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Hepatotoxic Medication

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161. Possible Hepatotoxicity of IQOS Full Text available with Trip Pro

Possible Hepatotoxicity of IQOS 30131373 2019 03 15 1468-3318 27 Suppl 1 2018 11 Tobacco control Tob Control Possible hepatotoxicity of IQOS. s39-s40 10.1136/tobaccocontrol-2018-054320 Chun Lauren L Department of Medicine, University of California, San Francisco, San Francisco, California, USA. Moazed Farzad F Department of Medicine, University of California, San Francisco, San Francisco, California, USA. Matthay Michael M Department of Medicine, University of California, San Francisco, San (...) Francisco, California, USA. Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA. Department of Anesthesia, University of California, San Francisco, San Francisco, California, USA. Calfee Carolyn C Department of Medicine, University of California, San Francisco, San Francisco, California, USA. Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA. Department of Anesthesia, University of California

2018 Tobacco Control

162. Atorvastatin mitigates cyclophosphamide-induced hepatotoxicity via suppression of oxidative stress and apoptosis in rat model Full Text available with Trip Pro

Atorvastatin mitigates cyclophosphamide-induced hepatotoxicity via suppression of oxidative stress and apoptosis in rat model Cyclophosphamide (CP), as a chemotherapy drug, induces hepatotoxicity through causing oxidative stress. Atorvastatin (ATV) at a low dose has antioxidant and anti-inflammatory properties. The present study was designed to investigate the protective effects of ATV against CP-induced hepatotoxicity in rat. In this experimental study, 32 rats were treated with ATV orally

2018 Research in pharmaceutical sciences

163. Cytotoxic and Hepatocurative Effect of Aqueous Fraction of Tapinanthus bangwensis Against Paracetamol-Induced Hepatotoxicity Full Text available with Trip Pro

Cytotoxic and Hepatocurative Effect of Aqueous Fraction of Tapinanthus bangwensis Against Paracetamol-Induced Hepatotoxicity Medicinal plants over time have proven to have potential to manage a huge number of diseases and disorders and thus have become a great source of pharmaceutical drugs. One of such plants is Tapinanthus bangwensis (African mistletoe). It is a semiparasitic and epiphytic plant growing on citrus tree, obtaining its food photosynthetically while its nutrient and water is got

2018 Journal of Evidence-based Integrative Medicine

164. Subchronic Toxicity Studies of Cortex Dictamni Extracts in Mice and Its Potential Hepatotoxicity Mechanisms in Vitro Full Text available with Trip Pro

toxic components in Cortex Dictamni with dictamnine as the most potentially hepatotoxic component, whose potential hepatotoxicity mechanism may be associated with cell apoptosis. Moreover, this study could provide valuable data for clinical drug safety research of Cortex Dictamni and a good example for safety study of other Chinese herbal medicines. (...) Subchronic Toxicity Studies of Cortex Dictamni Extracts in Mice and Its Potential Hepatotoxicity Mechanisms in Vitro Cortex Dictamni is a commonly-used traditional Chinese herbal medicine for the treatment of skin inflammation, tinea, and eczema. Recently, some studies reported that Cortex Dictamni might induce liver injury, suggesting more attention to its safety. The current study was designed to investigate subchronic toxicity of Cortex Dictamni aqueous extract (CDAE) and ethanol extract

2018 Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

165. In vivo investigation on the chronic hepatotoxicity induced by intraperitoneal administration of 10-nm silicon dioxide nanoparticles Full Text available with Trip Pro

In vivo investigation on the chronic hepatotoxicity induced by intraperitoneal administration of 10-nm silicon dioxide nanoparticles Silicon dioxide (silica) nanoparticles (SDNPs) are widely used in nanotechnology and medicine, but these nanomaterials may carry a high risk for human health while little is known about their toxicity.We investigated the alterations in morphometry, biochemistry, hematology, histology of liver tissue and gene expression of drug-metabolizing enzymes induced by 10-nm (...) and plateletcrit. Levels of alkaline phosphatase, lactate dehydrogenase, low-density lipids, procalcitonin, aspartate aminotransferase and alanine aminotransferase, as well as potassium, phosphorus and iron concentrations, were increased. Histopathology revealed that SDNPs could induce hydropic degeneration, sinusoidal dilatation, hyperplasia of Kupffer cells, karyopyknosis and infiltration of inflammatory cells in the liver. SDNPs reduced the expression of 12 genes of drug-metabolizing enzymes significantly

