Drug-induced hepatotoxicity covers the clinical and pathological expressions of almost any acute or chronic liver disease. Liver damage is due to intrinsic toxicity of the drug (paracetamol) and/or immunoallergic mechanisms (halothane). Acute injury may be cytotoxic or cholestatic. Cytotoxic injury is characterized by necrosis (paracetamol, halothane) or steatosis (valproate). Cholestatic injury can be associated with immune-mediated portal inflammation (chlorpromazine) or solely attributed to inhibition of transport systems (cyclosporin A). Chronic drug-induced disorders include chronic active hepatitis (methyldopa), autoimmune hepatitis (tienilic acid), alcoholic steatohepatitis-like reactions (amiodarone), indolent fibrosis (methotrexate), chronic cholestatic diseases, vascular lesions, and hepatic neoplasms. The clinical and morphological picture of many drug-induced liver diseases is nonspecific. Diagnosis is based on thorough drug history, temporal relationship, time-course of liver dysfunction, and the exclusion of other causes. Treatment consists of instant withdrawal of the suspected drug and administration of acetylcysteine as early as possible in case of paracetamol intoxication. Drug-induced liver diseases are usually reversible, but prolonged treatment leads to progression and liver cirrhosis.
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Theranostics
January 2025
Medicinal Materials Research Center, Biomedical Research Division, Korea Institute of Science and Technology (KIST), Seoul 02792, Republic of Korea.
Acute liver failure (ALF) is characterized by rapid hepatic dysfunction, primarily caused by drug-induced hepatotoxicity. Due to the lack of satisfactory treatment options, ALF remains a fatal clinical disease, representing a grand challenge in global health. For the drug repositioning to ALF of mesalamine, which is clinically approved for the treatment of inflammatory bowel disease (IBD), we propose a supramolecular prodrug nanoassembly (SPNs).
View Article and Find Full Text PDFSci Rep
January 2025
School of Medicine, Yichun University, 576 XueFu Road, Yuanzhou District, Yichun, 336000, Jiangxi, P.R. China.
Sodium aescinate (SA), a natural plant extract with various bioactivities, is widely used to treat oedema and inflammation in clinics. However, adverse events, including liver injury, kidney injury, and phlebitis, have been reported in patients with SA in recent years. In this study, we used BALB/c mice and L02 cells to evaluate the role of ferroptosis in SA-induced liver injury.
View Article and Find Full Text PDFBackground: Cirrhosis is the end stage of chronic liver disease. Cirrhosis causes portal hypertension, which, in turn, can lead to acute on chronic liver failure (ACLF), which is defined as acute decompensation combined with failure of the liver, coagulation system, kidneys, lungs, and/or circulatory system, or hepatic encephalopathy.
Methods: This review is based on a selective literature search for international publications in the NCBI database using the keywords "liver cirrhosis" and "ACLF.
Pharmaceutics
December 2024
Department of Medical Zoology, School of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea.
: Clonorchiasis is a foodborne parasitic disease that can lead to severe biliary fibrosis and cholangiocarcinoma. While praziquantel (PZQ) is available for clonorchiasis treatment, it cannot revert the histopathological damage incurred through parasite-induced fibrosis. Curcumin (CUR) is an emerging experimental drug possessing anti-inflammatory and fibrosis-alleviating effects, thus signifying its potential as an anthelmintic drug.
View Article and Find Full Text PDFToxics
November 2024
Laboratory of Metabolic Biochemistry, Institute of Exact and Biological Sciences, UFOP, Ouro Preto 35402-136, MG, Brazil.
Paracetamol (APAP) overdose is the leading cause of drug-induced liver injury, leading to acute liver failure. However, the role of concurrent acute or chronic ethanol ingestion in this context requires further clarification. In this study, we investigated the effects of acute and chronic ethanol ingestion on APAP-induced hepatotoxicity.
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