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Last update 08 May 2025

Chemical and Drug Induced Liver Injury, Chronic

Last update 08 May 2025

Basic Info

Synonyms

Chemical Induced Liver Injury, Chronic, Chemical and Drug Induced Liver Injury, Chronic, Chemical-Induced Liver Injury, Chronic

+ [47]

Introduction

Liver disease lasting six months or more, caused by an adverse effect of a drug or chemical. The adverse effect may be caused by drugs, drug metabolites, chemicals from the environment, or an idiosyncratic response.

Drugs associated with Chemical and Drug Induced Liver Injury, Chronic

Anti-human IL11RA antibody(Biocytogen)

Target

IL-11RA

Mechanism

IL-11RA antagonists

Active Org.

Biocytogen Pharmaceuticals (Beijing) Co., Ltd.

Originator Org.

Biocytogen Pharmaceuticals (Beijing) Co., Ltd.

Active Indication

Chemical and Drug Induced Liver Injury, Chronic

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Chemical and Drug Induced Liver Injury, Chronic

NCT06258525

/ Not yet recruitingPhase 2IIT

A Phase II, Open-Label Trial of S-Adenosylmethionine (SAMe) in Prevention of Oxaliplatin Associated Liver Injury

This is an open-label, phase II study that may provide evidence that taking S-adenosylmethionine (SAMe) supplementation prevents oxaliplatin, a type of chemotherapy drug, associated liver toxicity in patients with resectable colorectal liver metastases. Resectable means that it is able to removed with surgery. Patients will take two SAMe tablets in the morning and one tablet in the evening for 3-6 months (about 6-8 cycles of chemotherapy) in addition to oxaliplatin based chemotherapy followed by surgical removal of the colorectal liver metastases.

Start Date15 Apr 2025

Sponsor / Collaborator

Cedars-Sinai Medical Center

[+1]

NCT06383325

/ Not yet recruitingNot ApplicableIIT

Evaluation of Liver Function Test to Identify Hepatotoxcicity Among Acute Leukemia Patients Who Are Receiving Chemotherapy Induction

Detection of hepatotoxcicity in acute leukemia and study the outcome of acute leukemia patients that suffer from hepatic toxiciyt

Start Date01 May 2024

Sponsor / Collaborator

Assiut University

NCT05014087

/ RecruitingPhase 2IIT

Digoxin In Treatment of Alcohol Associated Hepatitis (DIGIT-AlcHep)

Prospective, single center, open label, randomized controlled trial to explore whether digoxin treatment affects cytokine levels as biomarkers of inflammation in patients with acute alcohol associated hepatitis, digoxin administration and dose adjustment.
The study intervention will be intravenous digoxin (renal-based dosing for maximum of 28 days) versus no digoxin in an open-label 1:1 randomized allocation of patients with severe acute alcohol associated hepatitis.

Start Date08 Oct 2021

Sponsor / Collaborator

Yale University

100 Clinical Results associated with Chemical and Drug Induced Liver Injury, Chronic

100 Translational Medicine associated with Chemical and Drug Induced Liver Injury, Chronic

0 Patents (Medical) associated with Chemical and Drug Induced Liver Injury, Chronic

250

Literatures (Medical) associated with Chemical and Drug Induced Liver Injury, Chronic

01 May 2025·Environmental Toxicology

Coleus vettiveroides Root Extract Protects Against Thioacetamide‐Induced Chronic Liver Injury by Inhibiting NF‐κB Signaling Pathway

Article

Author: Karthick, Munusamy ; Shree Harini, Karthik ; Ezhilarasan, Devaraj ; Mohamed Azar, Kadmad Abdul Hameed ; Kumar, Venkatesan

ABSTRACTThe roots of Coleus vettiveroides (CV) have been traditionally used in Indian medicinal systems such as Ayurveda and Siddha for its antioxidant, anti‐inflammatory, and antidiabetic effects. This study examines the antifibrotic potential of CV ethanolic root extract (CVERE) against thioacetamide (TAA)‐induced liver fibrosis in Wistar rats. TAA was administered via i.p., thrice weekly for 11 weeks to induce liver fibrosis in rats. In separate groups, rats were administered with TAA and were concurrently treated with CVERE 125 mg/kg, CVERE 250 mg/kg, and silymarin (SIL) 100 mg/kg. Liver marker enzymes of hepatotoxicity, oxidative stress markers, proinflammatory marker gene expression (TNF‐α, NF‐κB, COX, and ILs), fibrotic marker gene expression (collagen I and III), immune histochemical expression of fibrosis marker proteins, and histopathologic changes were analyzed. TAA administration led to a significant (p < 0.001) increase in the serum level of hepatotoxic marker enzymes. The TAA‐treated group showed higher levels (p < 0.001) of MDA and reduced activities of SOD and CAT in the liver. TAA administration increased CYP2E1 expression, proinflammatory, and fibrotic marker gene expressions in rat liver. The histopathology of the liver confirms TAA‐induced architectural distortion and fibrotic changes. CVERE and SIL simultaneous treatments significantly protected against TAA‐induced oxidative stress, inflammation, and liver fibrosis. In conclusion, CVERE inhibited TAA‐induced liver fibrosis through downregulation of TAA metabolic activation, redox imbalance, and inflammation through repression of the NF‐κB pathway.

