Risk of transient hyperammonemic encephalopathy in cancer patients who received continuous infusion of 5-fluorouracil with the complication of dehydration and infection

Liaw, Chuang-Chi; Wang, Hung‐Ming; Wang, Cheng‐Hsu; Yang, Tsung‐Lin; Chen, Jen‐Shi; Chang, Hsien-Khun; Lin, Yung‐Chang; Liaw, Shiumn-Jen; Yeh, Chau‐Ting

doi:10.1097/00001813-199903000-00004

Cited by 70 publications

(38 citation statements)

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“…The pathogenic mechanism is thought to be related to an acquired deficiency of glutamine synthetase of unknown cause. [60][61][62][63][64][65] Miscellaneous causes of hyperammonemia Hypoglycin (Jamaican vomiting sickness) This is caused by a toxin present in the unripe ackee fruit. The Jamaican vomiting sickness, which has a high mortality rate (up to 50%), is characterized by vomiting, lethargy, hallucinations, coma, hypoglycemia, hyperammonemia, and abnormal liver enzymes, which occur when this unripe fruit is ingested [6].…”

Section: Drug Related Causesmentioning

confidence: 99%

Hyperammonemia in review: pathophysiology, diagnosis, and treatment

2011

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Ammonia is an important source of nitrogen and is required for amino acid synthesis. It is also necessary for normal acid-base balance. When present in high concentrations, ammonia is toxic. Endogenous ammonia intoxication can occur when there is impaired capacity of the body to excrete nitrogenous waste, as seen with congenital enzymatic deficiencies. A variety of environmental causes and medications may also lead to ammonia toxicity. Hyperammonemia refers to a clinical condition associated with elevated ammonia levels manifested by a variety of symptoms and signs, including significant central nervous system (CNS) abnormalities. Appropriate and timely management requires a solid understanding of the fundamental pathophysiology, differential diagnosis, and treatment approaches available. The following review discusses the etiology, pathogenesis, differential diagnosis, and treatment of hyperammonemia.

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Section: Drug Related Causesmentioning

confidence: 99%

Hyperammonemia in review: pathophysiology, diagnosis, and treatment

2011

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“…Although there were various possible causes of the encephalopathy with hyperammonemia in the present case, dehydration was the most likely cause of the encephalopathy because the encephalopathy was improved by correction of dehydration without branched-chain amino acid within a short period of time. Dehydration reportedly inhibits metabolism of 5-FU [2], and correction of dehydration may be effective for encephalopathy with hyperammonemia induced by 5-FU [3]. Adequate wholebody management may cure encephalopathy within 72 h (average 15 h) [2] [4].…”

Section: Discussionmentioning

confidence: 99%

Rechallenge with 5-fluorouracil in a patient who developed encephalopathy caused by 5-fluorouracil for colon cancer

et al. 2016

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We report a case involving a patient with colon cancer who underwent 5-fluorouracil (5-FU) rechallenge and maintained an oncological effect for a long period after encephalopathy caused by 5-FU. Our patient was a 61-year-old man who was diagnosed with adenocarcinoma of the ascending colon with direct liver invasion. He underwent right hemicolectomy with partial liver resection followed by adjuvant chemotherapy with modified FOL-FOX6 (mFOLFOX6). Ten months after completion of mFOLFOX6, his carcinoembryonic antigen concentration increased, and ascites was revealed by computed tomography 2 months later. We started FOLFIRI, and he was taken to our hospital by ambulance because of loss of consciousness 10 days after the start of the third cycle of FOLFIRI. Laboratory investigations showed hyperammonemia and elevations of his serum creatinine and blood urea nitrogen concentrations. Brain computed tomography demonstrated no abnormalities. Transfusion of 1500 ml of crystalloid fluid resulted in gradual recovery over the next 12 h. His ammonia concentration decreased to a normal level. Twelve days after onset of the encephalopathy, we restarted FOLFIRI, but the dose of continuous 5-FU was decreased by 20 %. The patient's carcinoembryonic antigen concentration considerably decreased from 376.5 to 19.9 ng/ml, and his ascites disappeared. Nineteen months after the resumption of FOLFIRI, he underwent 34 courses of FOLFIRI and maintained stable disease. The encephalopathy did not recur.

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“…Hyperammonemic encephalopathy sometimes occurs in patients with hematologic malignancies during the period of neutropenia following cytoreductive therapy or high-dose chemotherapy for bone marrow transplantation, or in patients with solid organ malignancies treated with fluorouracil [7,8]. It is uncommon for patients with hepatic malignant infiltration to develop hyperammonemic encephalopathy, except in primary hepatocellular carcinomas or neuroendocrine tumors with hepatic metastases [9].…”

Section: Discussionmentioning

confidence: 99%

Regorafenib-Induced Hyperammonemic Encephalopathy in Metastatic Colon Cancer

Kitamoto¹,

Satake²,

Hatachi³

et al. 2015

JCPCR

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Regorafenib, a multi-targeted tyrosine kinase inhibitor (TKI), is used in metastatic colorectal cancer (mCRC) and gastrointestinal stromal tumors (GIST) for salvageline therapy. From clinical trials, the most commonly reported adverse events of regorafenib are hand-foot skin reactions, fatigue, diarrhea and hypertension. We report two cases of hyperammonemic encephalopathy induced by regorafenib in patients with mCRC. Hyperammonemic encephalopathy is a life-threatening complication in patients with severe liver cirrhosis, and is often observed in liver dysfunction/failure cases. Cases of hyperammonemic encephalopathy have been reported with various multi-targeted TKIs. The underlying mechanism of encephalopathy remains unclear, but in light of similar presentations, it can be reasonably suspected to be a result of a class effect of these TKIs. We suggest checking ammonia levels in patients on regorafenib presenting with altered consciousness, even if they have normal liver function. Discontinuation of regorafenib, as well as ammonia-lowering therapy, is essential to the management of this adverse effect, and recommencement of regorafenib should be discouraged.

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Risk of transient hyperammonemic encephalopathy in cancer patients who received continuous infusion of 5-fluorouracil with the complication of dehydration and infection

Cited by 70 publications

References 0 publications

Hyperammonemia in review: pathophysiology, diagnosis, and treatment

Hyperammonemia in review: pathophysiology, diagnosis, and treatment

Rechallenge with 5-fluorouracil in a patient who developed encephalopathy caused by 5-fluorouracil for colon cancer

Regorafenib-Induced Hyperammonemic Encephalopathy in Metastatic Colon Cancer

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