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Key Points The biological basis for most instances of drug-induced liver injury (DILI) is unknown, but variation in host metabolic, detoxification, liver-regeneration and immune-response pathways has been implicated Results of studies in animal models and humans suggest a role for variation in the expression of CD44 in acetaminophen hepatotoxicity Genomic approaches have demonstrated that variation in the host immune response could help to explain susceptibility to DILI induced by treatment with ximelagatran, lumiracoxib or flucloxacillin Informative animal models of DILI and in vitro test systems to predict drug hypersensitivity reactions are currently lacking A bedside-to-bench approach involving the collection of biological samples from patients with well-characterized DILI could improve our understanding of the risk factors and mechanisms of DILI This is a preview of subscription content, access via your institution Access options Subscribe to this journal Receive 12 print issues and online access 186,36 per year only 15,53 per issue Buy this article Purchase on SpringerLink Instant access to the full article PDF
H., DAINTY, J
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