A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine
Cancer patients presenting with altered mental status demand a broad differential with early recognition of the etiology. Failure to do so is associated with increased morbidity and mortality. Causes that must be considered include organ involvement of the cancer, electrolytes abnormalities, and eve...
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Case Reports in Oncological Medicine |
| Online Access: | http://dx.doi.org/10.1155/2020/4216752 |
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| author | Michael Chahin Nithya Krishnan Hardik Chhatrala Marwan Shaikh |
| author_facet | Michael Chahin Nithya Krishnan Hardik Chhatrala Marwan Shaikh |
| author_sort | Michael Chahin |
| collection | DOAJ |
| description | Cancer patients presenting with altered mental status demand a broad differential with early recognition of the etiology. Failure to do so is associated with increased morbidity and mortality. Causes that must be considered include organ involvement of the cancer, electrolytes abnormalities, and even chemotherapeutic agents. A 32-year-old female patient had been recently started on FOLFOX for metastatic colon cancer. Her initial treatments were uneventful, but she later developed encephalopathy during day three of cycle five. During her evaluation, she was found to have hyperammonemia (84 mcmol/L), without hepatic failure, that resolved with stopping chemotherapy and supportive care. After a trial of home infusion fluorouracil, she developed hyperammonemic encephalopathy again. During both admissions, her symptoms resolved with IV hydration and cessation of chemotherapy. She was then successfully challenged with capecitabine (1000 mg/m2 daily), and additional hydration, and continued chemotherapy without recurrence of symptoms. Hyperammonemia is associated with fluorouracil though the mechanism is unclear. Suspected etiologies include either elevated levels of the drug due to slower metabolism or accumulation of certain metabolites. Additionally, risk factors such urease-producing bacterial infections, dehydration, and increased catabolism are thought to increase the risk for hyperammonemia. This case demonstrates the need for greater awareness of fluorouracil as a cause of hyperammonemic encephalopathy. Knowledge of this may allow for earlier recognition and reduced unnecessary testing. |
| format | Article |
| id | doaj-art-89b7a7c09f364e08a8fd71d9692b4203 |
| institution | Kabale University |
| issn | 2090-6706 2090-6714 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Case Reports in Oncological Medicine |
| spelling | doaj-art-89b7a7c09f364e08a8fd71d9692b42032025-02-03T01:25:19ZengWileyCase Reports in Oncological Medicine2090-67062090-67142020-01-01202010.1155/2020/42167524216752A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with CapecitabineMichael Chahin0Nithya Krishnan1Hardik Chhatrala2Marwan Shaikh3University of Florida College of Medicine–Jacksonville, Department of Medicine, Division of Internal Medicine, USAUniversity of Florida College of Medicine–Jacksonville, Department of Medicine, Division of Internal Medicine, USAUniversity of Florida College of Medicine–Jacksonville, Department of Medicine, Division of Hematology and Oncology, USAUniversity of Florida College of Medicine–Jacksonville, Department of Medicine, Division of Hematology and Oncology, USACancer patients presenting with altered mental status demand a broad differential with early recognition of the etiology. Failure to do so is associated with increased morbidity and mortality. Causes that must be considered include organ involvement of the cancer, electrolytes abnormalities, and even chemotherapeutic agents. A 32-year-old female patient had been recently started on FOLFOX for metastatic colon cancer. Her initial treatments were uneventful, but she later developed encephalopathy during day three of cycle five. During her evaluation, she was found to have hyperammonemia (84 mcmol/L), without hepatic failure, that resolved with stopping chemotherapy and supportive care. After a trial of home infusion fluorouracil, she developed hyperammonemic encephalopathy again. During both admissions, her symptoms resolved with IV hydration and cessation of chemotherapy. She was then successfully challenged with capecitabine (1000 mg/m2 daily), and additional hydration, and continued chemotherapy without recurrence of symptoms. Hyperammonemia is associated with fluorouracil though the mechanism is unclear. Suspected etiologies include either elevated levels of the drug due to slower metabolism or accumulation of certain metabolites. Additionally, risk factors such urease-producing bacterial infections, dehydration, and increased catabolism are thought to increase the risk for hyperammonemia. This case demonstrates the need for greater awareness of fluorouracil as a cause of hyperammonemic encephalopathy. Knowledge of this may allow for earlier recognition and reduced unnecessary testing.http://dx.doi.org/10.1155/2020/4216752 |
| spellingShingle | Michael Chahin Nithya Krishnan Hardik Chhatrala Marwan Shaikh A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine Case Reports in Oncological Medicine |
| title | A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine |
| title_full | A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine |
| title_fullStr | A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine |
| title_full_unstemmed | A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine |
| title_short | A 5-Fluorouracil-Induced Hyperammonemic Encephalopathy Challenged with Capecitabine |
| title_sort | 5 fluorouracil induced hyperammonemic encephalopathy challenged with capecitabine |
| url | http://dx.doi.org/10.1155/2020/4216752 |
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