Hayakawa T, Funakoshi S, Hamamoto Y, Hirata K, Kanai T. Sunitinib-induced hyperammonemic encephalopathy in metastatic gastrointestinal stromal tumors: A case report. World J Clin Cases 2023; 11(31): 7629-7634 [PMID: 38078122 DOI: 10.12998/wjcc.v11.i31.7629]
Corresponding Author of This Article
Yasuo Hamamoto, MD, PhD, Assistant Professor, Doctor, Keio Cancer Center, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku 160-8582, Tokyo, Japan. yashmmt1971@gmail.com
Research Domain of This Article
Oncology
Article-Type of This Article
Case Report
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Takaoki Hayakawa, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Keio University School of Medicine, Shinjuku-ku 160-8582, Tokyo, Japan
Shinsuke Funakoshi, Division of Medical Oncology, Department of Internal Medicine, Tokyo Saiseikai Central Hospital, Minato-ku 108-0073, Tokyo, Japan
Yasuo Hamamoto, Kenro Hirata, Keio Cancer Center, Keio University School of Medicine, Shinjuku-ku 160-8582, Tokyo, Japan
Takanori Kanai, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku 160-8582, Tokyo, Japan
Author contributions: Hayakawa T obtained all the required data and drafted the article after a literature review; Hamamoto Y, Funakoshi S and Hirata K, a medical oncologist, revised the article; and Kanai T, a medical gastroenterologist, critically revised the article and approved its final version.
Informed consent statement: Written informed consent was obtained from the patient for the publication of this article and any accompanying images.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yasuo Hamamoto, MD, PhD, Assistant Professor, Doctor, Keio Cancer Center, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku 160-8582, Tokyo, Japan. yashmmt1971@gmail.com
Received: June 29, 2023 Peer-review started: June 29, 2023 First decision: September 26, 2023 Revised: October 10, 2023 Accepted: October 23, 2023 Article in press: October 23, 2023 Published online: November 6, 2023 Processing time: 130 Days and 7.8 Hours
Abstract
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.
Core Tip: This case is distinctive because the patient was diagnosed with a rare hyperammonemic encephalopathy caused by sunitinib, which was administered as treatment for gastrointestinal stromal tumors. We emphasize the need for systemic evaluation and prompt action for patients receiving tyrosine kinase inhibitors who present with adverse effects.