2018 International journal of nanomedicine

166. Phytochemistry, Antioxidant, and Hepatoprotective Potential of Acanthospermum hispidum DC Extracts against Diethylnitrosamine-Induced Hepatotoxicity in Rats Full Text available with Trip Pro

Phytochemistry, Antioxidant, and Hepatoprotective Potential of Acanthospermum hispidum DC Extracts against Diethylnitrosamine-Induced Hepatotoxicity in Rats Background: Burkina Faso is classified among the countries with a high prevalence (˃12%) of hepatitis. Hepatic diseases, such as cirrhosis—related to alcoholism—and hepatitis B and C, are the cause of the increase in cases of liver cancer. They promote the development of cancer by decreasing the natural cell death, causing (...) of Acanthopermum hispidum extracts would justify the observed hepatoprotective activity. These results confirmed that the plant is used in the treatment of liver diseases in traditional medicine in Burkina Faso.

2018 Medicines

167. Carnosic Acid, a Natural Diterpene, Attenuates Arsenic-Induced Hepatotoxicity via Reducing Oxidative Stress, MAPK Activation, and Apoptotic Cell Death Pathway Full Text available with Trip Pro

Carnosic Acid, a Natural Diterpene, Attenuates Arsenic-Induced Hepatotoxicity via Reducing Oxidative Stress, MAPK Activation, and Apoptotic Cell Death Pathway The present studies have been executed to explore the protective mechanism of carnosic acid (CA) against NaAsO2-induced hepatic injury. CA exhibited a concentration dependent (1-4 μM) increase in cell viability against NaAsO2 (12 μM) in murine hepatocytes. NaAsO2 treatment significantly enhanced the ROS-mediated oxidative stress (...) in the hepatic cells both in in vitro and in vivo systems. Significant activation of MAPK, NF-κB, p53, and intrinsic and extrinsic apoptotic signaling was observed in NaAsO2-exposed hepatic cells. CA could significantly counteract with redox stress and ROS-mediated signaling and thereby attenuated NaAsO2-mediated hepatotoxicity. NaAsO2 (10 mg/kg) treatment caused significant increment in the As bioaccumulation, cytosolic ATP level, DNA fragmentation, and oxidation in the liver of experimental mice (n = 6

2018 Oxidative medicine and cellular longevity

168. Membrane Remodeling as a Key Player of the Hepatotoxicity Induced by Co-Exposure to Benzo[a]pyrene and Ethanol of Obese Zebrafish Larvae Full Text available with Trip Pro

Membrane Remodeling as a Key Player of the Hepatotoxicity Induced by Co-Exposure to Benzo[a]pyrene and Ethanol of Obese Zebrafish Larvae The rise in prevalence of non-alcoholic fatty liver disease (NAFLD) constitutes an important public health concern worldwide. Including obesity, numerous risk factors of NAFLD such as benzo[a]pyrene (B[a]P) and ethanol have been identified as modifying the physicochemical properties of the plasma membrane in vitro thus causing membrane remodeling-changes (...) in membrane fluidity and lipid-raft characteristics. In this study, the possible involvement of membrane remodeling in the in vivo progression of steatosis to a steatohepatitis-like state upon co-exposure to B[a]P and ethanol was tested in obese zebrafish larvae. Larvae bearing steatosis as the result of a high-fat diet were exposed to ethanol and/or B[a]P for seven days at low concentrations coherent with human exposure in order to elicit hepatotoxicity. In this condition, the toxicant co-exposure raised

