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Silent toxicity: A rare case of 5-fluorouracil-induced hyperammonemic encephalopathy
Areti Kalfoutzou1, Cleopatra Rapti2, Eleftheria Bagiokou3
1Second Propaedeutic Department of Internal Medicine, Attikon General Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Abstract:
Hyperammonemic encephalopathy (HE) is a rare but serious neurological condition characterized by an acute alteration in mental status due to elevated serum ammonia levels, occurring in the absence of known liver disease. The build-up of ammonia, a by-product of protein metabolism, in the bloodstream leads to its crossing of the blood-brain barrier, where it acts as a neurotoxin, causing potentially reversible brain damage. Chemotherapeutic agents such as 5-fluorouracil (5-FU) are known to cause drug-induced HE. Our case reports a 63-year-old woman who presented with several episodes of reduced consciousness shortly after 5-FU administration, highlighting the necessity of monitoring serum ammonia levels in patients treated with 5-FU who develop neurological symptoms, and the need for expert consultation in attempting a 5-FU rechallenge.
Insights
Hyperammonemic encephalopathy (HE) is a serious neurological condition caused by high ammonia levels. Chemotherapy drug 5-fluorouracil (5-FU) can induce HE, necessitating ammonia monitoring in patients with neurological symptoms.
Area of Science:
- Neurology
- Oncology
- Toxicology
Background:
- Hyperammonemic encephalopathy (HE) is a neurological condition characterized by altered mental status due to elevated serum ammonia.
- Ammonia, a protein metabolism byproduct, crosses the blood-brain barrier, acting as a neurotoxin and causing reversible brain damage.
- Drug-induced HE is a known complication of certain chemotherapeutic agents, including 5-fluorouracil (5-FU).
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