Studies on the Use of the van den Bergh Reagent for Determination of Serum Bilirubin

1959 ◽  
Vol 5 (5) ◽  
pp. 470-478 ◽  
Author(s):  
Samuel Meites ◽  
Cecelia K Hogg
Keyword(s):  
Reaction Time ◽  
Hydrochloric Acid ◽  
Sodium Nitrite ◽  
Serum Bilirubin ◽  
Sulfanilic Acid ◽  
Total Serum Bilirubin ◽  
Total Serum ◽  
Bilirubin Concentration ◽  
Effects Of Temperature

Abstract 1. By increasing the concentration of hydrochloric acid, sulfanilic acid, and sodium nitrite in the van den Bergh reagent used for determining total serum bilirubin it is possible to increase the absorbance of azobilirubin and to accelerate its reaction time to less than 10 minutes. A modified reagent is proposed for the Malloy and Evelyn procedure. 2. The effects of temperature, urea, and protein on the coupling of serum bilirubin are discussed. 3. Hemolysis seriously affects the coupling of bilirubin. The decrease in azobilirubin production appears to vary directly with the amount of hemolysis. When the amount of hemolysis is constant, the decrease in azobilirubin production appears to vary inversely with the bilirubin concentration. The interfering effect of hemoglobin is unexplained.

Spurious hyperbilirubinemia in uremic patients on propranolol therapy.

1979 ◽  
Vol 25 (10) ◽  
pp. 1761-1765 ◽  
Author(s):  
W J Stone ◽  
T D McKinney ◽  
L G Warnock
Keyword(s):  
Serum Bilirubin ◽  
Flow Analysis ◽  
Total Serum Bilirubin ◽  
Total Serum ◽  
Low Grade ◽  
Bilirubin Concentration ◽  
Uremic Serum ◽  
Uremic Patients ◽  
Serum Bilirubin Concentration

Abstract Chronic, low-grade, unexplained increases of total serum bilirubin concentration were observed in 16 of 132 (12%) chronic dialysis patients. Cessation of antihypertensive medication in four patients resulted in disappearance of hyperbilirubinemia. Propranolol was the only antihypertensive drug common to all 16 patients. Daily dosage varied among the patients, but the mean dose was 308 mg (+/- 51 SEM). Serial determinations of sera from individual patients given different doses and from the group as a whole demonstrated a linear relationship between propranolol dose and apparent total serum bilirubin concentration with continuous-flow analysis. When serum specimens from uremic patients receiving propranolol were treated with diazotized fulfanilic acid and examined spectrophotometrically, an absorbance peak distinct from but overlapping that of bilirubin was consistently demonstrated. The material producing the peak disappeared when the drug was stopped, did not dialyze, and was not reproduced by the in vitro addition of propranolol to uremic serum. We postulate that a metabolite(s) of propranolol is retained in uremic serum and interferes with the bilirubin determination.

scholarly journals A Robust Procedure for the Automated Measurement of Total Serum Bilirubin Using Potassium Ferricyanide

1993 ◽  
Vol 30 (2) ◽  
pp. 175-179 ◽  
Author(s):  
Niall O'Leary ◽  
A Pembroke ◽  
P F Duggan
Keyword(s):  
Serum Bilirubin ◽  
Potassium Ferricyanide ◽  
Total Serum Bilirubin ◽  
Total Serum ◽  
Automated Measurement ◽  
Bilirubin Concentration

Bilirubin is oxidized to biliverdin by 1·0 mmol/L potassium ferricyanide in the presence of caffeine. The absorbance decline at 480 nm with blanking at 660 nm is proportional to bilirubin concentration. The assay is linear up to 1000μmol/L and is suitable for the measurement of bilirubin in adult and neonatal patients. The assay is accurate and precise and is not significantly affected by haemolysis up to 5·0 g/L haemoglobin. Reagents and calibration are stable for at least 3 months.

Direct Spectrophotometry of Total Serum Bilirubin in the Newborn

1960 ◽  
Vol 6 (5) ◽  
pp. 421-428 ◽  
Author(s):  
Samuel Meites ◽  
Cecelia K Hogg
Keyword(s):  
Spectrophotometric Method ◽  
Phosphate Buffer ◽  
Serum Bilirubin ◽  
Wave Length ◽  
Total Serum Bilirubin ◽  
Total Serum ◽  
Direct Spectrophotometry ◽  
Similar Equation

Abstract A simple, rapid direct spectrophotometric method for the determination of total serum bilirubin on a micro basis, with a 1:21 dilution of serum in phosphate buffer, is presented for use with the Junior Coleman spectrophotometer. The formula, mg./100 ml. bilirubin = 50 A455 - 119 A575, is applied, where A represents the absorbancy at the wave length specified. The method for obtaining this or a similar equation is presented. The spectrophotometric method, when applied to sera obtained from newborns, gives apparently reliable results in the presence or absence of hemolysis. An evaluation of the method and its limitations is presented.

Two Different UGT1A1 Mutations causing Crigler–Najjar Syndrome types I and II in an Iranian Family

2015 ◽  
Vol 24 (4) ◽  
pp. 523-526 ◽  
Author(s):  
Yoshihiro Maruo ◽  
Mahdiyeh Behnam ◽  
Shinichi Ikushiro ◽  
Sayuri Nakahara ◽  
Narges Nouri ◽  
...  
Keyword(s):  
Serum Bilirubin ◽  
Total Serum Bilirubin ◽  
Total Serum ◽  
Compound Heterozygous ◽  
Type I ◽  
Syndrome Type ◽  
Type Ii ◽  
Wild Type ◽  
Iranian Family ◽  
Udp Glucuronosyltransferase

Background: Crigler–Najjar syndrome type I (CN-1) and type II (CN-2) are rare hereditary unconjugated hyperbilirubinemia disorders. However, there have been no reports regarding the co-existence of CN-1 and CN-2 in one family. We experienced a case of an Iranian family that included members with either CN-1 or CN-2. Genetic analysis revealed a mutation in the bilirubin UDP-glucuronosyltransferase (UGT1A1) gene that resulted in residual enzymatic activity.Case report: The female proband developed severe hyperbilirubinemia [total serum bilirubin concentration (TB) = 34.8 mg/dL] with bilirubin encephalopathy (kernicterus) and died after liver transplantation. Her family history included a cousin with kernicterus (TB = 30.0 mg/dL) diagnosed as CN-1. Her great grandfather (TB unknown) and uncle (TB = 23.0 mg/dL) developed jaundice, but without any treatment, they remained healthy as CN-2. Results: The affected cousin was homozygous for a novel frameshift mutation (c.381insGG, p.C127WfsX23). The affected uncle was compound heterozygous for p.C127WfsX23 and p.V225G linked with A(TA)7TAA. p.V225G-UGT1A1 reduced glucuronidation activity to 60% of wild-type. Thus, linkage of A(TA)7TAA and p.V225G might reduce UGT1A1 activity to 18%–36 % of the wild-type. Conclusion: Genetic and in vitro expression analyses are useful for accurate genetic counseling for a family with a history of both CN-1 and CN-2. Abbreviations: CN-1: Crigler–Najjar syndrome type I; CN-2: Crigler–Najjar syndrome type II; GS: Gilbert syndrome; UGT1A1: bilirubin UDP-glucuronosyltransferase; WT: Wild type; TB: total serum bilirubin.

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