Case reports in hepatology · 2026
Amoxicillin-Induced Drug-Induced Liver Injury Superimposed on Acute Hepatitis C Infection in a Patient With Hurler Syndrome: A Diagnostic Challenge Assessed by the Updated RUCAM.
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Garg Archit, Seshie Prosper, Chouthai Abhishek, Raval Sahil, Santharaman Aadhithyaraman, Manzoor Adil, Broder Arkady
Аннотация
BACKGROUND: Drug-induced liver injury (DILI) refers to hepatotoxicity caused by conventional chemical drugs or xenobiotics, whereas herb-induced liver injury (HILI) is attributed to herbal and dietary supplements. Both these conditions pose diagnostic challenges, particularly when concurrent etiologies such as acute viral hepatitis are present. Hurler syndrome (mucopolysaccharidosis Type I) causes hepatocyte and Kupffer cell vacuolization and can predispose to DILI. Early diagnosis is critical given the high fatality rates associated with DILI.
CASE REPORT: We present a case of a 28-year-old male with Hurler syndrome who presented with acute onset of nausea, vomiting, and jaundice. Liver function tests (LFTs) revealed markedly elevated liver enzymes. Serological workup identified newly acquired acute hepatitis C virus (HCV) infection. The patient had recent amoxicillin use and was taking hibiscus tea daily. Causality assessment using the updated Roussel Uclaf Causality Assessment Method (RUCAM) of 2016 yielded a score of 6 (probable DILI). Liver biopsy confirmed DILI. The patient showed clinical improvement with N-acetylcysteine and corticosteroids, with progressive normalization of liver enzymes.
CONCLUSIONS: This case highlights the importance of differentiating DILI from acute viral hepatitis: strong clinical suspicion, temporal relation with offending drug, liver biopsy, and treatment response assessment. Clinicians should have a high index of suspicion for DILI even in the presence of concurrent acute HCV infection, especially in patients with underlying hepatic dysfunction such as Hurler syndrome in our case.
CASE REPORT: We present a case of a 28-year-old male with Hurler syndrome who presented with acute onset of nausea, vomiting, and jaundice. Liver function tests (LFTs) revealed markedly elevated liver enzymes. Serological workup identified newly acquired acute hepatitis C virus (HCV) infection. The patient had recent amoxicillin use and was taking hibiscus tea daily. Causality assessment using the updated Roussel Uclaf Causality Assessment Method (RUCAM) of 2016 yielded a score of 6 (probable DILI). Liver biopsy confirmed DILI. The patient showed clinical improvement with N-acetylcysteine and corticosteroids, with progressive normalization of liver enzymes.
CONCLUSIONS: This case highlights the importance of differentiating DILI from acute viral hepatitis: strong clinical suspicion, temporal relation with offending drug, liver biopsy, and treatment response assessment. Clinicians should have a high index of suspicion for DILI even in the presence of concurrent acute HCV infection, especially in patients with underlying hepatic dysfunction such as Hurler syndrome in our case.