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Amitriptyline-induced prolonged cholestasis.

D Larrey1, G Amouyal, D Pessayre

  • 1Unité de Recherches de Physiopathologie Hépatique, INSERM U24, Hôpital Beaujon, Clichy, France.

Gastroenterology
|January 1, 1988
PubMed
Summary
This summary is machine-generated.

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Amitriptyline can cause prolonged cholestasis (bile flow obstruction) in patients, leading to jaundice and itching for months. Susceptibility to this liver injury may not be linked to genetic metabolism differences.

Area of Science:

  • Hepatology
  • Clinical Pharmacology
  • Toxicology

Background:

  • Amitriptyline is a commonly prescribed tricyclic antidepressant.
  • Drug-induced liver injury (DILI) is a significant clinical concern.
  • The metabolic pathways of amitriptyline can influence its toxicity.

Observation:

  • A patient developed prolonged cholestasis, jaundice, and pruritus after 5 weeks of amitriptyline use.
  • Liver biopsies revealed progressive lesions, including inflammation, fibrosis, and bile duct loss.
  • The patient was identified as an extensive metabolizer for dextromethorphan, indicating efficient drug metabolism.

Findings:

  • Amitriptyline administration was associated with prolonged cholestasis lasting over 19 months.
  • The liver injury progressed from the hepatic venule to portal tract lesions.

Related Experiment Videos

  • The patient's extensive metabolizer phenotype suggests genetic factors in drug hydroxylation are not the sole determinant of amitriptyline-induced liver injury.

    • Implications:

    • Amitriptyline can be a cause of prolonged cholestatic liver injury.
    • The risk of developing amitriptyline-induced liver injury may be independent of the debrisoquine poor metabolizer phenotype.
    • Further research is needed to elucidate the mechanisms underlying amitriptyline hepatotoxicity.