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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Clin Cases. Sep 26, 2026; 14(27): 127697
Published online Sep 26, 2026. doi: 10.12998/wjcc.127697
Letter to the Editor: Hepatocellular pattern is compatible with fenbendazole-associated drug-induced liver injury
Arunkumar Krishnan, Tinsay A Woreta
Arunkumar Krishnan, Department of Medicine, Atrium Health Levine Cancer, Charlotte, NC 28204, United States
Arunkumar Krishnan, Department of Supportive Oncology, Atrium Health Wake Forest Baptist Comprehensive Cancer Center, Charlotte, NC 28204, United States
Tinsay A Woreta, Division of Gastroenterology and Hepatology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States
Author contributions: Krishnan A conceptualized and designed the research, performed interpretation of data and wrote the original draft; Woreta TA supervised the project; Krishnan A and Woreta TA performed the review and editing of the draft; both authors revised the manuscript for important intellectual content; all authors approved the final version of the article, including the authorship list.
AI contribution statement: The authors declare that no AI tools were used in the development or writing of this manuscript and take full responsibility for its integrity, accuracy, and originality.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Arunkumar Krishnan, MD, Department of Medicine, Atrium Health Levine Cancer, No. 1021 Morehead Medical Dr, Charlotte, NC 28204, United States. dr.arunkumar.krishnan@gmail.com
Received: September 4, 2026
Revised: October 1, 2026
Accepted: October 12, 2026
Published online: September 26, 2026
Processing time: 39 Days and 17.3 Hours
Abstract

We respond to Supple’s proposal, published in the World Journal of Clinical Cases, that liver injury following fenbendazole dose escalation in a patient receiving nivolumab/relatlimab represented immunogenic tumor-cell death. Marked aminotransferase elevation with modest alkaline phosphatase elevation is compatible with hepatocellular injury; neither this pattern nor an aspartate aminotransferase: alanine aminotransferase ratio near unity identifies its cause. The exposure history, improvement after withdrawal without corticosteroids, and subsequent tolerance of immunotherapy supported our original clinical interpretation of fenbendazole-associated drug-induced liver injury. Concurrent nosode exposure and possible immune-mediated or combination effects limit single-agent attribution. The reported R ratio and Roussel Uclaf Causality Assessment Method score cannot be independently verified from the available information; neither is presented here as an established error or a newly adjudicated result. Tumor necrosis was not demonstrated, although the reported investigations cannot exclude microscopic necrosis. These limitations do not establish anticancer benefit. The clinical priority remains evaluation of potentially serious liver injury and avoidance of deliberate diagnostic fenbendazole rechallenge.

Keywords: Fenbendazole; Drug-induced liver injury; Hepatocellular injury; Immune checkpoint inhibitor; Roussel Uclaf Causality Assessment Method; Tumor onconecrosis

Core Tip: Modest alkaline phosphatase elevation does not contradict hepatocellular drug-induced liver injury, and the aspartate aminotransferase:alanine aminotransferase ratio cannot establish tumor onconecrosis. Our original clinical assessment favored fenbendazole-associated injury on the overall course, with residual uncertainty from co-exposures. The reported R ratio and Roussel Uclaf Causality Assessment Method score remain unresolved verification needs rather than established errors; this limitation does not validate an alternative mechanism. Severe liver injury should prompt clinical evaluation and should not be interpreted as evidence of anticancer efficacy.

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