How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

28,914 results for

Alcoholic Hepatitis

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

261. Randomized placebo-controlled trial of emricasan for non-alcoholic steatohepatitis-related cirrhosis with severe portal hypertension. (Abstract)

Randomized placebo-controlled trial of emricasan for non-alcoholic steatohepatitis-related cirrhosis with severe portal hypertension. Emricasan, an oral pan-caspase inhibitor, decreased portal pressure in experimental cirrhosis and in an open-label study in patients with cirrhosis and severe portal hypertension, defined as a hepatic venous pressure gradient (HVPG) ≥12 mmHg. We aimed to confirm these results in a placebo-controlled study in patients with non-alcoholic steatohepatitis (NASH (...) hypertension. Compensated patients with higher baseline HVPG had evidence of a small treatment effect. Emricasan treatment appeared safe and well-tolerated.Cirrhosis (scarring of the liver) is the main consequence of non-alcoholic steatohepatitis (NASH). Cirrhosis leads to high pressure in the portal vein which accounts for most of the complications of cirrhosis. Reducing portal pressure is beneficial in patients with cirrhosis. We studied the possibility that emricasan, a drug that improves inflammation

2020 Journal of Hepatology

262. Insulin sensitizer MSDC-0602K in non-alcoholic steatohepatitis: A randomized, double-blind, placebo-controlled phase IIb study. (Abstract)

to daily oral placebo, or 1 of 3 MSDC-0602K doses in a 52-week double-blind study. The primary efficacy endpoint was hepatic histological improvement of ≥2 points in non-alcoholic fatty liver disease activity score (NAS) with a ≥1-point reduction in either ballooning or lobular inflammation and no increase in fibrosis stage at 12 months. Secondary endpoints included NAS improvement without worsening fibrosis, NASH resolution, and fibrosis reduction. Exploratory endpoints included changes in insulin (...) Insulin sensitizer MSDC-0602K in non-alcoholic steatohepatitis: A randomized, double-blind, placebo-controlled phase IIb study. MSDC-0602K is a novel insulin sensitizer designed to preferentially target the mitochondrial pyruvate carrier while minimizing direct binding to the transcriptional factor PPARγ. Herein, we aimed to assess the efficacy and safety of MSDC-0602K in patients with non-alcoholic steatohepatitis.Patients with biopsy-confirmed NASH and fibrosis (F1-F3) were randomized

2020 Journal of Hepatology

263. A defect in endothelial autophagy occurs in patients with non-alcoholic steatohepatitis and promotes inflammation and fibrosis. (Abstract)

A defect in endothelial autophagy occurs in patients with non-alcoholic steatohepatitis and promotes inflammation and fibrosis. Previous studies demonstrated that autophagy is protective in hepatocytes and macrophages, but detrimental in hepatic stellate cells in chronic liver diseases. The role of autophagy in liver sinusoidal endothelial cells (LSECs) in non-alcoholic steatohepatitis (NASH) is unknown. Our aim was to analyze the potential implication of autophagy in LSECs in NASH and liver (...) in the early stages of NASH, but also favors more advanced stages of liver fibrosis.Autophagy is a physiological process controlling endothelial homeostasis in vascular beds outside the liver. This study demonstrates that autophagy is defective in the liver endothelial cells of patients with non-alcoholic steatohepatitis. This defect promotes liver inflammation and fibrosis at early stages of non-alcoholic steatohepatitis, but also at advanced stages of chronic liver disease.Copyright © 2019 European

2020 Journal of Hepatology

264. Risk of hepatocellular carcinoma in Danish outpatients with alcohol-related cirrhosis. (Abstract)

all Danish outpatients with a hospital diagnosis of alcoholic cirrhosis, except those with cancer, those with chronic viral hepatitis or autoimmune liver disease, and those older than 80 years. We followed them through 2018 and described the cumulative risk of HCC and the cumulative risk of death from HCC, variceal bleeding, or trauma.Of the 4553 included patients, 181 developed HCC and 2274 died. The cumulative risk of HCC was 0.9% (95% confidence interval [CI] 0.7 to 1.3) after 1 year, 3.6% (95 (...) Risk of hepatocellular carcinoma in Danish outpatients with alcohol-related cirrhosis. Accurate estimates of the risk of hepatocellular carcinoma (HCC) in patients with cirrhosis are important for clinical decisions about HCC surveillance. We described HCC risk among outpatients with alcoholic cirrhosis and contrasted the risk of death from HCC with the risk of death from variceal bleeding or trauma.This was a nationwide, registry-based historical cohort study between 2006 and 2018. We included

