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Alcoholic Hepatitis

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241. Metabolic syndrome, but not non-alcoholic fatty liver disease, increases 10-year mortality: A prospective, community-cohort study. (Abstract)

Metabolic syndrome, but not non-alcoholic fatty liver disease, increases 10-year mortality: A prospective, community-cohort study. Data on outcomes of non-alcoholic fatty liver disease (NAFLD) from South Asia are lacking. We compared mortality, among those with- and without-NAFLD, after 10-years follow-up among urban, adult Sri Lankans.Participants (aged 35-64 years), selected by age-stratified random sampling, were screened by structured-interview in 2007. Anthropometric measurements, liver (...) ultrasonography and biochemical/serological tests were done. NAFLD was diagnosed on ultrasound criteria, safe-alcohol consumption (Asian-standards) and absence of hepatitis B/C. Subjects without NAFLD were those without any ultrasound criteria of fatty liver, safe-alcohol consumption and absence of hepatitis B/C. The cohort was re-evaluated to assess mortality in 2017. Participants or their households were contacted by telephone/post, and deaths confirmed by home-visits and death certificate review. Cox

2020 Liver International

242. A diabetologist's perspective of non-alcoholic steatohepatitis (NASH): Knowledge gaps and future directions. Full Text available with Trip Pro

A diabetologist's perspective of non-alcoholic steatohepatitis (NASH): Knowledge gaps and future directions. There is a close link between steatohepatitis (NASH) and Type 2 diabetes (T2DM). Recently, the American Diabetes Association (ADA) recommended screening for NASH and advanced fibrosis in patients with diabetes and hepatic steatosis or elevated plasma alanine aminotransferase (ALT). This is because as many as ~30% to 40% may have NASH and ~10% to 15% advanced fibrosis. The role

2020 Liver International

243. Mesenchymal iron deposition is associated with adverse long-term outcome in non-alcoholic fatty liver disease. Full Text available with Trip Pro

Mesenchymal iron deposition is associated with adverse long-term outcome in non-alcoholic fatty liver disease. Approximately one-third of patients with non-alcoholic fatty liver disease (NAFLD) show signs of mild-to-moderate iron overload. The impact of histological iron deposition on the clinical course of patients with NAFLD has not been established.For this retrospective study, 299 consecutive patients with biopsy-proven NAFLD and a mean follow-up of 8.4 (±4.1; range: 0.3-18.0) years were (...) allocated to one of four groups according to presence of hepatic iron in the reticuloendothelial system (RES) and/or hepatocytes (HC): 156 subjects (52%) showed no stainable iron (NONE), 58 (19%) exclusively reticuloendothelial (xRES), 19 (6%) exclusively hepatocellular (xHC) and 66 (22%) showed a mixed (HC/RES) pattern of iron deposition. A long-term analysis for overall survival, hepatic, cardiovascular or extrahepatic-malignant events was conducted. Based on multivariate Cox proportional hazards

2020 Liver International

244. Oxidative Stress Is Associated with Suspected Non-Alcoholic Fatty Liver Disease and All-Cause Mortality in the General Population. Full Text available with Trip Pro

Oxidative Stress Is Associated with Suspected Non-Alcoholic Fatty Liver Disease and All-Cause Mortality in the General Population. Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation, inflammation and an imbalanced redox homeostasis. We hypothesized that systemic free thiol levels, as a proxy of systemic oxidative stress, are associated with NAFLD.Protein-adjusted serum free thiol concentrations were determined in participants from the Prevention of Renal (...) and Vascular End-Stage Disease (PREVEND) cohort study (n=5,562). Suspected NAFLD was defined by the Fatty Liver Index (FLI≥60) and Hepatic Steatosis Index (HSI>36).Protein-adjusted serum free thiols were significantly reduced in subjects with FLI≥60 (n=1,651). In multivariable logistic regression analyses, protein-adjusted serum free thiols were associated with NAFLD (FLI≥60) (OR per doubling of concentration: 0.78 [95% CI 0.64-0.96], P=0.016) even when adjusted for potential confounding factors, including

2020 Liver International

245. Type 2 Diabetes and Metformin Use Associate With Outcomes of Patients With Non-alcoholic Steatohepatitis-related, Child-Pugh A Cirrhosis. (Abstract)