2018 Biomolecules

169. Mitochondrial–Lysosomal Axis in Acetaminophen Hepatotoxicity Full Text available with Trip Pro

Mitochondrial–Lysosomal Axis in Acetaminophen Hepatotoxicity Acetaminophen (APAP) toxicity is the most common cause of acute liver failure and a major indication for liver transplantion in the United States and Europe. Although significant progress has been made in understanding the molecular mechanisms underlying APAP hepatotoxicity, there is still an urgent need to find novel and effective therapies against APAP-induced acute liver failure. Hepatic APAP metabolism results in the production (...) of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI), which under physiological conditions is cleared by its conjugation with glutathione (GSH) to prevent its targeting to mitochondria. APAP overdose or GSH limitation leads to mitochondrial NAPQI-protein adducts formation, resulting in oxidative stress, mitochondrial dysfunction, and necrotic cell death. As mitochondria are a major target of APAP hepatotoxicity, mitochondrial quality control and clearance of dysfunctional mitochondria through

2018 Frontiers in pharmacology

170. Hold the Gaba: A Case of Gabapentin-induced Hepatotoxicity Full Text available with Trip Pro

Hold the Gaba: A Case of Gabapentin-induced Hepatotoxicity A drug-induced liver injury is one of the most common causes of acute liver failure. While acetaminophen is the most common etiology, other offending medications include amoxicillin-clavulanic acid, amiodarone, isoniazid, and fluoroquinolones to name a few. Gabapentin, a gamma-aminobutyric acid (GABA) analogue, has infrequently been reported to cause liver injury; however, the causality in the previous reports is contested. Herein, we

2018 Cureus

171. Investigating the CYP2E1 Potential Role in the Mechanisms Behind INH/LPS-Induced Hepatotoxicity Full Text available with Trip Pro

Investigating the CYP2E1 Potential Role in the Mechanisms Behind INH/LPS-Induced Hepatotoxicity Tuberculosis (TB) is one of the oldest infectious diseases that affected humankind and remains one of the world's deadliest communicable diseases that could be considered as global emergency, but the discovery and development of isoniazid (INH) in the 1950s paved the way to an effective single and/or combined first-line anti-TB therapy. However, administration of INH induces severe hepatic toxicity (...) in some patients. Previously, we establish a rat model of INH hepatotoxicity utilizing the inflammatory stress theory, in which bacterial lipopolysaccharide (LPS) potentially enhanced INH toxicity. These enhancing activities ranged between augmenting the inflammatory stress, oxidative stress, alteration of bile acid homeostasis, and CYP2E1 over-expression. Although pre-treatment with dexamethasone (DEX) helped overcome both inflammatory and oxidative stress which ended-up in alleviation of LPS

2018 Frontiers in pharmacology

172. Discovery of Hepatotoxic Equivalent Combinatorial Markers from Dioscorea bulbifera tuber by Fingerprint-Toxicity Relationship Modeling Full Text available with Trip Pro

Discovery of Hepatotoxic Equivalent Combinatorial Markers from Dioscorea bulbifera tuber by Fingerprint-Toxicity Relationship Modeling Due to extremely chemical complexity, identification of potential toxicity-related constituents from an herbal medicine (HM) still remains challenging. Traditional toxicity-guided separation procedure suffers from time- and labor-consumption and neglects the additive effect of multi-components. In this study, we proposed a screening strategy called "hepatotoxic (...) equivalent combinatorial markers (HECMs)" for a hepatotoxic HM, Dioscorea bulbifera tuber (DBT). Firstly, the chemical constituents in DBT extract were globally characterized. Secondly, the fingerprints of DBT extracts were established and their in vivo hepatotoxicities were tested. Thirdly, three chemometric tools including partial least squares regression (PLSR), back propagation-artificial neural network (BP-ANN) and cluster analysis were applied to model the fingerprint-hepatotoxicity relationship

2018 Scientific reports

173. Cuscuta arvensis Beyr “Dodder”: In Vivo Hepatoprotective Effects Against Acetaminophen-Induced Hepatotoxicity in Rats Full Text available with Trip Pro

Cuscuta arvensis Beyr “Dodder”: In Vivo Hepatoprotective Effects Against Acetaminophen-Induced Hepatotoxicity in Rats Cuscuta arvensis Beyr. is a parasitic plant, and commonly known as "dodder" in Europe, in the United States, and "tu si zi shu" in China. It is one of the preferred spices used in sweet and savory dishes. Also, it is used as a folk medicine for the treatment particularly of liver problems, knee pains, and physiological hepatitis, which occur notably in newborns (...) and their mothers in the southeastern part of Turkey. The purpose of this study was to investigate the hepatoprotective effects and antioxidant activities of aqueous and methanolic extracts of C. arvensis Beyr. on acetaminophen (APAP)-induced acute hepatotoxicity in rats. The results were supported by subsequent histopathological studies. The hepatoprotective activity of both the aqueous and methanolic extracts at an oral dose of 125 and 250 mg/kg was investigated by observing the reduction levels

