Abstract
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.
Highlights
In 1957, Heidelberger et al reported the use of 5-FU as a new antitumoral drug [1], and at present, 5-FU is one of the most commonly used anticancer drugs around the world
Due to the rapid clearance of 5-FU, we evaluated the patient’s dihydropyrimidine dehydrogenase (DPD) activity using the urinary dihydrouracil to uracil ratio (DHU/U)
Previous studies have investigated the relationship between DPD activity and 5-FU toxicity [7,8,9,10,11]
Summary
In 1957, Heidelberger et al reported the use of 5-FU as a new antitumoral drug [1], and at present, 5-FU is one of the most commonly used anticancer drugs around the world. As is the case for other anticancer drugs, the most common side effects of 5-FU, such as diarrhea, mucositis, neutropenia, and anemia, are due to its effects on the bone marrow and gastrointestinal epithelium. These common adverse effects are observed in more than half of the patients treated with 5-FU-containing regimens [2]. The prevalence of 5-FU-induced hyperammonemia has been reported to range within 5.7%– 7.0% [3,4,5]. We report a patient who developed recurrent hyperammonemia
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