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Alcoholic Hepatitis

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161. Time course of compromised urea synthesis in patients with alcoholic hepatitis. (Abstract)

Time course of compromised urea synthesis in patients with alcoholic hepatitis. Alcoholic hepatitis (AH) markedly decreases the urea synthesis capacity. We aimed to investigate the time course of this compromised essential liver function in patients with AH and its relation to treatment and survival.Thirty patients with AH were included in a prospective cohort study. We measured the substrate-independent urea synthesis capacity, i.e., the functional hepatic nitrogen clearance (FHNC (...) ), in the patients at study entry and again at three months (survivors/available: n = 17). Patients with severe disease (Glasgow Alcoholic Hepatitis Score ≥9, n = 17) were randomized to receive either prednisolone or pentoxifylline and were in addition examined after 14 days (n = 9).FHNC (normal range = 25-45 L/h) was markedly decreased at study entry (median = 5.6 (IQR = 3.0-9.6) L/h) and increased by three-fold in survivors at three months (15.1 (12.0-22.9) L/h; p < .001). In patients with severe AH, FHNC

2018 Scandinavian journal of gastroenterology Controlled trial quality: uncertain

162. Prevalence, severity and mortality associated with alcoholic hepatitis and drinking in patients with COVID-19: a systematic review and meta-analysis

Prevalence, severity and mortality associated with alcoholic hepatitis and drinking in patients with COVID-19: a systematic review and meta-analysis Print | PDF PROSPERO This information has been provided by the named contact for this review. CRD has accepted this information in good faith and registered the review in PROSPERO. The registrant confirms that the information supplied for this submission is accurate and complete. CRD bears no responsibility or liability for the content

2020 PROSPERO

163. Efficacy of granulocyte colony-stimulating factor therapy in patients with severe alcoholic hepatitis

Efficacy of granulocyte colony-stimulating factor therapy in patients with severe alcoholic hepatitis Print | PDF PROSPERO This information has been provided by the named contact for this review. CRD has accepted this information in good faith and registered the review in PROSPERO. The registrant confirms that the information supplied for this submission is accurate and complete. CRD bears no responsibility or liability for the content of this registration record, any associated files

2020 PROSPERO

164. The hepatic BMAL1/AKT/Lipogenesis axis protects against alcoholic liver disease via promoting PPARα pathway. Full Text available with Trip Pro

The hepatic BMAL1/AKT/Lipogenesis axis protects against alcoholic liver disease via promoting PPARα pathway. Alcohol liver disease (ALD) is one of the major chronic liver diseases worldwide, ranging from fatty liver, alcoholic hepatitis, cirrhosis, and potentially, hepatocellular carcinoma. Epidemiological studies suggest a potential link between ALD and impaired circadian rhythms, but the role of hepatic circadian proteins in the pathogenesis of ALD remains unknown. Here we show (...) hepatic fatty acid oxidation but also alleviates ethanol-induced fatty liver and liver injury. Furthermore, hepatic over-expression of lipogenic transcription factor ChREBP, but not SREBP-1c, in the liver of Bmal1-LKO mice also increases fatty acid oxidation and partially reduces ethanol-induced fatty liver and liver injury.we identified a novel protective role of BMAL1 in hepatocytes against ALD. The protective action of BMAL1 during alcohol consumption depends on its ability to couple ChREBP-induced

2018 Hepatology

165. Alcohol-dysregulated microRNAs in hepatitis B virus-related hepatocellular carcinoma. Full Text available with Trip Pro

Alcohol-dysregulated microRNAs in hepatitis B virus-related hepatocellular carcinoma. Alcohol consumption and chronic hepatitis B virus (HBV) infection are two well-established risk factors for Hepatocellular carcinoma (HCC); however, there remains a limited understanding of the molecular pathway behind the pathogenesis and progression behind HCC, and how alcohol promotes carcinogenesis in the context of HBV+ HCC. Using next-generation sequencing data from 130 HCC patients and 50 normal liver (...) tissues, we identified a panel of microRNAs that are significantly dysregulated by alcohol consumption in HBV+ patients. In particular, two microRNAs, miR-944 and miR-223-3p, showed remarkable correlation with clinical indication and genomic alterations. We confirmed the dysregulation of these two microRNAs in liver cell lines treated by alcohol and acetaldehyde, and showed that manipulation of miR-223-3p and miR-944 expression induces significant changes in cellular proliferation, sensitivity

2017 PLoS ONE

166. Human neutrophil peptide-1 promotes alcohol-induced hepatic fibrosis and hepatocyte apoptosis. Full Text available with Trip Pro

of Bcl2 in a concentration-dependent manner in vitro.HNP-1 secreted by neutrophils may exacerbate alcohol-induced hepatic fibrosis and hepatocyte apoptosis with a decrease in Bcl2 expression and an increase in miR-34a-5p expression. (...) Human neutrophil peptide-1 promotes alcohol-induced hepatic fibrosis and hepatocyte apoptosis. Neutrophil infiltration of the liver is a typical feature of alcoholic liver injury. Human neutrophil peptide (HNP)-1 is an antimicrobial peptide secreted by neutrophils. The aim of this study was to determine if HNP-1 affects ethanol-induced liver injury and to examine the mechanism of liver injury induced by HNP-1.Transgenic (TG) mice expressing HNP-1 under the control of a β-actin-based promoter

