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A case report of hyperammonemic encephalopathy induced by high-dose continuous infusion of 5-fluorouracil in a patient with rectal cancer.
AME Case Rep
October 2024
Department of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, China.
Background: Hyperammonemic encephalopathy caused by high-dose infusion of 5-fluorouracil (5-FU) is a rare adverse reaction in rectal cancer patients with an incidence rate of 5.7%. Although the patient could be restored to normal after supportive treatments, the occurrence of this side effect was still inevitable.
View Article and Find Full Text PDFBeyond Chemotherapy: Exploring 5-FU Resistance and Stemness in Colorectal Cancer.
Eur J Pharmacol
January 2025
School of Biotechnology, KIIT Deemed to be University, Bhubaneswar - 751024, Odisha, India. Electronic address:
Colorectal cancer (CRC) remains a significant global health challenge, demanding continuous advancements in treatment strategies. This review explores the complexities of targeting colorectal cancer stem cells (CSCs) and the mechanisms contributing to resistance to 5-fluorouracil (5-FU). The efficacy of 5-FU is enhanced by combination therapies such as FOLFOXIRI and targeted treatments like bevacizumab, cetuximab, and panitumumab, particularly in KRAS wild-type tumors, despite associated toxicity.
View Article and Find Full Text PDFThe Frequency of c.557A>G in the Dominican Population and Its Association with African Ancestry.
Pharmaceutics
December 2024
Personalized Medicine and Mental Health Unit, University Institute for Bio-Sanitary Research of Extremadura, 06080 Badajoz, Spain.
Genetic polymorphism of the dihydropyrimidine dehydrogenase gene () is responsible for the variability found in the metabolism of fluoropyrimidines such as 5-fluorouracil (5-FU), capecitabine, or tegafur. The genotype is linked to variability in enzyme activity, 5-FU elimination, and toxicity. Approximately 10-40% of patients treated with fluoropyrimidines develop severe toxicity.
View Article and Find Full Text PDFDihydropyrimidine enzyme activity and its effect on chemotherapy toxicity: importance of genetic testing.
Cancer Chemother Pharmacol
January 2025
Markey Cancer Center, University of Kentucky, Lexington, KY, USA.
Purpose: Patients with partial or complete DPD deficiency have decreased capacity to degrade fluorouracil and are at risk of developing toxicity, which can be even life-threatening.
Case: A 43-year-old man with moderately differentiated rectal adenocarcinoma on capecitabine presented to the emergency department with complaints of nausea, vomiting, diarrhea, weakness, and lower abdominal pain for several days. Laboratory findings include grade 4 neutropenia (ANC 10) and thrombocytopenia (platelets 36,000).
Dihydropyrimidine dehydrogenase polymorphisms in patients with gastrointestinal malignancies and their impact on fluoropyrimidine tolerability: Experience from a single Italian institution.
World J Gastrointest Oncol
January 2025
Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples 80131, Campania, Italy.
Background: Fluoropyrimidines are metabolized in the liver by the enzyme dihydropyrimidine dehydrogenase (DPD), encoded by the gene. About 7% of the European population is a carrier of gene polymorphisms associated with reduced DPD enzyme activity.
Aim: To assess the prevalence of polymorphisms and their impact on fluoropyrimidine tolerability in Italian patients with gastrointestinal malignancies.
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