2018 Journal of medicinal food

174. Licorice root extract and magnesium isoglycyrrhizinate protect against triptolide-induced hepatotoxicity via up-regulation of the Nrf2 pathway Full Text available with Trip Pro

of triptolide. Licorice root extract contains various bioactive compounds and is potent hepatoprotective. Magnesium isoglycyrrhizinate, a magnesium salt of the 18α-glycyrrhizic acid stereoisomer of glycyrrhizic acid, is used clinically in China to treat chronic viral hepatitis and acute drug-induced liver injury. The aim of this study was to investigate the role of the factor erythroid 2-related factor 2 pathway in the protective effects of LE and MIG against triptolide-induced hepatotoxicity (...) Licorice root extract and magnesium isoglycyrrhizinate protect against triptolide-induced hepatotoxicity via up-regulation of the Nrf2 pathway Triptolide, the predominant biologically active component of the Chinese herb Tripterygium wilfordii Hook f., possesses numerous pharmacological activities, including anti-inflammatory, anti-fertility, anti-neoplastic, and immunosuppressive effects. However, toxicity and severe adverse effects, particularly hepatotoxicity, limit the clinical application

2018 Drug delivery

175. Interpretation the Hepatotoxicity Based on Pharmacokinetics Investigated Through Oral Administrated Different Extraction Parts of Polygonum multiflorum on Rats Full Text available with Trip Pro

(original and generated through EDG deglycosylation), and other free anthraquinones might be responsible for the hepatotoxicity of PM in vivo. PM extracts produced inhibitory effects on drug metabolic enzymes, include CYP3A4, CYP2C19, CYP2E1, UGT1A1, etc. And these effects may be related to its hepatotoxicity and pharmacokinetic behavior different. This information on hepatotoxicity and the pharmacokinetic comparison may be useful to understand the toxicological effects of PM. (...) Interpretation the Hepatotoxicity Based on Pharmacokinetics Investigated Through Oral Administrated Different Extraction Parts of Polygonum multiflorum on Rats The liver injury induced by Polygonum multiflorum (PM) used for clinical treatment has recently received widespread attention. This study aimed to determine the hepatotoxicity of PM through pharmacokinetics studies. The extract of PM was separated to isolate the anthraquinone fraction, the tannin and polysaccharide fraction

2018 Frontiers in pharmacology

176. Low risk of hepatotoxicity from rifampicin when used for cholestatic pruritus: a cross-disease cohort study. Full Text available with Trip Pro

Low risk of hepatotoxicity from rifampicin when used for cholestatic pruritus: a cross-disease cohort study. The use of rifampicin for cholestatic pruritus is accompanied by concerns over safety, but the availability of real-world prescribing data is relatively limited.We sought to describe the rate and characteristics of rifampicin-induced hepatitis in a mixed aetiology cohort of patients with established liver disease and cholestatic pruritus.Retrospective review of records for out-patients (...) rifampicin for a median of 131 days. Most had primary biliary cholangitis or primary sclerosing cholangitis; 40 (38.1%) were men and median age was 44 years (IQR: 32-57). 44 (41.9%) patients had baseline serum bilirubin ≥2 × ULN and 28 (26.7%) ALT ≥3 × ULN. 5 (4.8%) developed rifampicin-induced hepatitis at a median of 70(range 27-130) days after drug initiation. No individual or laboratory baseline characteristics were significantly associated with subsequent development of hepatitis. All cases

2018 Alimentary Pharmacology & Therapeutics

177. Increased MMAB level in mitochondria as a novel biomarker of hepatotoxicity induced by Efavirenz. Full Text available with Trip Pro

