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Sunitinib-induced hyperammonemic encephalopathy in metastatic gastrointestinal stromal tumors: A case report
Takaoki Hayakawa1, Shinsuke Funakoshi2, Yasuo Hamamoto3
1Department of Internal Medicine, Division of Gastroenterology and Hepatology, Keio University School of Medicine, Shinjuku-ku 160-8582, Tokyo, Japan.
Background:
Sunitinib, a multi-targeted tyrosine kinase inhibitor (TKI), has been approved for the salvage treatment of gastrointestinal stromal tumors (GIST). Hyperammonemic encephalopathy is a rare but severe complication of sunitinib use. Here, we present the case of a 66-year-old male with metastatic GIST without underlying liver cirrhosis who developed sunitinib-induced hyperammonemic encephalopathy.
Case Summary:
A 66-year-old male with metastatic GIST was admitted because of reduced consciousness. Imatinib was administered as the first-line systemic therapy. He experienced repeated episodes of peritonitis due to tumor perforation, and surgery was performed. Progressive disease was confirmed based on increased liver metastasis, and sunitinib was initiated as a salvage treatment. However, 23 d after the third course of sunitinib, he presented to the emergency room with an episode of altered consciousness and behavioral changes. Based on the patient clinical history and examination findings, sunitinib-induced encephalopathy was suspected. Sunitinib was discontinued, and the patient was treated for hyperammonemia. The patient had a normal level of consciousness four days later, and the serum ammonia level gradually decreased. No further neurological symptoms were reported in subsequent follow-ups.
Conclusion:
TKI-induced hyperammonemic encephalopathy is potentially life-threatening. Patients receiving TKIs experiencing adverse reactions should undergo systemic evaluation and prompt treatment.
Insights
Sunitinib, a tyrosine kinase inhibitor (TKI), can cause rare but severe hyperammonemic encephalopathy in gastrointestinal stromal tumor (GIST) patients. Prompt evaluation and treatment are crucial for managing this potentially life-threatening TKI side effect.
Area of Science:
- Oncology
- Pharmacology
- Neurology
Background:
- Sunitinib, a multi-targeted tyrosine kinase inhibitor (TKI), is approved for advanced gastrointestinal stromal tumors (GIST).
- Hyperammonemic encephalopathy is a rare but serious complication associated with sunitinib therapy.
- This report details a case in a metastatic GIST patient without pre-existing liver cirrhosis.
Observation:
- A 66-year-old male with metastatic GIST developed altered consciousness and behavioral changes after initiating sunitinib salvage therapy.
- The patient experienced symptoms 23 days after the third course of sunitinib.
- Neurological decline was suspected to be linked to sunitinib administration.
Findings:
- Discontinuation of sunitinib and treatment for hyperammonemia led to the patient's full recovery of consciousness within four days.
- Serum ammonia levels normalized with treatment, and no further neurological sequelae were observed.
- This case highlights a severe adverse reaction to sunitinib in a GIST patient.
Implications:
- Tyrosine kinase inhibitor (TKI)-induced hyperammonemic encephalopathy is a potentially fatal condition.
- Clinicians should maintain a high index of suspicion for hyperammonemic encephalopathy in patients on TKIs presenting with neurological symptoms.
- Systemic evaluation and immediate intervention are critical for managing TKI-induced hyperammonemic encephalopathy.
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