Abstract
Drug-induced liver injury (DILI) is typically divided into two categories: “intrinsic” and “idiosyncratic.” Intrinsic DILI is dose-dependent and usually predictable. In contrast, idiosyncratic DILI is difficult to predict as it has a complex dose-response relationship, its onset is typically delayed, and it is often observed in only a small percentage of treated patients. Both intrinsic and idiosyncratic DILI involve some level of direct drug-induced stress or injury to liver cells through three major mechanisms: mitochondrial dysfunction, oxidative stress, and alterations in bile acid homeostasis. In some cases of idiosyncratic hepatocellular DILI, hepatocyte stress leads to an adaptive immune response that in combination with loss of immune tolerance is ultimately responsible for clinically important liver injury. Both properties intrinsic to the drug as well as host factors determine susceptibility to DILI. New cell culture, preclinical animal, and computational models hold promise for guiding an improved understanding and prediction of DILI.
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