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A Case of Non-cirrhotic Hyperammonemic Encephalopathy in a Patient With Metastatic Gastrointestinal Stromal Tumor

Acute toxic encephalopathy (ATE) is a widely recognized medical emergency with an expansive differential. One particular known etiology for ATE is elevated ammonia, a powerful neurotoxin that often presents with clinical findings of confusion, disorientation, tremors, and in severe cases, coma and d...

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Detalles Bibliográficos
Autores principales: Jeong, Il Seok D, Abiri, Parinaz, Cai, Johnny, Yim, Catherine, Powell, Leland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10182871/
https://www.ncbi.nlm.nih.gov/pubmed/37193452
http://dx.doi.org/10.7759/cureus.37541
Descripción
Sumario:Acute toxic encephalopathy (ATE) is a widely recognized medical emergency with an expansive differential. One particular known etiology for ATE is elevated ammonia, a powerful neurotoxin that often presents with clinical findings of confusion, disorientation, tremors, and in severe cases, coma and death. Hyperammonemia is most commonly associated with liver disease and presents as hepatic encephalopathy in the setting of decompensated cirrhosis; however, in rare cases, a patient may suffer from non-cirrhotic hyperammonemic encephalopathy. We describe the case of a 61-year-old male with metastatic gastrointestinal stromal tumor who was diagnosed with non-cirrhotic hyperammonemic encephalopathy, and briefly explore the literature describing its mechanisms.