Type 2 Diabetes and Metformin Use Associate With Outcomes of Patients With Non-alcoholic Steatohepatitis-related, Child-Pugh A Cirrhosis. Factors that affect outcomes of patients with non-alcoholic steatohepatitis (NASH) related cirrhosis are unclear. We studied associations of type 2 diabetes, levels of hemoglobin A1c (HbA1c), and use antidiabetic medications with survival and liver-related events in patients with NASH and compensated cirrhosis.We collected data from 299 patients with biopsy (...) -proven NASH with Child-Pugh A cirrhosis from tertiary hospitals in Spain, Australia, Hong Kong, and Cuba, from April 1995 through December 2016. We obtained information on presence of type 2 diabetes, level of HbA1c, and use of antidiabetic medications. Cox proportional and competing risk models were used to estimate and compare rates of transplant-free survival, hepatic decompensation, and hepatocellular carcinoma (HCC).Two-hundred and twelve patients had type 2 diabetes at baseline and 8/87

2020 Clinical Gastroenterology and Hepatology

246. Tolerogenic properties of liver macrophages in non-alcoholic steatohepatitis. (Abstract)

liver macrophages phenotype and costimulatory/inhibitory properties upon exposure to lipopolysaccharide or interleukin 4. We did phagocytosis and antigen presentation assays to investigate liver macrophages function as scavengers and immune response initiators. Using immunofluorescence staining, we further determined, in human liver tissue of patients with simple steatosis, non-alcoholic steatohepatitis and chronic hepatitis B infection, the expression of the co-inhibitory protein CD274 (Programmed (...) -death ligand 1) and major histocompatibility complex (MHC) class II.Both in humans and mice, within chronically inflamed fatty livers, liver macrophages acquired immunomodulatory properties by reducing the expression of MHC class II, and by enhancing co-inhibitory signalling. Liver macrophages circumscribed endotoxin-mediated inflammatory response by upregulating anti-inflammatory genes arginase 1 and interleukin-10. While hepatic macrophages isolated from mice with normal livers were capable

2020 Liver International

247. Dietary fatty acid oxidation is decreased in non-alcoholic fatty liver disease: A palmitate breath test study. (Abstract)

Dietary fatty acid oxidation is decreased in non-alcoholic fatty liver disease: A palmitate breath test study. Hepatic fat excess in non-alcoholic fatty liver disease (NAFLD) reflects an imbalance between fat accumulation and disposal. Conflicting data exist for the role of fatty acid oxidation (FAO), one of the disposal pathways, and have mostly come from the studies delivering fatty acids (FAs) intravenously. Whether FAO of orally provided FAs is affected in NAFLD is unknown.We performed (...) acid oxidation was 27% lower in 43 subjects with NAFLD compared to 11 controls (CPDR 9.5 ± 2.4% vs 13.1 ± 3.7%, P = .0001) and this persisted after correcting for acetate (29.3 ± 10.5 vs 36.6 ± 13.9, P = .03). The decrease in FAO was not because of the delayed transit as the time to peak 13 C detection did not differ between groups (4.9 ± 1.2 hours vs 4.7 ± 0.8 hours, P = .7). Rates of PA oxidation were not correlated with obesity, hepatic or adipose insulin resistance, alanine aminotransferase

2020 Liver International

248. Cytolysin-positive Enterococcus faecalis is not increased in patients with non-alcoholic steatohepatitis. (Abstract)

Cytolysin-positive Enterococcus faecalis is not increased in patients with non-alcoholic steatohepatitis. Several studies show associations between gut bacterial dysbiosis and chronic liver diseases, but causative mechanisms are largely unclear. We recently identified cytolysin, a bacterial exotoxin expressed and secreted by Enterococcus faecalis to cause liver damage in the setting of alcohol-related liver disease. Cytolysin was increased and highly correlated with liver disease severity (...) and mortality in alcoholic hepatitis patients. In this study, we investigated if faecal cytolysin-positivity can be linked to non-alcoholic fatty liver disease, a highly prevalent disease where new biomarkers and treatment targets are urgently needed. In contrast to what we observed in alcoholic hepatitis, only seven out of 96 non-alcoholic fatty liver disease patients were cytolysin-positive, and these patients did not have increased liver disease activity compared with cytolysin-negative patients