2020 Journal of Hepatology

265. Blocking integrin α<sub>4</sub>β<sub>7</sub>-mediated CD4 T cell recruitment to the intestine and liver protects mice from western diet-induced non-alcoholic steatohepatitis. (Abstract)

Blocking integrin α4β7-mediated CD4 T cell recruitment to the intestine and liver protects mice from western diet-induced non-alcoholic steatohepatitis. The heterodimeric integrin receptor α4β7 regulates CD4 T cell recruitment to inflamed tissues, but its role in the pathogenesis of nonalcoholic steatohepatitis (NASH) is unknown. Here we examined the role of α4β7-mediated recruitment of CD4 T cells to the intestine and liver in NASH.Male littermate F11r+/+ (control (...) ) and junctional adhesion molecule A knockout F11r-/- mice were fed a normal diet or a Western diet (WD) for eight weeks. Liver and intestinal tissues were analyzed by histology, qRT-PCR, 16s rRNA sequencing and flow cytometry. Colonic mucosa-associated microbiota was analyzed using 16s rRNA sequencing. Liver biopsies from NASH patients were analyzed by confocal imaging and qRT-PCR.WD-fed knockout mice developed NASH and had increased hepatic and intestinal α4β7+ CD4 T cells relative to control mice which

2020 Journal of Hepatology

266. ER stress-induced upregulation of NNMT contributes to alcohol-related fatty liver development. (Abstract)

and upregulates hepatic NNMT expression. ER stress inducers upregulated NNMT expression in both AML-12 hepatocytes and mice. PERK-ATF4 pathway activation is the main contributor in ER stress-mediated NNMT upregulation in the liver. Alcohol consumption fails to upregulate NNMT in liver-specific ATF4 knockout mice. Both adenoviral NNMT knockdown and NNMT inhibitor administration prevents fatty liver development induced by chronic alcohol feeding, which is associated with the downregulation of an array of genes (...) involved in de novo lipogenesis pathway, including Srebf1, Acaca, Acacb and Fasn. Further investigations revealed that NNMT inhibition-induced lipogenic pathway activation was independent of its NAD+-enhancing action; however, incremental cellular NAD+ contents due to NNMT inhibition was associated with marked liver AMPK activation.ER stress, in specific, the PERK-ATF4 pathway activation, is mechanistically involved in hepatic NNMT upregulation in response to chronic alcohol exposure and NNMT

2020 Journal of Hepatology

267. Reply to HEP-20-0871 Letter to the Editors: Cilofexor in patients with non-alcoholic steatohepatitis (NASH): Is it really effective? (Abstract)

of cilofexor as monotherapy and in combination with other compounds that includes histologic endpoints (NCT03449446). Although reductions in liver transaminases were not statistically significant, dose-dependent improvements in GGT and hepatic fat by MRI-PDFF occurred. The proportion of patients with a ≥30% reduction in PDFF at week 24 was 13% in the placebo group, 14% in the cilofexor 30 mg group (p=0.87), and 39% in the 100 mg group (p=0.011).This article is protected by copyright. All rights reserved. (...) Reply to HEP-20-0871 Letter to the Editors: Cilofexor in patients with non-alcoholic steatohepatitis (NASH): Is it really effective? We thank Drs. Jindal and Sarin for their correspondence regarding our study of the nonsteroidal FXR agonist cilofexor in NASH. The objective of this Phase 2a study was to obtain preliminary evidence regarding the safety, pharmacokinetics, pharmacodynamics, and efficacy of cilofexor, including dose response. Indeed, our observations informed the 48-week ATLAS trial

2020 Hepatology

268. Volixibat in adults with non-alcoholic steatohepatitis: 24-week interim analysis from a randomized, phase II study. Full Text available with Trip Pro

