S5605 A Case of Off-Label Fenbendazole-Associated Liver Injury in a Patient With Underlying Liver Disease

Introduction: Fenbendazole is a veterinary anthelmintic used to treat parasitic infections in animals. It is not currently approved by the FDA and its pharmacokinetics and safety in humans has limited support in medical literature. We report a case of a 68-year-old man with hepatocellular carcinoma (HCC) and metabolic dysfunction-associated steatohepatitis (MASH) cirrhosis who developed drug-induced liver injury (DILI) after self-administering fenbendazole without professional medical oversight. This case highlights fenbendazole’s hepatotoxic potential and the risks of unregulated alternative therapies in patients with cirrhosis and HCC. Case Description/Methods: A 68-year-old man with hepatocellular carcinoma and MASH cirrhosis presented with 8 days of progressive jaundice and fatigue. His labs were notable for a cholestatic predominant liver injury. No recent illnesses, alcohol, acetaminophen use, and no new medications except self-administration of fenbendazole for a month based on anecdotal reports of cancer cure. Initial labs showed alanine aminotransferase 638 U/L, aspartate aminotransferase 670 U/L, alkaline phosphatase 197 U/L, total bilirubin 8.2 mg/dL, Direct bilirubin 4.5 mg/dL, and international normalized ratio 1.3. Workup for viral, autoimmune, and infectious causes were negative. Cross sectional imaging of the abdomen revealed evidence of known HCC, but otherwise no acute findings. Liver biopsy showed findings that were consistent with drug-induced liver injury. Fenbendazole was discontinued, and ursodiol started. Liver chemistries eventually returned to baseline over the course of 2 months. He continues to recover in the outpatient setting. Discussion: Fenbendazole disrupts microtubule formation and has shown potential anti-neoplastic effects in preclinical studies, though no human data confirm its safety or efficacy. This case raises key concerns: cirrhotic patients are especially vulnerable to hepatotoxicity due to limited hepatic reserve, and unregulated medication or supplement use—often fueled by anecdotal reports and misinformation—is increasing in oncology. While supportive care is primary, ursodiol may have helped improve the cholestatic injury. Timely identification and withdrawal of fenbendazole were critical to recovery. Clinicians should routinely ask about alternative therapies in patients with abnormal liver tests, especially those with liver disease or cancer.

Authors

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001149880.58386.06
Primary Topic
Drug-Induced Hepatotoxicity and Protection
Type
article
Field-Weighted Citation Impact
0.00
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article

S5605 A Case of Off-Label Fenbendazole-Associated Liver Injury in a Patient With Underlying Liver Disease

Jonathan Rice, A. R. Colón, Tafadzwa Amani, Colin Jenks
The American Journal of Gastroenterology
Drug-Induced Hepatotoxicity and Protection
article

S5605 A Case of Off-Label Fenbendazole-Associated Liver Injury in a Patient With Underlying Liver Disease

Jonathan Rice, A. R. Colón, Tafadzwa Amani, Colin Jenks
article en

Abstract

Introduction: Fenbendazole is a veterinary anthelmintic used to treat parasitic infections in animals. It is not currently approved by the FDA and its pharmacokinetics and safety in humans has limited support in medical literature. We report a case of a 68-year-old man with hepatocellular carcinoma (HCC) and metabolic dysfunction-associated steatohepatitis (MASH) cirrhosis who developed drug-induced liver injury (DILI) after self-administering fenbendazole without professional medical oversight. This case highlights fenbendazole’s hepatotoxic potential and the risks of unregulated alternative therapies in patients with cirrhosis and HCC. Case Description/Methods: A 68-year-old man with hepatocellular carcinoma and MASH cirrhosis presented with 8 days of progressive jaundice and fatigue. His labs were notable for a cholestatic predominant liver injury. No recent illnesses, alcohol, acetaminophen use, and no new medications except self-administration of fenbendazole for a month based on anecdotal reports of cancer cure. Initial labs showed alanine aminotransferase 638 U/L, aspartate aminotransferase 670 U/L, alkaline phosphatase 197 U/L, total bilirubin 8.2 mg/dL, Direct bilirubin 4.5 mg/dL, and international normalized ratio 1.3. Workup for viral, autoimmune, and infectious causes were negative. Cross sectional imaging of the abdomen revealed evidence of known HCC, but otherwise no acute findings. Liver biopsy showed findings that were consistent with drug-induced liver injury. Fenbendazole was discontinued, and ursodiol started. Liver chemistries eventually returned to baseline over the course of 2 months. He continues to recover in the outpatient setting. Discussion: Fenbendazole disrupts microtubule formation and has shown potential anti-neoplastic effects in preclinical studies, though no human data confirm its safety or efficacy. This case raises key concerns: cirrhotic patients are especially vulnerable to hepatotoxicity due to limited hepatic reserve, and unregulated medication or supplement use—often fueled by anecdotal reports and misinformation—is increasing in oncology. While supportive care is primary, ursodiol may have helped improve the cholestatic injury. Timely identification and withdrawal of fenbendazole were critical to recovery. Clinicians should routinely ask about alternative therapies in patients with abnormal liver tests, especially those with liver disease or cancer.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 52%
Drug-Induced Hepatotoxicity and Protection
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