucopyranosiduronic acid, with the acyl radical being that of the phenylazo derivative of bilirubin. The 3-C-hydroxymethylriburonic acid, isolated as one of the components of the hexuronosylhexuronide, is the first natural branched-chain hexuronic acid to be detected, and the first branched-chain sugar ever detected in humans.

Azo Compounds↗
PubMed1981

The relationship between serum bilirubin and reserve albumin for binding of bilirubin during phototherapy of preterm infants.

Thirty-four preterm newborn infants suffering from uncomplicated hyperbilirubinaemia were studied. The infants received ordinary phototherapy continuously during 48 hours. The serum unconjugated bilirubin concentration decreased significantly during the treatment, and a significant correlation between the changes in the serum bilirubin concentration and the changes in the serum reserve albumin concentration for binding of bilirubin measured by the [14C]MADDS method was found. The regression coefficients were -0.50 and -0.48 after 24 and 48 hours of treatment, respectively. Thus, it can be concluded that the risk of bilirubin encephalopathy is reduced by phototherapy in preterm infants.

Bilirubin↗
PubMed1982

Low reserve albumin for binding of bilirubin in neonates with deficiency of bilirubin excretion and bronze baby syndrome.

The plasma reserve albumin concentration for binding of bilirubin was found to be low in four newborn infants with deficiency of bilirubin excretion, of whom two had the bronze baby syndrome. Thus, the risk of bilirubin encephalopathy was increased. Also the ratio of binding fraction of albumin, i.e. unconjugated bilirubin plus reserve albumin, to total albumin was low. Possible causes of the low reserve albumin concentration and the ratio are discussed.

Bile↗
PubMed1975

Bilirubin binding to hepatic Y and Z protein (ligandin): tissue bilirubin concentrations in phenobarbital treated Gunn rats (38466).

NaP treatment significantly reduced plasma bilirubin levels in the (jj) Gunn rat. It is suggested that NaP significantly increased extravascular bilirubin binding in the liver by induction of the synthesis of Y anion binding protein. The changes in bilirubin concentration of blood and other tissues subsequent to NaP treatment were consistent with the establishment of a new tissue bilirubin equilibrium.

Adipose Tissue↗
PubMed1975

Bilirubin as a cholestatic agent. IV. Effect of bilirubin and sulfobromophthalein (BSP) on biliary manganese excretion.

These experiments demonstrate that the adminstration of bilirubin does not significantly alter biliary manganese excretion in manganese-loaded animals. Sulfobromophthalein sodium (BSP), which has been shown to afford prophylaxis against manganese-bilirubin cholestasis, significantly increases the biliary excretion of manganese. These results are meaningful in that they indicate that the amount of manganese per se in the bile is not critical in this cholestasis, and suggest that intracanalicular reactions are probably not etiologically critical in this model. They point to the conclusion that the critical cholestatic events are occurring within the hepatocyte. The results also indicate that the biliary excretion of manganese is obligate, and to some extent independent of bile flow. The critical cholestatic events are presumably mediated through the biochemical effects of either a manganese-bilirubin complex or of manganese and bilirubin acting separately but synergistically.

Animals↗
PubMed1975

[Lowering of serum bilirubin following experimental ligation of the bile duct. Affinity-chromatography binding of bilirubin to albumin conjugated with agarose].

Principle and procedure of a new method in the treatment of experimental hyperbilirubinemia for removing protein-bound, not dialyzable substances from blood by extracorporeal hemoperfusion are described. In six out of eight experiments a decrease of serum bilirubin levels between 11 and 36% has been accomplished. Changes in hemograms are reported and correlations between serum bilirubin value, amount bilirubin bound by the agarose beads and bilirubin clearance rate are discussed.

Animals↗
PubMed1985

Elimination of the "chromogen oxidase" activity of bilirubin oxidase added to obviate bilirubin interference in hydrogen peroxide/peroxidase detecting systems.

The use of bilirubin oxidase to remove interference by bilirubin in hydrogen peroxide/peroxidase detecting systems is hampered by its inherent "chromogen oxidase" activity (its ability to oxidize the chromogens used in the systems). This unwanted activity is greater than 99% inhibited by 0.5 mmol/L cyanide, 97% inhibited by 20 mmol/L azide. At these same concentrations, they inhibit bilirubin oxidase activity by 95% and 73%, respectively. Sequential addition of reagents allows the use of bilirubin oxidase without interference by the chromogen oxidase activity.

5'-Nucleotidase↗
PubMed1994

Bilirubin UDP-glucuronosyltransferase 1 is the only relevant bilirubin glucuronidating isoform in man.

Crigler-Najjar syndrome type I (CN-I) is caused by an inherited absence of UDP-glucuronosyltransferase activity toward bilirubin (B-UGT), resulting in severe non-hemolytic unconjugated hyperbilirubinemia. Based on the expression of cDNAs in COS cells, two UGT isoforms in human liver, B-UGT1 and B-UGT2, have been reported to catalyze bilirubin glucuronidation. These isoforms, which are derived from a single gene, ugt1, have identical carboxyl-terminal domains that are encoded by four consecutive exons shared by both isoforms. A critical lesion in any of these common exons should inactivate both B-UGT isoforms, giving rise to CN-I. The amino-terminal domains of the B-UGT isoforms are unique, each being encoded by a different 5' exon. If both B-UGT isoforms contribute significantly to bilirubin glucuronidation, a mutation in one of these unique 5' exons should affect a single isoform, while the other isoforms should provide residual B-UGT activity. However, in two patients with CN-I, we found a mutation only in the unique exon of B-UGT1, the other exons being normal. To clarify this apparent paradox, we expressed the cDNA for each B-UGT isoform in COS cells and determined the specific B-UGT activity. These studies show that only B-UGT1 has quantitatively significant catalytic activity. Furthermore, we show that the mutation in B-UGT1 observed in each of the two CN-I patients inactivates B-UGT1. Together, the results indicate that B-UGT1 is the only physiologically relevant isoform in bilirubin glucuronidation.

Animals↗