ReviewPharmacological reviews2009
Inflammatory stress and idiosyncratic hepatotoxicity: hints from animal models.
Review in Pharmacological reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 136 citations in OpenAlex.
- Diclofenac Immune-Mediated Hepatitis: Identification of Innate and Adaptive Immune Responses at Clinically Relevant Doses.International journal of molecular sciences · 2025Article
- Recent advancement in prevention against hepatotoxicity, molecular mechanisms, and bioavailability of gallic acid, a natural phenolic compound: challenges and perspectives.Frontiers in pharmacology · 2025Review
- Are the Common Genetic 3'UTR Variants in ADME Genes Playing a Role in Tolerance of Breast Cancer Chemotherapy?International journal of molecular sciences · 2024Article
- Optimization and pharmacological evaluation of phytochemical-rich Cuscuta reflexa seed extract for its efficacy against chlorpyrifos-induced hepatotoxicity in murine models.Scientific reports · 2024Article
- Mechanistic Understanding of Idiosyncratic Drug-Induced Hepatotoxicity Using Co-Cultures of Hepatocytes and Macrophages.Antioxidants (Basel, Switzerland) · 2023Article
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
- Exploration of the Components and Pharmacological Mechanisms of Keyin Pill-Induced Liver Injury Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The Function of NF-Kappa B During Epilepsy, a Potential Therapeutic Target.Frontiers in neuroscience · 2022Review
- Mechanisms of immune checkpoint inhibitor-mediated liver injury.Acta pharmaceutica Sinica. B · 2021Review
- Critical Review of Gaps in the Diagnosis and Management of Drug-Induced Liver Injury Associated with Severe Cutaneous Adverse Reactions.Journal of clinical medicine · 2021Review
- Characterisation of Drug-Induced Liver Injury in Patients with COVID-19 Detected by a Proactive Pharmacovigilance Program from Laboratory Signals.Journal of clinical medicine · 2021Article
- Drug-induced organ injury in coronavirus disease 2019 pharmacotherapy: Mechanisms and challenges in differential diagnosis and potential protective strategies.Journal of biochemical and molecular toxicology · 2021Review
- Oxidative Stress in Drug-Induced Liver Injury (DILI): From Mechanisms to Biomarkers for Use in Clinical Practice.Antioxidants (Basel, Switzerland) · 2021Review
- Modeling the Bioactivation and Subsequent Reactivity of Drugs.Chemical research in toxicology · 2021Article
- The hepatotoxicity of Polygonum multiflorum: The emerging role of the immune-mediated liver injury.Acta pharmacologica Sinica · 2021Review
- Metabolic Forest: Predicting the Diverse Structures of Drug Metabolites.Journal of chemical information and modeling · 2020Article
- An adverse outcome pathway for immune-mediated and allergic hepatitis: a case study with the NSAID diclofenac.Archives of toxicology · 2020Article
- Lipidomics Analysis Indicates Disturbed Hepatocellular Lipid Metabolism inFrontiers in pharmacology · 2020Article
- Research Progress on the Animal Models of Drug-Induced Liver Injury: Current Status and Further Perspectives.BioMed research international · 2019Review
- Model-based identification of TNFα-induced IKKβ-mediated and IκBα-mediated regulation of NFκB signal transduction as a tool to quantify the impact of drug-induced liver injury compounds.NPJ systems biology and applications · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Adverse drug reactions (ADRs) present a serious human health problem. They are major contributors to hospitalization and mortality throughout the world (Lazarou et al., 1998; Pirmohamed et al., 2004). A small fraction (less than 5%) of ADRs can be classified as "idiosyncratic." Idiosyncratic ADRs (IADRs) are caused by drugs with diverse pharmacological effects and occur at various times during drug therapy. Although IADRs affect a number of organs, liver toxicity occurs frequently and is the primary focus of this review. Because of the inconsistency of clinical data and the lack of experimental animal models, how IADRs arise is largely undefined. Generation of toxic drug metabolites and induction of specific immunity are frequently cited as causes of IADRs, but definitive evidence supporting either mechanism is lacking for most drugs. Among the more recent hypotheses for causation of IADRs is that inflammatory stress induced by exogenous or endogenous inflammagens is a susceptibility factor. In this review, we give a brief overview of idiosyncratic hepatotoxicity and the inflammatory response induced by bacterial lipopolysaccharide. We discuss the inflammatory stress hypothesis and use as examples two drugs that have caused IADRs in human patients: ranitidine and diclofenac. The review focuses on experimental animal models that support the inflammatory stress hypothesis and on the mechanisms of hepatotoxic response in these models. The need for design of epidemiological studies and the potential for implementation of inflammation interaction studies in preclinical toxicity screening are also discussed briefly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.