5-Fluorouracil rechallenge after 5-fluorouracil-induced hyperammonemic encephalopathy

Alice Boilève, Camille Wicker, Benjamin Verret, Florence Leroy, David Malka, Mathieu Jozwiake, Clément Pontoizeau, Chris Ottolenghi, Pascale De Lonlay, Michel Ducreux, Antoine Hollebecque

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13 Scopus citations


For several decades, 5-Fluorouracil (5-FU) has been the backbone of many chemotherapy regimens for various tumor types. Its most common side effects are gastrointestinal disorders, mucositis, myelosuppression, hand-foot syndrome, and rarely cardiac toxicity. More rarely, 5-FU infusion can induce hyperammonemic encephalopathy. 5-FU toxicities can be worsened by complete or partial genetic and/or phenotypic dihydropyrimidine dehydrogenase deficiency. Here, we report the case of a patient who initially developed a 5-FU-induced hyperammonemic encephalopathy after receiving FOLFIRINOX (oxaliplatin, irinotecan, folinic acid, and 5-FU) chemotherapy with bevacizumab to treat a metastatic gastrointestinal cancer of unknown primary. Thereafter, the patient was rechallenged successfully by the same chemotherapy regimen (FOLFIRINOX) for more than 6 months with a protocol consisting in a free protein diet, and administration of ammonium chelators, and Krebs and urea cycle intermediates, to prevent further hyperammonemia. We also present a review of the literature on 5-FU rechallenge after 5-FU-induced hyperammonemic encephalopathy.

Original languageEnglish
Pages (from-to)313-317
Number of pages5
JournalAnti-Cancer Drugs
Issue number3
StatePublished - 1 Mar 2019
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2018 Wolters Kluwer Health, Inc. All rights reserved.


  • 5-fluorouracil
  • Cancer
  • Hyperammonemic encephalopathy
  • Krebs cycle
  • Metabolomic disease


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