Volixibat in adults with non-alcoholic steatohepatitis: 24-week interim analysis from a randomized, phase II study. Volixibat is an inhibitor of the apical sodium-dependent bile acid transporter (ASBT) that has been hypothesized to improve non-alcoholic steatohepatitis (NASH) by blocking bile acid reuptake and stimulating hepatic bile acid production. We studied the safety, tolerability and efficacy of volixibat in patients with NASH.In this double-blind, phase II dose-finding study, adults (...) with ≥5% steatosis and NASH without cirrhosis (N = 197) were randomized to receive volixibat (5, 10 or 20 mg) or placebo once daily for 48 weeks. The endpoints of a predefined interim analysis (n = 80), at week 24, were: ≥5% reduction in MRI-proton density fat fraction and ≥20% reduction in serum alanine aminotransferase levels. The primary endpoint was a ≥2-point reduction in non-alcoholic fatty liver disease activity score without worsening fibrosis at week 48.Volixibat did not meet either interim

2020 Journal of Hepatology

269. Inhibition of PU.1 ameliorates metabolic dysfunction and non-alcoholic steatohepatitis. (Abstract)

Inhibition of PU.1 ameliorates metabolic dysfunction and non-alcoholic steatohepatitis. Obesity is a well-established risk factor for type 2 diabetes (T2D) and non-alcoholic steatohepatitis (NASH), but the underlying mechanisms remain incompletely understood. Herein, we aimed to identify novel pathogenic factors (and possible therapeutic targets) underlying metabolic dysfunction in the liver.We applied a tandem quantitative proteomics strategy to enrich and identify transcription factors (TFs (...) in the whole liver, but not hepatocytes alone, significantly improved glucose homeostasis and suppressed liver inflammation. Consistently, treatment with the PU.1 inhibitor DB1976 markedly reduced inflammation and improved glucose homeostasis and dyslipidemia in DIO mice, and strongly suppressed glucose intolerance, liver steatosis, inflammation, and fibrosis in a dietary NASH mouse model. Furthermore, hepatic PU.1 expression was positively correlated with insulin resistance and inflammation in liver

2020 Journal of Hepatology

270. Genome-wide association study of non-alcoholic fatty liver and steatohepatitis in a histologically-characterised cohort. Full Text available with Trip Pro

Genome-wide association study of non-alcoholic fatty liver and steatohepatitis in a histologically-characterised cohort. Genetic factors associated with non-alcoholic fatty liver disease (NAFLD) remain incompletely understood. To date, most GWAS studies have adopted radiologically assessed hepatic triglyceride content as reference phenotype and so cannot address steatohepatitis or fibrosis. We describe a genome-wide association study (GWAS) encompassing the full spectrum of histologically

2020 Journal of Hepatology

271. TGF-β-driven reduction of cytoglobin leads to oxidative DNA damage in stellate cells during non-alcoholic steatohepatitis. Full Text available with Trip Pro

TGF-β-driven reduction of cytoglobin leads to oxidative DNA damage in stellate cells during non-alcoholic steatohepatitis. Cytoglobin (CYGB) is a respiratory protein that acts as a scavenger of reactive oxygen species. Although CYGB is expressed uniquely in hepatic stellate cells (HSCs) in the liver, the molecular role of CYGB in human HSC activation and human liver disease remains uncharacterised. The aim of this study was to reveal the mechanism by which TGF-β1/SMAD2 pathway regulates human (...) CYGB promoter and the pathophysiological function of CYGB in human non-alcoholic steatohepatitis (NASH).Immunohistochemical staining was performed using human NASH biopsy specimens. Molecular and biochemical analysis were performed by western blotting, quantitative PCR, and luciferase and immunoprecipitation assays. Hydroxyl radicals (•OH) and oxidative DNA damage were measured using an •OH-detectable probe and 8-hydroxy-2'-deoxyguanosine (8-OHdG) ELISA.In culture, TGF-β1-pretreated human hepatic

2020 Journal of Hepatology

272. Impact of Alcohol Use Disorder Treatment on Clinical Outcomes Among Patients With Cirrhosis. (Abstract)

Impact of Alcohol Use Disorder Treatment on Clinical Outcomes Among Patients With Cirrhosis. Despite the significant medical and economic consequences of coexisting alcohol use disorder (AUD) in patients with cirrhosis, little is known about AUD treatment patterns and their impact on clinical outcomes in this population. We aimed to characterize the use of and outcomes associated with AUD treatment in patients with cirrhosis.This retrospective cohort study included Veterans with cirrhosis who (...) , 5,088 (14%) received AUD treatment, including 4,461 (12%) who received behavioral therapy alone, 159 (0.4%) who received pharmacotherapy alone, and 468 (1%) who received both behavioral therapy and pharmacotherapy. In adjusted analyses, behavioral and/or pharmacotherapy-based AUD treatment was associated with a significant reduction in incident hepatic decompensation (6.5% vs. 11.6%, adjusted odds ratio [AOR], 0.63; 95% confidence interval [CI], 0.52, 0.76), a nonsignificant decrease in short-term