2020 Liver International

249. Association of HSD17B13 rs72613567:TA with non-alcoholic fatty liver disease in Hispanics/Latinos. (Abstract)

Association of HSD17B13 rs72613567:TA with non-alcoholic fatty liver disease in Hispanics/Latinos. Non-alcoholic fatty liver disease (NAFLD) disproportionately affects Hispanic/Latinos and rates of NAFLD vary among Hispanics from different background groups. Genetic variants and continental ancestry contribute to NAFLD disparities among Hispanics. We evaluated two newly identified NAFLD-associated single nucleotide polymorphisms of HSD17B13, rs72613567:TA and rs62305723:A in Hispanics (...) /Latinos.Clinical data, genotypes of variants of interest and estimates of continental ancestry were extracted from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) database, which includes a cohort of 16 415 US Hispanic/Latinos. Surrogate endpoints for NAFLD were suspected NAFLD based on unexplained aminotransferase elevation, continuous ALT levels and FIB-4 scores to estimate hepatic fibrosis.In all, 9342 participants were included for analysis. The rs72613567:TA allele was found in 15.3

2020 Liver International

250. Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma. Full Text available with Trip Pro

Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma. Osteopontin, a multifunctional protein and inflammatory cytokine, is overexpressed in adipose tissue and liver in obesity and contributes to the induction of adipose tissue inflammation and non-alcoholic fatty liver (NAFL). Studies performed in both mice and humans also point to a potential role for OPN in malignant transformation and tumour growth. To fully understand the role of OPN (...) on the development of NAFL-derived hepatocellular carcinoma (HCC), we applied a non-alcoholic steatohepatitis (NASH)-HCC mouse model on osteopontin-deficient (Spp1-/- ) mice analysing time points of NASH, fibrosis and HCC compared to wild-type mice.Two-day-old wild-type and Spp1-/- mice received a low-dose streptozotocin injection in order to induce diabetes, and were fed a high-fat diet starting from week 4. Different cohorts of mice of both genotypes were sacrificed at 8, 12 and 19 weeks of age to evaluate

2020 Liver International

251. Prediction of liver fibrosis severity in alcoholic liver disease by human microfibrillar-associated protein 4. Full Text available with Trip Pro

for detection of hepatitis C virus (HCV)-related fibrosis.To evaluate the diagnostic accuracy of MFAP4 to detect ALD-induced fibrosis.We performed a prospective, liver biopsy-controlled study involving 266 patients with prior or current alcohol overuse. Patients were split into a training and a validation cohort.MFAP4 was present in fibrotic hepatic tissue and serum MFAP4 levels increased with fibrosis grade. The area under the receiver operating characteristic curve (AUROC) for detection of cirrhosis (...) Prediction of liver fibrosis severity in alcoholic liver disease by human microfibrillar-associated protein 4. Alcoholic liver disease (ALD) is a public health concern that is the cause of half of all cirrhosis-related deaths. Early detection of fibrosis, ideally in the precirrhotic stage, is a key strategy for improving ALD outcomes and for preventing progression to cirrhosis. Previous studies identified the blood-borne marker human microfibrillar-associated protein 4 (MFAP4) as a biomarker

2020 Liver International

252. Impact of sleeve gastrectomy and Roux-en-Y gastric bypass on biopsy-proven non-alcoholic fatty liver disease. (Abstract)

Impact of sleeve gastrectomy and Roux-en-Y gastric bypass on biopsy-proven non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease (NAFLD)/steatohepatitis (NASH) is the hepatic manifestation of metabolic syndrome. Our aim was to study the long-term effects of sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB) on NAFLD/NASH.Between 2008 and 2015, 3813 patients had an intraoperative liver biopsy performed at the time of primary RYGB and SG at a single academic center