2017 PLoS ONE

167. DEPTOR Suppresses Lipogenesis and Ameliorates Hepatic Steatosis and Acute-on-Chronic Liver Injury in Alcoholic Liver Disease. Full Text available with Trip Pro

overexpression of hepatic DEPTOR suppressed mTORC1 signaling and ameliorated alcoholic hepatosteatosis, inflammation, and acute-on-chronic liver injury. Mechanistically, the lipid-lowering effect of hepatic DEPTOR was attributable to decreased proteolytic processing, nuclear translocation, and transcriptional activity of the lipogenic transcription factor sterol regulatory element-binding protein-1 (SREBP-1). DEPTOR-dependent inhibition of mTORC1 also attenuated alcohol-induced cytoplasmic accumulation (...) DEPTOR Suppresses Lipogenesis and Ameliorates Hepatic Steatosis and Acute-on-Chronic Liver Injury in Alcoholic Liver Disease. Alcoholic liver disease (ALD) is characterized by lipid accumulation and liver injury. However, how chronic alcohol consumption causes hepatic lipid accumulation remains elusive. The present study demonstrates that activation of the mechanistic target of rapamycin complex 1 (mTORC1) plays a causal role in alcoholic steatosis, inflammation, and liver injury. Chronic-plus

2018 Hepatology

168. The prognostic value of Acute-on-Chronic Liver Failure during the course of severe alcoholic hepatitis. (Abstract)

The prognostic value of Acute-on-Chronic Liver Failure during the course of severe alcoholic hepatitis. A better identification of factors predicting death is needed in alcoholic hepatitis (AH). Acute-on-chronic liver failure (ACLF) occurs during the course of liver disease and can be identified when AH is diagnosed (prevalent ACLF [pACLF]) or during follow-up (incidental ACLF [iACLF]). This study analyzed the impact of ACLF on outcomes in AH and the role of infection on the onset of ACLF (...) the course of severe alcoholic hepatitis. In severe alcoholic hepatitis, acute-on-chronic liver failure is associated with high mortality and frequently occurs after an infection.Copyright © 2018 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

2018 Journal of Hepatology

169. Aflatoxin B<sub>1</sub> exposure increases the risk of hepatocellular carcinoma associated with hepatitis C virus infection or alcohol consumption. Full Text available with Trip Pro

Aflatoxin B1 exposure increases the risk of hepatocellular carcinoma associated with hepatitis C virus infection or alcohol consumption. Hepatocarcinogenicity of aflatoxin B1 (AFB1) has rarely been studied in populations with hepatitis C virus (HCV) infection and those without hepatitis B virus (HBV) and HCV infection (non-B-non-C). This case-control study nested in a community-based cohort aimed to investigate the HCC risk associated with AFB1 in HCV-infected and non-B-non-C (...) )], but not in non-B-non-C participants without alcohol drinking habit. AFB1 exposure remained an independent risk predictor for HCV-related HCC after adjustment for other HCC predictors (multivariate-adjusted OR [95% CI], 3.65 [1.32-10.10]).AFB1 exposure contributes to the development of HCC in participants with significant risk factors for cirrhosis including alcohol and HCV infection.Copyright © 2018 Elsevier Ltd. All rights reserved.

2018 European Journal of Cancer

170. Periodontitis is associated with significant hepatic fibrosis in patients with non-alcoholic fatty liver disease. Full Text available with Trip Pro

Periodontitis is associated with significant hepatic fibrosis in patients with non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease (NAFLD) has a bidirectional association with metabolic syndrome. It affects up to 30% of the general population, 70% of individuals with diabetes and 90% with obesity. The main histological hallmark of progressive NAFLD is fibrosis. There is a bidirectional epidemiological link between periodontitis and metabolic syndrome. NAFLD, periodontitis (...) -based study, consenting patients with biopsy-proved NAFLD (or with liver indices too mild to justify biopsy) underwent dental examination. Basic Periodontal Examination score was recorded.In NHANES, periodontitis was significantly associated with steatosis in 8172 adults even after adjusting for sociodemographic factors. However, associations were fully explained after accounting for features of metabolic syndrome. In the patient-based study, periodontitis was significantly more common in patients

2017 PLoS ONE

171. Improvement of Hepatic Fibrosis and Patient-Reported Outcomes in Non-Alcoholic Steatohepatitis Treated with Selonsertib. (Abstract)