2020 Hepatology

273. Study of 18 mg Selincro® As-needed Use, in the Treatment of Patients With Alcohol Dependence in Primary Care

: Selincro® 18 mg with continuous psychosocial support: Cohort A Other: Initial psychosocial support: Cohort B Phase 4 Detailed Description: 635 patients are planned (total number of patients) with 475 patients treated with Selincro® (Cohort A) and 160 patients not treated with Selincro® (Cohort B) to determine the reduction in alcohol consumption in patients with alcohol dependence. Cohort A will comprise patients who maintain a high drinking risk level (DRL, defined by World Health Organization (WHO (...) and telephone number. Exclusion Criteria: The patient has one or more contraindications to the prescription of Selincro®: hypersensitivity to the active substance or to any of the excipients taking opioid analgesics current or recent opioid addiction acute symptoms of opioid withdrawal recent use of opioids suspected severe hepatic impairment (Child-Pugh classification) severe renal impairment (eGFR <30 ml/min per 1.73 m2) a recent history of acute alcohol withdrawal syndrome (including hallucinations

2014 Clinical Trials

274. Standard Definitions and Common Data Elements for Clinical Trials in Patients With Alcoholic Hepatitis: Recommendation From the NIAAA Alcoholic Hepatitis Consortia Full Text available with Trip Pro

Standard Definitions and Common Data Elements for Clinical Trials in Patients With Alcoholic Hepatitis: Recommendation From the NIAAA Alcoholic Hepatitis Consortia 26921783 2016 08 08 2019 01 18 1528-0012 150 4 2016 Apr Gastroenterology Gastroenterology Standard Definitions and Common Data Elements for Clinical Trials in Patients With Alcoholic Hepatitis: Recommendation From the NIAAA Alcoholic Hepatitis Consortia. 785-90 10.1053/j.gastro.2016.02.042 S0016-5085(16)00233-X Crabb David W DW (...) , National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland. Sanyal Arun A Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, School of Medicine, Virginia Commonwealth University, Richmond, Virginia. Shah Vijay V Gastroenterology Research Unit, Department of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. Szabo Gyongyi G Division of Gastroenterology, Department of Medicine, University of Massachusetts

2016 Gastroenterology

275. A Prospective study of the utility of plasma biomarkers to diagnose alcoholic hepatitis. Full Text available with Trip Pro

A Prospective study of the utility of plasma biomarkers to diagnose alcoholic hepatitis. The diagnosis of alcoholic hepatitis (AH) often requires a transjugular liver biopsy (TJLB), a procedure that is not always readily accessible. We analyzed plasma biomarkers to estimate the presence of histological features of AH among patients with clinical suspicion of AH. Using enzyme-linked immunosorbent assay, we tested M65 and M30 (circulating fragments of cytokeratin-18) and their respective fraction

2017 Hepatology

276. Ginsenoside Rg1 inhibits inflammatory responses via modulation of the nuclear factor-κB pathway and inhibition of inflammasome activation in alcoholic hepatitis Full Text available with Trip Pro

Ginsenoside Rg1 inhibits inflammatory responses via modulation of the nuclear factor-κB pathway and inhibition of inflammasome activation in alcoholic hepatitis Ginsenoside Rg1 (G‑Rg1) is an active ingredient of Panax ginseng, which has previously been reported to attenuate alcohol‑induced hepatic damage; however, the underlying mechanisms remain largely unknown. The present study aimed to investigate the protective effects of G‑Rg1 on alcohol‑induced cell injury in vitro and on a rat model (...) of alcoholic hepatitis in vivo. For the in vitro model, L‑O2 cells were incubated with ethanol in the presence or absence of G‑Rg1. For the in vivo model, rats were administered ethanol by intragastric injection and were treated with G‑Rg1, or dexamethasone as a control. The results indicated that serum biochemical parameters, including alanine aminotransferase, aspartate aminotransferase and total bilirubin, as well as the expression of nuclear factor (NF)‑κB pathway‑associated inflammatory cytokines

2017 International journal of molecular medicine

277. Hepatic toxicity assessment of cationic liposome exposure in healthy and chronic alcohol fed mice Full Text available with Trip Pro