2020 Surgical endoscopy

253. Incretin combination therapy for the treatment of non-alcoholic steatohepatitis. (Abstract)

Incretin combination therapy for the treatment of non-alcoholic steatohepatitis. To test specific mono-agonists to the glucagon-like peptide-1 receptor (GLP-1R), glucagon receptor (GCGR) and glucose-dependent insulinotropic peptide receptor (GIPR), individually and in combination, in a mouse model of diet-induced non-alcoholic steatohepatitis (NASH) and fibrosis in order to decipher the contribution of their activities and potential additive effects to improving systemic and hepatic (...) 1-GCG or 3-GIP alone did not influence body weight, liver lipids and histology, their combination with 2-GLP1 provided additional weight loss, reduction in liver triglycerides and improvement in histological disease activity score. Notably, 4-dual-GLP-1R/GCGR and the triple combination of selective mono-agonists led to a significantly stronger reduction in the histological non-alcoholic fatty liver disease activity score compared to high-dose liraglutide, at the same extent of body weight

2020 obesity & metabolism

254. Elevated fructose and uric acid via aldose reductase contribute to experimental and human alcoholic liver disease. (Abstract)

Elevated fructose and uric acid via aldose reductase contribute to experimental and human alcoholic liver disease. Alcohol-associated liver disease (ALD) is a common chronic liver disease worldwide with high morbidity and mortality, and no FDA-approved therapies. Fructose (dietary or endogenous), its metabolite uric acid, and aldose reductase (AR, the only endogenous enzyme that produces fructose) are strongly associated with the development of non-alcoholic fatty liver disease (NAFLD). However (...) , the role of AR or its metabolites in ALD remains understudied and was examined using human specimens, cultured cells and mouse model systems. We demonstrated for the first time in liver specimens from alcoholic hepatitis (AH) patients, AR upregulation and elevated AR metabolites (sorbitol, fructose, and uric acid) which correlated significantly with (i) increased lipid peroxidation byproducts and ER stress, (ii) decreased protective ER chaperones, and (iii) greater cell death and liver injury. Further

2020 Hepatology

255. Risk of Cirrhosis and Hepatocellular Cancer in Patients with Non-Alcoholic Fatty Liver Disease and Normal Liver Enzymes. (Abstract)

Risk of Cirrhosis and Hepatocellular Cancer in Patients with Non-Alcoholic Fatty Liver Disease and Normal Liver Enzymes. The long term risk of disease for patients with NAFLD in the absence of elevated enzymes is unclear. We conducted a retrospective cohort study utilizing the Corporate Data Warehouse of the Veterans Health Administration. We classified patients into 3 groups: patients with steatosis/normal ALT, steatosis/elevated ALT, and no steatosis/normal ALT. We examined incidence rates (...) (IR) for cirrhosis and hepatocellular carcinoma (HCC) and conducted cause specific hazard models to evaluate the risk of cirrhosis and HCC. We identified 3,522 patients with steatosis/normal ALT, 15,419 patients with steatosis/elevated ALT, and 9,267 patients with no steatosis/normal ALT. Mean age in each group was 58.9, 54.7 and 59.3 years, respectively; over 90% were men. Compared to patients with hepatic steatosis/normal ALT, those with steatosis/elevated ALT were younger and more likely

2020 Hepatology

256. Glutamate signaling in alcoholic fatty liver: « PAS DE DEUX ». (Abstract)

Glutamate signaling in alcoholic fatty liver: « PAS DE DEUX ». Alcoholic liver disease (ALD) is characterized by histological hallmarks including steatosis, inflammation and fibrosis that result from complex interrelated pathophysiological events in the context of chronic alcohol exposure. Several studies have shown that alcohol-induced oxidative stress is a key event in the pathogenesis of ALD. Thus, continuous alcohol exposure is associated with a marked induction of microsomal cytochrome (...) P450 2E1 (CYP2E1) leading to generation of reactive oxygen species (ROS) in hepatocytes that promote depletion of the hepatic antioxidant tripeptide glutathione.This article is protected by copyright. All rights reserved.

