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CASE REPORT
Imatinib and liver toxicity
  1. Mohammad Inamul Haq1,
  2. Joanna Nixon2 and
  3. Adrian J Stanley3
  1. 1 Department of Gastroenterology, Glasgow Royal Infirmary, Glasgow, UK
  2. 2 Beatson West of Scotland Cancer Centre, Glasgow, UK
  3. 3 Department of Gastroenterology, Glasgow Royal Infirmary, Glasgow, UK
  1. Correspondence to Dr Mohammad Inamul Haq, m.haq1{at}nhs.net

Abstract

Imatinib is a specific tyrosine kinase inhibitor which has been approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukaemia and c-KIT (CD117)-positive gastrointestinal stromal tumours. It has been associated with hepatotoxicity ranging from abnormal liver function tests to acute liver failure along with chronic hepatitis B reactivation. We report the case of a patient who was started on adjuvant treatment with imatinib following resection of a primary gastrointestinal stromal cell tumour of jejunum and developed severe hepatotoxicity. There was no history of risk factors for liver disease, and a search for the underlying causes of hepatotoxicity was unremarkable. Imatinib was stopped and she was treated with steroids which resulted in dramatic improvement of liver function tests. Liver biopsy in this case was not performed because liver function tests improved following discontinuation of imatinib and treatment with steroids. Repeat imaging did not reveal any evidence of tumour recurrence.

  • gastric cancer
  • chemotherapy
  • liver disease

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Footnotes

  • Contributors MIH, JN and AJS discussed the case and conceived the idea to write. MIH wrote the manuscript with input from JN and AJS. Patient was consented by JN. All authors approved the final manuscript. Final manuscript was submitted by MIH.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.