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Related Concept Videos

Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
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Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
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Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
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Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...

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Related Experiment Video

Updated: Jul 14, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

[Irinotecan and liver dysfunctions].

Marie-Paule Sablin1, Christophe Le Tourneau, Sandrine Faivre

  • 1Service Inter Hospitalier de Cancérologie Bichat-Beaujon, Hôpital Beaujon, 100 boulevard du Général Leclerc, 92118 Clichy Cedex, France.

Therapie
|June 22, 2007
PubMed
Summary

Irinotecan is a key cancer drug, but liver issues complicate its use. Patients with hyperbilirubinemia or UGT1A1 gene variations may need dose adjustments to avoid toxicity.

Area of Science:

  • Oncology
  • Pharmacology
  • Hepatology

Background:

  • Irinotecan is an established cytotoxic chemotherapy agent for various cancers.
  • Hepatic metabolism is the primary route for irinotecan, posing challenges in patients with liver dysfunction.
  • Existing data suggest hyperbilirubinemia necessitates irinotecan dose reduction and UGT1A1 gene polymorphism increases toxicity risk.

Purpose of the Study:

  • To review the challenges and considerations for irinotecan administration in patients with liver dysfunction.
  • To highlight the impact of hyperbilirubinemia and UGT1A1 gene polymorphism on irinotecan therapy.
  • To underscore the need for further research into optimizing irinotecan use in hepatically impaired patients.

Main Methods:

  • Literature review of studies on irinotecan in cancer patients with liver dysfunction.

Related Experiment Videos

Last Updated: Jul 14, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

  • Analysis of data concerning irinotecan metabolism, pharmacokinetics, and toxicity.
  • Examination of the role of hyperbilirubinemia and UGT1A1 gene variants in irinotecan treatment outcomes.

    • Main Results:

    • Liver dysfunction, particularly hyperbilirubinemia, is a significant factor influencing irinotecan dosing.
    • UGT1A1 gene polymorphism is a validated predictor of irinotecan-induced toxicity.
    • Current evidence indicates a need for tailored irinotecan regimens in patients with compromised liver function.

    Conclusions:

    • Optimizing irinotecan therapy in patients with liver dysfunction requires careful consideration of metabolic capacity and genetic factors.
    • Dose adjustments based on bilirubin levels and UGT1A1 genotype are crucial for managing irinotecan toxicity.
    • Further clinical studies are essential to establish definitive guidelines for irinotecan use in this patient population.