2020 Hepatology

257. The L-α-lysophosphatidylinositol/GPR55 system induces the development of non-alcoholic steatosis and steatohepatitis. Full Text available with Trip Pro

unknown.We measured: 1) GPR55 expression in the liver of patients with NAFLD, compared with non-obese individuals without liver disease, as well as animal models with steatosis and non-alcoholic steatohepatitis (NASH); and 2) the effects of LPI and genetic disruption of GPR55 in mice, human hepatocytes and human hepatic stellate cells. Notably, we found that circulating LPI and liver expression of GPR55 were upregulated in patients with NASH. LPI induced- AMP-activated protein kinase (AMPK) activation (...) The L-α-lysophosphatidylinositol/GPR55 system induces the development of non-alcoholic steatosis and steatohepatitis. G protein-coupled receptor 55 (GPR55) is a putative cannabinoid receptor, and l-α-lysophosphatidylinositol (LPI) is its only known endogenous ligand. Although GPR55 has been linked to energy homeostasis in different organs, its specific role in lipid metabolism in the liver and its contribution to the pathophysiology of non-alcoholic fatty liver disease (NAFLD) remains

2020 Hepatology

258. IL-17 signaling in steatotic hepatocytes and macrophages promotes hepatocellular carcinoma in alcohol-related liver disease. (Abstract)

IL-17 signaling in steatotic hepatocytes and macrophages promotes hepatocellular carcinoma in alcohol-related liver disease. Chronic alcohol consumption is a leading risk factor for the development of hepatocellular carcinoma (HCC), which is associated with a marked increase in hepatic expression of pro-inflammatory IL-17A and its receptor IL-17RA.Genetic deletion and pharmacological blocking were used to characterize the role of IL-17A/IL-17RA signaling in the pathogenesis of HCC in mouse (...) (deficient in IL-17RA in hepatic stellate cells). Deletion of Il-17ra in myeloid cells ameliorated tumorigenesis via suppression of pro-tumorigenic/inflammatory and pro-fibrogenic responses in alcohol-fed Il-17raΔMΦ mice. Remarkably, despite a normal inflammatory response, alcohol-fed Il-17raΔHep mice developed the fewest tumors (compared with Il-17raΔMΦ mice), with reduced steatosis and fibrosis. Steatotic IL-17RA-deficient hepatocytes downregulated the expression of Cxcl1 and other chemokines

2020 Journal of Hepatology

259. Long-term outcomes in patients with decompensated alcohol-related liver disease, steatohepatitis and Maddrey's discriminant function <32. Full Text available with Trip Pro

Long-term outcomes in patients with decompensated alcohol-related liver disease, steatohepatitis and Maddrey's discriminant function <32. Patients with alcoholic hepatitis and a modified Maddrey's discriminant function (mDF) <32 have a low risk of short-term mortality. However, few data exist concerning long-term outcomes. The aims of this study were to evaluate 5-year survival rates and to identify predictive factors for long-term prognosis in this patient population.We studied patients (...) from 2 centers who were admitted for hepatic decompensation (ascites, hepatic encephalopathy, or jaundice) and who had histological findings of steatohepatitis and an mDF <32. Clinical and biological parameters were recorded at the time of liver biopsy and alcohol consumption was recorded during follow-up. We performed Cox proportional hazard survival analysis to identify factors associated with 5-year survival.One hundred and twenty-one patients were included (male: 64%, mean age: 51.5 ± 10.3

2020 Journal of Hepatology

260. ARRB1 inhibits non-alcoholic steatohepatitis progression by promoting GDF15 maturation. Full Text available with Trip Pro

ARRB1 inhibits non-alcoholic steatohepatitis progression by promoting GDF15 maturation. Non-alcoholic steatohepatitis (NASH) is associated with the dysregulation of lipid metabolism and hepatic inflammation. The causal mechanism underlying NASH is not fully elucidated. This study investigated the role of β-Arrestin1 (ARRB1) in the progression of NASH.Liver tissue from patients with NASH and controls were obtained to evaluate ARRB1 expression. NASH models were established in Arrb1-knockout (...) , the severity of liver disease in patients with NASH was negatively correlated with ARRB1 expression.ARRB1 acts as a vital regulator in the development of NASH by facilitating the translocation of GDF15 to the Golgi apparatus and its subsequent maturation. Thus, ARRB1 is a potential therapeutic target for the treatment of NASH.Non-alcoholic steatohepatitis (NASH) is associated with the progressive dysfunction of lipid metabolism and a consequent inflammatory response. Decreased ARRB1 is observed in patients

2020 Journal of Hepatology

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