Drug-induced Liver Injury
Drug-induced Liver Injury - Related Videos
07:27
The Murine Choline-Deficient, Ethionine-Supplemented (CDE) Diet Model of Chronic Liver Injury
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Cited by 14 •
2017
Here we describe a common method to induce chronic liver injury in mice by feeding of a choline-deficient and ethionine-supplemented (CDE) diet. We demonstrate health monitoring, liver perfusion, isolation, and preservation. A time course of six weeks can inform about liver injury, pathohistology, fibrosis, inflammatory, and liver progenitor cell responses.
09:32
Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
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2025
Here, we study hepatotoxicity caused by lapatinib and neratinib through SASP-driven macrophage polarization, which offers a deeper mechanistic understanding beyond traditional toxicity tests. This approach demonstrates how senescent hepatocytes influence immune responses. This is particularly valuable for assessing long-term drug effects and discovering new therapeutic targets for managing drug-induced hepatotoxicity.
11:06
Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
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Cited by 11 •
2022
Drug-induced liver injury (DILI) is a major cause of drug failure. A protocol has been developed to accurately predict the DILI liability of a compound using a liver microphysiological system (MPS). The liver model uses the coculture of primary hepatic cells and translationally relevant endpoints to assess cellular responses to treatment.
10:45
Histological Analyses of Acute Alcoholic Liver Injury in Zebrafish
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Cited by 27 •
2017
This protocol describes histological analyses of the livers from zebrafish larvae that have been treated with 2% ethanol for 24 h. Such acute ethanol treatment results in hepatic steatosis and swelling of the hepatic vasculature.
04:24
Bipolar Radiofrequency-Based Hemorrhage Arrest in Solid Organ Injury: A Technique to Arrest Bleeding in Porcine Model With Liver Injury Using Electrosurgery
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2025
This video demonstrates a technique of bipolar radiofrequency energy-based transcollation for hemorrhage arrest in solid organ injury in a porcine model. This method is helpful for the surgical management of traumatic injury by achieving hemostasis by arresting bleeding at the injury site.
FAQs
Predictable toxicity generally follows dose-dependent exposure, making its relationship to the medicine more consistent. Idiosyncratic reactions are less predictable and may reflect reactive metabolites, mitochondrial stress, oxidative injury, or immune-mediated damage to hepatocytes. This distinction matters in pharmacology because predictable effects can be evaluated through dose and exposure, whereas idiosyncratic risk requires attention to biological mechanisms and individual susceptibility.
Several processes can injure hepatocytes, including formation of reactive metabolites, disruption of mitochondrial function, oxidative injury, and immune-mediated cellular damage. These mechanisms provide different explanations for how a medicine or its metabolites can produce liver injury. Identifying the likely process helps researchers interpret toxicity findings and supports efforts to design medicines with improved safety profiles.
Susceptibility varies among individuals, even when people receive medicines used for similar purposes. The overview links this variation to differences in how injury mechanisms affect the liver, including responses to reactive metabolites, mitochondrial stress, oxidative injury, or immune-mediated damage. Understanding this variability is important for pharmacology because it helps explain why risk cannot always be predicted from dose alone.
Evaluation combines patterns of liver-enzyme elevation with symptoms, the patient’s exposure history, and recovery after the suspected medicine is withdrawn. Clinicians also use these findings to distinguish medication-related injury from other liver disorders. Considering several types of evidence together is important because no single observation in the overview is presented as sufficient by itself.
Improvement after withdrawal of the suspected medicine is one part of assessing whether exposure contributed to liver injury. It is interpreted alongside enzyme-elevation patterns, symptoms, and exposure history rather than in isolation. This approach supports timely clinical decisions while helping clinicians distinguish a suspected medication-related process from other possible liver disorders.
Research on this problem supports safer drug design, preclinical screening, and post-market surveillance. Investigators examine potential injury mechanisms and evaluate liver-related findings before and after medicines reach broader use. These activities help identify safety concerns, improve understanding of variable susceptibility, and inform clinical decisions when possible liver injury emerges during treatment.