Pharmacokinetic and toxicodynamic concepts in idiosyncratic, drug-induced liver injury

Expert Opin Drug Metab Toxicol. 2022 Jul-Aug;18(7-8):469-481. doi: 10.1080/17425255.2022.2113379. Epub 2022 Aug 24.

Abstract

Introduction: Idiosyncratic drug-induced liver injury (IDILI) causes morbidity and mortality in patients and leads to curtailed use of efficacious pharmaceuticals. Unlike intrinsically toxic reactions, which depend on dose, IDILI occurs in a minority of patients at therapeutic doses. Much remains unknown about causal links among drug exposure, a mode of action, and liver injury. Consequently, numerous hypotheses about IDILI pathogenesis have arisen.

Areas covered: Pharmacokinetic and toxicodynamic characteristics underlying current hypotheses of IDILI etiology are discussed and illustrated graphically.

Expert opinion: Hypotheses to explain IDILI etiology all involve alterations in pharmacokinetics, which lead to plasma drug concentrations that rise above a threshold for toxicity, or in toxicodynamics, which result in a lowering of the toxicity threshold. Altered pharmacokinetics arise, for example, from changes in drug metabolism or from transporter polymorphisms. A lowered toxicity threshold can arise from drug-induced mitochondrial injury, accumulation of toxic endogenous factors or harmful immune responses. Newly developed, interactive freeware (DemoTox-PK; https://bit.ly/DemoTox-PK) allows the user to visualize how such alterations might lead to a toxic reaction. The illustrations presented provide a framework for conceptualizing idiosyncratic reactions and could serve as a stimulus for future discussion, education, and research into modes of action of IDILI.

Keywords: Drug toxicity; idiosyncrasy; idiosyncratic; liver injury; liver toxicity; pharmacodynamics; pharmacokinetics; toxicity threshold; toxicodynamics.

MeSH terms

  • Chemical and Drug Induced Liver Injury* / etiology
  • Humans
  • Liver / metabolism