Bilirubin in clinical practice: a review

@article{Fevery2008BilirubinIC,
  title={Bilirubin in clinical practice: a review},
  author={Johan Fevery},
  journal={Liver International},
  year={2008},
  volume={28}
}
  • J. Fevery
  • Published 1 May 2008
  • Medicine, Biology
  • Liver International
Bilirubin is an endogenous compound that can be toxic under certain conditions but, on the other hand, mild unconjugated hyperbilirubinaemia might protect against cardiovascular diseases and tumour development. Serum bilirubin levels are often enhanced under a variety of clinical conditions. These are discussed and the mechanisms are outlined. 
View on Wiley
onlinelibrary.wiley.com
230 Citations
Highly Influential Citations
14
Background Citations
87
Methods Citations
7
Results Citations
1

230 Citations

Conjugated bilirubin as a reflex test for increased total bilirubin in apparently healthy population

The aim of this study was to investigate whether using increased total bilirubin as a reflex test can reduce conjugated bilirUBin (CBIL) test.

The molecular basis of jaundice: An old symptom revisited

A low serum bilirubin level has emerged as an important predisposing factor or a biomarker of these pathologic conditions including cardiovascular, tumour, and possibly neurodegenerative diseases.

A novel mutation in the biliverdin reductase‐A gene combined with liver cirrhosis results in hyperbiliverdinaemia (green jaundice)

Background: Hyperbiliverdinaemia is a poorly defined clinical sign that has been infrequently reported in cases of liver cirrhosis or liver carcinoma, usually indicating a poor long‐term prognosis.

Bilirubin concentration and cardiovascular risk profile

The results of this retrospective epidemiological investigation show that plasma bilirubin concentration is not associated with variations of hsCRP and the lipid profile in a large population of outpatients with no biochemical markers of liver disease.

Measurement and clinical usefulness of bilirubin in liver disease

For accurate diagnosis, alterations in bilirubin concentrations should be assessed in relation to patient anamnesis, the degree of the alteration, and the pattern of concurrent biochemical alterations.

Bilirubin and beyond: a review of lipid status in Gilbert's syndrome and its relevance to cardiovascular disease protection.

Bilirubin, platelet activation and heart disease: a missing link to cardiovascular protection in Gilbert's syndrome?

An Introduction to Anemia and Bilirubinemia

An overview of two serious medical conditions, anemia and bilirubinemia, which are associated with changes in the contents of specific chromophores present in the blood stream, and their causes, types, symptoms and treatment options are provided.

Circulating bilirubin and defense against kidney disease and cardiovascular mortality: mechanisms contributing to protection in clinical investigations.

This is the first review to examine the clinical evidence and summarize the potential mechanisms of action that link bilirubin to protection from kidney damage, subsequent kidney failure, and dialysis-related mortality.

Bilirubin chemistry and metabolism; harmful and protective aspects.

Although, UCB was long thought to be a non-functional waste product, recent studies have shown that the antioxidant effects of mildly elevated serum UCB levels, as well as activation of heme oxygenase, may protect against diseases associated with oxidative stress, such as atherosclerosis.
...

References

SHOWING 1-10 OF 119 REFERENCES

Chemoprevention of severe neonatal hyperbilirubinemia.

The uses of synthetic heme analogues that are competitive inhibitors of heme oxygenase, the rate-limiting enzyme in the production of bilirubin, represent a novel means of controlling severe…

Glucuronidation of bilirubin and the occurrence of pigment gallstones in patients with chronic haemolytic diseases

A clearcut separation from normal values was not obtained, suggesting at least in the present group of patients that Gilbert's syndrome represents only one end of a continuum of bilirubin conjugation rates and not a separate entity.

Unconjugated hyperbilirubinemia. Physiologic evaluation and experimental approaches to therapy.

Of the hereditary disorders of bilirubin metabolism, Gilbert's syndrome is common but innocuous, whereas Crigler-Najjar syndrome is rare but devastating, and various modalities used in an attempt to reduce her plasma bilIRubin concentration by either increasing bilirubsin clearance or reducing bilirUBin turnover are described.

Serum bilirubins in hepatobiliary disease: Comparison with other liver function tests and changes in the postobstructive period

Using this criterion, the AMHPLC result in the clinical anicteric patients (n = 39) was more frequently abnormal than the corresponding value of fasting serum bile acids, SGPT, total bilirubins, alkaline phosphatase, or γ‐glutamyl transpeptidase.

Enterohepatic cycling of bilirubin: a putative mechanism for pigment gallstone formation in ileal Crohn's disease.

Intestinal colonization leading to fecal urobilinoid excretion may play a role in the pathogenesis of neonatal jaundice.

The urobilinoid production during the first week of life is quantitatively insufficient to contribute significantly to the removal of bilirubin, but enhancement of the microbial conversion of bilIRubin could decrease the intestinal concentration of bil irubin and may decrease the degree or enhance the removalof neonatal hyperbilirubinemia.

Renal bilirubin clearance in liver patients.

Serum bilirubin levels in the U.S. Population: Gender effect and inverse correlation with colorectal cancer

The observed inverse correlation between serum bilirubin concentrations and a history of nondermatological malignancy, particularly colorectal cancer, warrants further investigation of a potentially important chemopreventive function of bilirUBin.

Hepatic uptake of organic anions affects the plasma bilirubin level in subjects with Gilbert's syndrome mutations in UGT1A1

The lower BSP uptake in Gilbert's syndrome is not secondary to the hyperbilirubinemia, but probably caused by an independent, genetically determined defect in hepatic transport mechanism(s), shared by BSP and bilirubin, that is likely necessary for phenotypic expression of GS.

Molecular basis of bilirubin-induced neurotoxicity.

...