Increased MMAB level in mitochondria as a novel biomarker of hepatotoxicity induced by Efavirenz. Efavirenz (EFV), a non-nucleoside reverse transcriptase inhibitor (NNRTI), has been widely used in the therapy of human immunodeficiency virus (HIV) infection. Some of its toxic effects on hepatic cells have been reported to display features of mitochondrial dysfunction through bioenergetic stress and autophagy, etc. However, alteration of protein levels, especially mitochondrial protein levels (...) expressed proteins were quantified by real time RT-PCR. We also detected the expression of mitochondrial precursor Cob(I)yrinic acid a,c-diamide adenosyltransferase (MMAB) by immunohistochemistry analysis in clinical samples. The expression levels of MMAB and ROS were detected in EFV-treated Huh-7 cells with and without shRNA used to knock down MMAB, and in primary hepatocytes (PHC). The effects of other anti-HIV drugs (nevirapine (NVP) and tenofovirdisoproxil (TDF)), and hydrogen peroxide (H2O2) were

2017 PLoS ONE

178. HLA-DR7 and HLA-DQ2: Transgenic mouse strains tested as a model system for ximelagatran hepatotoxicity. Full Text available with Trip Pro

HLA-DR7 and HLA-DQ2: Transgenic mouse strains tested as a model system for ximelagatran hepatotoxicity. The oral thrombin inhibitor ximelagatran was withdrawn in the late clinical trial phase because it adversely affected the liver. In approximately 8% of treated patients, drug-induced liver injury (DILI) was expressed as transient alanine transaminase (ALT) elevations. No evidence of DILI had been revealed in the pre-clinical in vivo studies. A whole genome scan study performed on the clinical (...) association of both ximelagatran (pro-drug) and melagatran (active drug) to the antigen-presenting groove of the homology modelled HLA-DR7 molecule suggesting "altered repertoire" as a key initiating event driving development of DILI in humans. Transgenic mouse strains (tgms) expressing HLA of serotype HLA-DR7 (HLA-DRB1*0701, -DRA*0102), and HLA-DQ2 (HLA-DQB1*0202,-DQA1*0201) were created. These two lines were crossed with a human (h)CD4 transgenic line, generating the two tgms DR7xhCD4 and DQ2xhCD4

2017 PLoS ONE

179. Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses. Full Text available with Trip Pro

Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses. Oleanolic acid (OA) is a triterpenoid that exists widely in fruits, vegetables and medicinal herbs. OA is included in some dietary supplements and is used as a complementary and alternative medicine (CAM) in China, India, Asia, the USA and European countries. OA is effective in protecting against various hepatotoxicants, and one of the protective mechanisms is reprogramming the liver (...) of time of OA exposure differentiate the ability of OA to produce hepatoprotection vs hepatotoxicity. Hepatotoxicity produced by herbs is increasingly recognized and is of global concern. Given the appealing nature of OA in dietary supplements and its use as an alternative medicine around the world, as well as the development of OA derivatives (CDDO-Im and CDDO-Me) as therapeutics, it is important to understand not only that they program the liver to protect against hepatotoxic chemicals, but also how

2018 Liver International

180. Incidence of Hepatitis B Virus Reactivation and Hepatotoxicity in Patients Receiving Long-term Treatment With Tumor Necrosis Factor Antagonists. Full Text available with Trip Pro

Incidence of Hepatitis B Virus Reactivation and Hepatotoxicity in Patients Receiving Long-term Treatment With Tumor Necrosis Factor Antagonists. Tumor necrosis factor (TNF) antagonists are the first-line treatment for many autoimmune diseases. However, they have been associated with reactivation of hepatitis B virus (HBV). We determined the rate of HBV reactivation and hepatotoxicity grade 3 or 4 (HT ≥3) in patients treated with an anti-TNF agent for an autoimmune disease.We collected data from (...) of the 178 patients who were HBsAg negative and positive for the hepatitis B core antibody (anti-HBc+) had HBV reactivation. HBV reactivation occurred in 1/5 HBsAg+ patients who received prophylactic antiviral therapy and 8/18 who did not (P = .61). No one with HBV reactivation had liver failure. HT ≥3 occurred in 273 patients (2.7%), but only 3 cases were attributed to HBV. Cirrhosis was significantly associated with HT ≥3 (P < .001).In a retrospective analysis of patients treated with TNF antagonists

2018 Clinical Gastroenterology and Hepatology

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