01 Apr 2025·Fitoterapia

Hepatoprotective potential of Ceiba chodatii Hassl. Against carbon tetrachloride-induced chronic liver damage supported with phytochemical investigation

Article

Author: Saber, Entesar Ali ; Fahim, John Refaat ; Matsunami, Katsuyoshi ; Fawzy, Michael Atef ; Kamel, Mohamed Salah ; Samy, Mamdouh Nabil ; Sugimoto, Sachiko ; Ibrahem, Engy Saadalah ; Attia, Eman Zekry

Hepatic fibrosis is a major health concern that can develop into other life-threatening pathologies, with no fully effective treatments are available to date. Ceiba is a genus of multipurpose trees with diverse therapeutic applications, including liver ailments. Prior research has also unveiled the protecting role of Ceiba plants in chemical liver injuries via a number of in vitro and in vivo tests. Due to the crucial need for alternative therapies to prevent liver damage and stop its progress, the present work evaluates the protective effects of the total extract of Ceiba chodatii Hassl. flowers and its derived fractions (I-IV) against CCl₄-induced chronic liver damage for the first time. The obtained results indicated the ability of C. chodatii flowers, particularly their chloroform- and ethyl acetate-soluble fractions (II and III), to alleviate liver damage in CCl₄-intoxicated rats via normalizing high liver injury hallmarks (e.g., ALT, AST, albumin, and total bilirubin), preventing the build-up of malondialdehyde, enhancing the antioxidant capacity of hepatocytes, mitigating aberrant histopathological changes, and reducing extracellular matrix accumulation. Further mechanistic studies showed the aptitude of C. chodatii flowers to attenuate inflammatory, fibrotic, and apoptotic responses via counteracting the production of inflammatory cytokines (e.g., IL-6 and TNF-α), reducing the levels of cleaved caspase-3, and inhibiting JAK2/STAT3 and TGF-β/Smad signaling pathways. Interestingly, the liver-protecting actions of fractions II and III were also comparable to those of silymarin (50 mg/kg). Moreover, phytochemical investigation of C. chodatii flowers led to the isolation and identification of a group of flavonoid glycosides (1-10), with good antioxidant and liver supporting properties, suggesting their potential contribution to the anti-fibrotic properties of C. chodatii. These data highlight the multi-target hepatoprotective effects of C. chodatii and its potential as an alternative source to develop natural therapeutic agents against liver fibrosis.

01 Apr 2025·Journal of Gastroenterology and Hepatology

Analysis of Immunometabolic Profiles in Patients With Chronic Drug‐Induced Liver Injury and Validation in Mice to Reveal Potential Mechanisms

Article

Author: Chang, Binxia ; Sun, Ying ; Bai, Zhaofang ; Zhu, Yun ; Huang, Ang ; Lu, Yawen ; Liu, Zherui ; Xie, Huan ; Wang, Jiabo ; Chen, Shaoting ; He, Xian ; Zhai, Xingran ; Xiao, Xiaohe ; Zou, Zhengsheng

ABSTRACTBackgroundThe mechanism underlying chronic drug‐induced liver injury (DILI) remains unclear. Immune activation is a common feature of DILI progression and is closely associated with metabolism. We explored the immunometabolic profile of chronic DILI and the potential mechanism of chronic DILI progression.MethodsPlasma and peripheral blood mononuclear cells from patients with chronic DILI were analyzed using multiplex immunoassays and untargeted metabolomics to reveal their immunometabolic profile. The effects and potential mechanisms of chronic DILI‐related metabolite on acute or chronic liver injury induced by LPS or CCl4 in mice were investigated.ResultsPatients with chronic DILI exhibited elevated plasma IL‐6, IL‐12p70, IL‐15 and reduced IL‐10 levels. The percentage of IL‐12+ monocytes was higher, while that of CD206+ monocytes, IL‐10+ monocytes, Th2, Treg, and IL‐10+ CD4+ T cells were lower in patients with chronic DILI compared to those with acute DILI. We identified the most significantly increased metabolite in patients with chronic DILI was cis‐aconitic acid (CAA). Administration of CAA can attenuate liver injury in mice with acute liver injury induced by LPS or CCl4 and promote the spontaneous resolution of liver fibrosis in mice with chronic live injury induced by CCl4. The protective mechanism of CAA against liver injury is associated with the inhibition of hepatic macrophage infiltration and polarization, which is achieved by inhibiting the secretion of neutrophil‐derived IL‐33 and subsequent phosphorylation of GATA3.ConclusionsCAA, which is elevated in patients with chronic DILI, protects against liver injury by inhibiting hepatic macrophage infiltration and polarization through the suppression of the IL‐33/GATA3 pathway, suggesting that CAA may serve as a potential target for regulating tissue repair in liver injury.

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Chemical and Drug Induced Liver Injury, Chronic

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