Hepatic toxicity assessment of cationic liposome exposure in healthy and chronic alcohol fed mice The utilisation of nanoparticles as the means of targeted delivery of therapeutics and/or imaging agents could greatly enhance the specific transport of biologically active payloads to target tissues while avoiding or reducing undesired side-effects. To allow for this to become a reality, the question of potential toxicological effects needs to be addressed. In the present investigation, a cationic (...) or chronically alcohol fed mice. Additionally, the in vitro material-induced adverse effects (cytotoxicity, inflammation or albumin secretion) were all also minimal. The data from this study demonstrated that the intravenous injection of cationic liposomes does not cause hepatic toxicity. This investigation is important as it investigates the toxicity of a nano-sized material in a model of alcoholic hepatic disease in vitro and in vivo. This is an area of research in the field of nanotoxicology

2017 Heliyon

278. [18F]-BMS-747158-02PET imaging for evaluating hepatic mitochondrial complex 1dysfunction in a mouse model of non-alcoholic fatty liver disease Full Text available with Trip Pro

[18F]-BMS-747158-02PET imaging for evaluating hepatic mitochondrial complex 1dysfunction in a mouse model of non-alcoholic fatty liver disease Mitochondrial dysfunction is one of the main causes of non-alcohol fatty liver disease (NAFLD). [18F]-BMS-747158-02 (18F-BMS) which was originally developed as a myocardial perfusion imaging agent was reported to bind mitochondrial complex-1 (MC-1). The aim of this study was to investigate the potential use of 18F-BMS for evaluating hepatic MC-1 activity (...) in mice fed a methionine- and choline-deficient (MCD) diet. Male C57BL/6J mice were fed a MCD diet for up to 2 weeks. PET scans with 18F-BMS were performed after 1 and 2 weeks of the MCD diet. 18F-BMS was intravenously injected into mice, and the uptake (standardized uptake value (SUV)) in the liver was determined. The binding specificity for MC-1 was assessed by pre-administration of rotenone, a specific MC-1 inhibitor. Hepatic MC-1 activity was measured using liver homogenates generated after each

2017 EJNMMI research

279. Alcohol and hepatitis virus-dysregulated lncRNAs as potential biomarkers for hepatocellular carcinoma Full Text available with Trip Pro

analysis of patient samples from The Cancer Genome Atlas database, we identified putative lncRNAs dysregulated in HCC and by its risk factors, hepatitis infection and alcohol consumption. We identified 184 lncRNAs dysregulated in HCC tumors versus paired normal samples, 53 lncRNAs dysregulated in alcohol-drinking patients with hepatitis B, and 5, 456 lncRNAs dysregulated in patients with hepatitis infection. A panel of these candidate lncRNAs' expressions correlated significantly with patient survival (...) Alcohol and hepatitis virus-dysregulated lncRNAs as potential biomarkers for hepatocellular carcinoma Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths because of frequent late detection and poor therapeutic outcomes, necessitating the need to identify effective biomarkers for early diagnosis and new therapeutic targets for effective treatment. Long noncoding RNAs (lncRNAs) have emerged as promising molecular markers for diagnosis and treatment. Through

2017 Oncotarget

280. Hepatic regulation of VLDL receptor by PPARβ/δ and FGF21 modulates non-alcoholic fatty liver disease Full Text available with Trip Pro

Hepatic regulation of VLDL receptor by PPARβ/δ and FGF21 modulates non-alcoholic fatty liver disease The very low-density lipoprotein receptor (VLDLR) plays an important role in the development of hepatic steatosis. In this study, we investigated the role of Peroxisome Proliferator-Activated Receptor (PPAR)β/δ and fibroblast growth factor 21 (FGF21) in hepatic VLDLR regulation.Studies were conducted in wild-type and Pparβ/δ-null mice, primary mouse hepatocytes, human Huh-7 hepatocytes (...) , and liver biopsies from control subjects and patients with moderate and severe hepatic steatosis.Increased VLDLR levels were observed in liver of Pparβ/δ-null mice and in Pparβ/δ-knocked down mouse primary hepatocytes through mechanisms involving the heme-regulated eukaryotic translation initiation factor 2α (eIF2α) kinase (HRI), activating transcription factor (ATF) 4 and the oxidative stress-induced nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathways. Moreover, by using a neutralizing antibody

2017 Molecular metabolism

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>