Transient hyperammonemia related to chemotherapy with continuous infusion of high-dose 5-fluorouracil

Liaw, Chuang-Chi; Liaw, Shiumn-Jen; Wang, Chen‐Hsu; Chiu, Mee-Chou; Huang, Jen‐Seng

doi:10.1097/00001813-199306000-00003

Cited by 33 publications

(19 citation statements)

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“…More close studies of the differences between the regulation of liver and intestinal CPSI, or the extent of damage in surgery or disease in either organ, would allow better understanding of the causes of hyperammonemia. More suggestive evidence that intestinal CPSI may significantly contribute to the regulation of serum ammonia homeostasis comes from findings in patients treated with cytostatic drugs, resulting in hyperammonemia in several cases (Fine et al 1989;Liaw et al 1993). Unfortunately, in none of these cases was intestinal mucosal damage or CPSI activity assessed, whereas the intestine is much more prone to damage by cytostatic treatment compared to liver.…”

Section: Potential Physiological Significance Of Intestinal Cpsimentioning

confidence: 99%

Intestinal Carbamoyl Phosphate Synthase I in Human and Rat: Expression During Development Shows Species Differences and Mosaic Expression in Duodenum of Both Species

Beers

Rings

Posthuma

et al. 1998

J Histochem Cytochem.

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SUMMARYThe clinical importance of carbamoyl phosphate synthase I (CPSI) relates to its capacity to metabolize ammonia, because CPSI deficiencies cause lethal serum ammonia levels. Although some metabolic parameters concerning liver and intestinal CPSI have been reported, the extent to which enterocytes contribute to ammonia conversion remains unclear without a detailed description of its developmental and spatial expression patterns. Therefore, we determined the patterns of enterocytic CPSI mRNA and protein expression in human and rat intestine during embryonic and postnatal development, using in situ hybridization and immunohistochemistry. CPSI protein appeared during human embryogenesis in liver at 31-35 e.d. (embryonic days) before intestine (59 e.d.), whereas in rat CPSI detection in intestine (at 16 e.d.) preceded liver (20 e.d.). During all stages of development there was a good correlation between the expression of CPSI protein and mRNA in the intestinal epithelium. Strikingly, duodenal enterocytes in both species exhibited mosaic CPSI protein expression despite uniform CPSI mRNA expression in the epithelium and the presence of functional mitochondria in all epithelial cells. Unlike rat, CPSI in human embryos was expressed in liver before intestine. Although CPSI was primarily regulated at the transcriptional level, CPSI protein appeared mosaic in the duodenum of both species, possibly due to post-transcriptional regulation. (J Histochem Cytochem 46:231-240, 1998)

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Section: Potential Physiological Significance Of Intestinal Cpsimentioning

confidence: 99%

Intestinal Carbamoyl Phosphate Synthase I in Human and Rat: Expression During Development Shows Species Differences and Mosaic Expression in Duodenum of Both Species

Beers

Rings

Posthuma

et al. 1998

J Histochem Cytochem.

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“…Initially described 30 years ago, chemotherapy-related HAE has been reported mostly in patients with hematologic malignancies undergoing intensive cytoreductive treatment or bone marrow transplantation [14][15][16]. Several case reports and small case series described development of HAE in patients treated with a variety of agents, including conventional cytotoxics, such as 5-fluorouracil, L-asparaginase, cytarabine, cyclophosphamide, oxaliplatin, vincristine, ©AlphaMed Press 2016…”

Section: Discussionmentioning

confidence: 99%

“…Encephalopathy With Fibrolamellar Hepatocellular Carcinoma CME etoposide, anthracyclines, busulfan, methotrexate, topotecan, vinorelbine, and gemcitabine [16][17][18][19]. Steroids, commonly used for premedication or as part of chemotherapeutic regimens, can contribute to the development of HAE [20][21][22].…”

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confidence: 99%

Hyperammonemic Encephalopathy Associated With Fibrolamellar Hepatocellular Carcinoma: Case Report, Literature Review, and Proposed Treatment Algorithm

et al. 2016

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We report a case of a 31-year-old man with metastatic fibrolamellar hepatocellular carcinoma (FLHCC) treated with gemcitabine and oxaliplatin complicated by hyperammonemic encephalopathy biochemically consistent with acquired ornithine transcarbamylase deficiency. Awareness of FLHCC-associated hyperammonemic encephalopathy and a pathophysiology-based management approach can optimize patient outcome and prevent serious complications. A discussion of the management, literature review, and proposed treatment algorithm of this rare metabolic complication are presented. The Oncologist 2016; 21:514-520Implications for Practice: Pathophysiology-guided management of cancer-associated hyperammonemic encephalopathy can improve patient outcome and prevent life-threatening complications. Community and academic oncologists should be aware of this serious metabolic complication of cancer and be familiar with its management.

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“…These common adverse effects are observed in more than half of the patients treated with 5-FU-containing regimens [ 2 ]. On the other hand, the prevalence of 5-FU-induced hyperammonemia has been reported to range within 5.7%–7.0% [ 3 – 5 ]. The exact mechanism responsible for 5-FU-induced hyperammonemia remains unknown.…”

Section: Introductionmentioning

confidence: 99%

A Case of Hyperammonemia Associated with High Dihydropyrimidine Dehydrogenase Activity

Nagaharu¹,

Ikemura

Yamashita

et al. 2016

Case Reports in Oncological Medicine

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Over the past decades, 5-Fluorouracil (5-FU) has been widely used to treat several types of carcinoma, including esophageal squamous cell carcinoma. In addition to its common side effects, including diarrhea, mucositis, neutropenia, and anemia, 5-FU treatment has also been reported to cause hyperammonemia. However, the exact mechanism responsible for 5-FU-induced hyperammonemia remains unknown. We encountered an esophageal carcinoma patient who developed hyperammonemia when receiving 5-FU-containing chemotherapy but did not exhibit any of the other common adverse effects of 5-FU treatment. At the onset of hyperammonemia, laboratory tests revealed high dihydropyrimidine dehydrogenase (DPD) activity and rapid 5-FU clearance. Our findings suggested that 5-FU hypermetabolism may be one of the key mechanisms responsible for hyperammonemia during 5-FU treatment.

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Transient hyperammonemia related to chemotherapy with continuous infusion of high-dose 5-fluorouracil

Cited by 33 publications

References 0 publications

Intestinal Carbamoyl Phosphate Synthase I in Human and Rat: Expression During Development Shows Species Differences and Mosaic Expression in Duodenum of Both Species

Intestinal Carbamoyl Phosphate Synthase I in Human and Rat: Expression During Development Shows Species Differences and Mosaic Expression in Duodenum of Both Species

Hyperammonemic Encephalopathy Associated With Fibrolamellar Hepatocellular Carcinoma: Case Report, Literature Review, and Proposed Treatment Algorithm

A Case of Hyperammonemia Associated with High Dihydropyrimidine Dehydrogenase Activity

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