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Related Experiment Video

Updated: Jan 20, 2026

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
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Drug-Induced Liver Injury with Eosinophilia: A Case-Control Study Using Electronic Medical Records.

Kimino Minagawa1, Hayato Akimoto1, Takashi Hayakawa2

  • 1Division of Genomic Epidemiology and Clinical Trials, Clinical Trials Research Center, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.

Biological & Pharmaceutical Bulletin
|January 18, 2026
PubMed
Summary

Idiosyncratic drug-induced liver injury with eosinophilia (DILI-Eos) is linked to many drugs, with varying risks even within drug classes. This study identifies specific drugs associated with DILI-Eos, highlighting immune-mediated pathways.

Keywords:
case–control studyeosinophiliahepatotoxicityidiosyncratic drug-induced liver injurysignal detection

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Area of Science:

  • Pharmacology and Toxicology
  • Hepatology
  • Immunology

Background:

  • Idiosyncratic drug-induced liver injury (iDILI) is a severe adverse drug reaction with suspected immune involvement.
  • The role of eosinophils in iDILI and drug-specific risks remain poorly understood, despite eosinophilia often marking hypersensitivity.

Purpose of the Study:

  • To evaluate drug-specific risks associated with drug-induced liver injury with eosinophilia (DILI-Eos).
  • To investigate the potential immune-mediated mechanisms underlying DILI-Eos.

Main Methods:

  • A case-control study utilizing electronic medical records of 17,129 Japanese adult patients.
  • Extraction of 631 DILI-Eos cases and 16,498 non-DILI-Eos controls.
  • Multivariable logistic regression analysis for 38 drugs prescribed within 60 days prior to liver injury onset.

Main Results:

  • Sulbactam/cefoperazone showed the strongest association with DILI-Eos (aOR 14.51), followed by meropenem (aOR 5.68) and tazobactam/piperacillin (aOR 3.55).
  • Common drugs like mosapride, lansoprazole, furosemide, and ambroxol were also significantly associated with increased DILI-Eos risk.
  • Significant variability in risk was observed within drug classes like β-lactam antibiotics and NSAIDs.

Conclusions:

  • DILI-Eos can be triggered by a wide range of drugs across therapeutic classes, potentially via immune-mediated pathways.
  • Drug-specific risk evaluation is crucial due to observed variability, even within the same drug classes.
  • Further research is needed to elucidate the causality and mechanisms of eosinophilic responses in DILI.