Bilirubin Metabolism and Jaundice

Wolkoff, Allan W.; Berk, Paul D.

doi:10.1002/9781119950509.ch6

Cited by 10 publications

(14 citation statements)

References 235 publications

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“…Bilirubin in bile is mostly diglucuronidated, but the proportion of monoglucuronide is over 20% instead of the normal 7%. 12 Homozygosity for this promoter mutation is necessary but not sufficient for hyperbilirubinemia to occur:…”

Section: Ugt1a1 Mutationsmentioning

confidence: 99%

“…The process of bilirubin conjugation and the function of UDP-glucuronosyl transferases have been extensively reviewed in several recent papers and chapters. [10][11][12] UGT1A1 (OMIM * 191740) appears to be the only enzyme that glucuronidates bilirubin.…”

Section: Conjugationmentioning

confidence: 99%

“…90 Induction of UGT1A1 by phenobarbital (60-120 mg per day) reduces the bilirubin concentration by >25%. 12 In most cases, basal or phenobarbital-induced UGT1A1 activity is sufficient to prevent bilirubin encephalopathy. However, neurologic sequelae may occur after an intercurrent illness, fasting, or any other event that temporarily increases the serum bilirubin concentration.…”

Section: Crigler-najjar Syndrome Type IImentioning

confidence: 99%

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Inherited Disorders of Bilirubin Transport and Conjugation: New Insights Into Molecular Mechanisms and Consequences

2014

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Section: Ugt1a1 Mutationsmentioning

confidence: 99%

Section: Conjugationmentioning

confidence: 99%

Section: Crigler-najjar Syndrome Type IImentioning

confidence: 99%

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Inherited Disorders of Bilirubin Transport and Conjugation: New Insights Into Molecular Mechanisms and Consequences

2014

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“…Excess bilirubin will undergo conjugation in the liver by enzyme glucuronyltransferase, turning into water‐soluble conjugated bilirubin. Further metabolism of conjugated bilirubin will produce urobilinogen, which is responsible for the dark amber color of urine in jaundice patient . Excess bilirubin in blood during hyperbilirubinemia results in yellowish discoloration of the hollow fibers in dialyzer.…”

Section: Discussionmentioning

confidence: 99%

Yellowish discoloration of dialyzer

Chiew¹,

Peng

Yang

2011

Hemodialysis International

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A 43-year-old Chinese man with chronic viral hepatitis and end-stage renal disease, receiving conventional hemodialysis for 6 years, presented with general malaise and abdominal fullness. After 4.5 hours of hemodialysis, the hollow fibers of the dialyzer turned yellow. Biochemistry studies showed hyperbilirubinemia. The actual serum bilirubin (7.4 mg/dL) could be proved. Abdominal echography survey was negative. Hyperbilirubinemia was secondary to acute exacerbation of chronic viral hepatitis. Anuria and skin hyperpigmentation in uremia lack the tea-color urine and mask clinical jaundice in the presence of hyperbilirubinemia. Careful observation of dialyzer yellowish discoloration gave us timely discovery of patient's hyperbilirubinemia.

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“…As between 5%‐10% of the population has Gilbert's Syndrome, it is likely that some patients enrolled in a cholestatic liver disease trial will also have this hereditary condition characterised by intermittent unconjugated (indirect) hyperbilirubinaemia in the absence of hepatocellular disease . Total bilirubin levels in Gilbert's Syndrome are usually mildly elevated, but rarely greater than 4‐5 mg/dL . Gilbert's Syndrome is caused by a reduction of the level of the enzyme uridine 5'‐diphospho‐‐glucuronyl‐transferase to 20‐30% of its normal amount which results in impaired conjugation of bilirubin with glucuronic acid .…”

Section: Additional Considerations For Clinical Trials Of Pbc and Pscmentioning

confidence: 99%

Consensus guidelines: best practices for detection, assessment and management of suspected acute drug‐induced liver injury occurring during clinical trials in adults with chronic cholestatic liver disease

Palmer

Regev

Lindor

et al. 2019

Aliment Pharmacol Ther

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Summary Background Improved knowledge of the molecular pathophysiology and immunopathogenesis of cholestatic liver diseases in recent years has led to an increased interest in developing novel therapies. Patients with cholestatic liver disease often require different approaches to assessment and management of suspected drug‐induced liver injury (DILI) compared to those with healthy livers and those with parenchymal liver diseases. At present, there are no regulatory guidelines or society position papers, that systematically address best practices pertaining to detection of DILI in these patients. Aims To outline best practices for detection, assessment and management of suspected acute DILI during clinical trials in adults with the cholestatic liver diseases – Primary Biliary Cholangitis (PBC) and Primary Sclerosing Cholangitis (PSC). Methods This is one of the several papers developed by the IQ DILI Initiative, which is comprised of members from 16 pharmaceutical companies, in collaboration with DILI experts from academia and regulatory agencies. The contents are the result of an extensive literature review, as well as in‐depth discussions among industry, regulatory and academic DILI experts, to achieve consensus recommendations on DILI‐related issues occurring during clinical trials for cholestatic liver diseases. Results Recommended best practices are outlined pertaining to hepatic eligibility criteria, monitoring of liver tests, approach to a suspected DILI signal, and hepatic discontinuation rules. Conclusions This paper provides a framework for the approach to detection, assessment and management of suspected acute DILI occurring during clinical trials in adults with cholestatic liver disease.

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Bilirubin Metabolism and Jaundice

Cited by 10 publications

References 235 publications

Inherited Disorders of Bilirubin Transport and Conjugation: New Insights Into Molecular Mechanisms and Consequences

Inherited Disorders of Bilirubin Transport and Conjugation: New Insights Into Molecular Mechanisms and Consequences

Yellowish discoloration of dialyzer

Consensus guidelines: best practices for detection, assessment and management of suspected acute drug‐induced liver injury occurring during clinical trials in adults with chronic cholestatic liver disease

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