5-Fluorouracil rechallenge after 5-fluorouracil-induced hyperammonemic encephalopathy. Issue 3 (March 2019)

• Record Type: Journal Article
• Authors: Boilève, Alice; Wicker, Camille; Verret, Benjamin; Leroy, Florence; Malka, David; Jozwiak, Mathieu; Pontoizeau, Clément; Ottolenghi, Chris; De Lonlay, Pascale; Ducreux, Michel; Hollebecque, Antoine
• Is Part Of: Anti-cancer drugs. Volume 30:Issue 3(2019)
• Publication Date: 2019-03
• Subjects: cancer -- 5-fluorouracil -- hyperammonemic encephalopathy -- Krebs cycle -- metabolomic disease; Antineoplastic agents -- Periodicals; Cancer -- Chemotherapy -- Periodicals; Antineoplastic Agents -- therapeutic use -- Periodicals; Drug Therapy -- Periodicals; 616.994061
• DOI: 10.1097/CAD.0000000000000730
• Languages: English
• ISSNs: 0959-4973

Abstract

Abstract : 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.