Improvement of Hepatic Fibrosis and Patient-Reported Outcomes in Non-Alcoholic Steatohepatitis Treated with Selonsertib. Patient-reported outcomes (PROs) represent patients' perspective about their well-being.To assess PRO changes in patients with non-alcoholic steatohepatitis (NASH) after treatment with selonsertib (SEL) and to associate them with different biomarkers.Patients with NASH and stage 2-3 fibrosis received SEL 6 mg or 18 mg orally QD alone or in combination with simtuzumab (SIM (...) -0.24 to -0.38, P < .05).A decrease in hepatic collagen is the most prominently associated with improvement of PROs in NASH patients with F2-F3 treated with SEL. Furthermore, serum cytokines are associated with baseline PROs and with treatment-emergent changes in PROs in patients with NASH.© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

2018 Liver International Controlled trial quality: uncertain

172. Liver Transplantation for Severe Alcoholic Hepatitis, Updated Lessons from the World's Largest Series. Full Text available with Trip Pro

Liver Transplantation for Severe Alcoholic Hepatitis, Updated Lessons from the World's Largest Series. Six-month sobriety before transplantation for alcoholic liver disease is typically required but poorly supported by data. We initiated a pilot program after a report of liver transplantation for severe alcoholic hepatitis (SAH) in which the 6-month rule was waived. We previously reported early outcomes; we now provide longer follow-up in the largest cohort of early liver transplantation (...) infection, malignancy, and rejection.Compared with patients with alcoholic cirrhosis, SAH patients were younger and with shorter drinking history and higher Model for End-Stage Liver Disease scores at listing and at transplantation. Of these patients, 46% received preoperative steroids; all were nonresponders by Lille score. At a median follow-up time of 532 days (interquartile range 281 to 998 days), there were no significant differences between groups by log-rank testing of Kaplan-Meier estimates

2018 Journal of the American College of Surgeons

173. Efficacy of Granulocyte Colony Stimulating Factor and N-acetyl Cysteine Therapies in Patients with Severe Alcoholic Hepatitis. Full Text available with Trip Pro

Efficacy of Granulocyte Colony Stimulating Factor and N-acetyl Cysteine Therapies in Patients with Severe Alcoholic Hepatitis. Patients with alcoholic hepatitis (AH) have high mortality, so new therapies are needed. Administration of granulocyte colony stimulating factor (G-CSF) increases survival times of patients with AH. It is not known whether addition of N-acetyl cysteine (NAC) to G-CSF could further increase survival time. We performed a randomized controlled pilot study to compare

2018 Clinical Gastroenterology and Hepatology Controlled trial quality: predicted high

174. Root bark of Ulmus davidiana var. japonica restrains acute alcohol-induced hepatic steatosis onset in mice by inhibiting ROS accumulation. Full Text available with Trip Pro

Root bark of Ulmus davidiana var. japonica restrains acute alcohol-induced hepatic steatosis onset in mice by inhibiting ROS accumulation. Alcohol-induced hepatic steatosis and inflammation are key drivers of alcohol-induced liver injury, mainly caused by oxidative stress. The roots bark of Ulmus davidiana var. japonica is well known for its substantial antioxidative and antitumorigenic potency. In this study, we examined whether this plant can ameliorate alcohol-induced liver injuries (...) characterized by hepatic steatosis and inflammation through its antioxidative activity. C57BL/6J mice were treated with the root bark extract of Ulmus davidiana var. japonica (RUE; 100 mg of extract/kg bodyweight; oral gavage) and alcohol (1 g/kg of bodyweight; oral gavage) for 5 days. Markers of acute alcohol-induced hepatic steatosis were determined and putative molecular mechanisms responsible for the protection of RUE were investigated. RUE noticeably protected against alcohol-induced hepatic steatosis

2017 PLoS ONE

175. Evaluation of the effects of dapagliflozin, an SGLT2 inhibitor, on hepatic steatosis and fibrosis by transient elastography in patients with type 2 diabetes and non-alcoholic fatty liver disease. (Abstract)

Evaluation of the effects of dapagliflozin, an SGLT2 inhibitor, on hepatic steatosis and fibrosis by transient elastography in patients with type 2 diabetes and non-alcoholic fatty liver disease. To investigate the effects of dapagliflozin on liver steatosis and fibrosis evaluated in patients with type 2 diabetes and non-alcoholic fatty liver disease (NAFLD).In a randomized, active-controlled, open-label trial, 57 patients with type 2 diabetes and NAFLD were randomized to a dapagliflozin group (...) (5 mg/d; n = 33) or a control group (n = 24) and were treated for 24 weeks. Hepatic steatosis and fibrosis were assessed using transient elastography to measure controlled attenuation parameter (CAP) and liver stiffness, respectively.Baseline liver stiffness measurement (LSM) was positively correlated with several markers and scoring systems for liver fibrosis. In week 24, there was a significant decrease in CAP from 314 ± 61 to 290 ± 73 dB/m (P = 0.0424) in the dapagliflozin group, while

2018 obesity & metabolism Controlled trial quality: uncertain

176. Bile acid homeostasis and intestinal dysbiosis in alcoholic hepatitis. Full Text available with Trip Pro

Bile acid homeostasis and intestinal dysbiosis in alcoholic hepatitis. Intestinal microbiota plays an important role in bile acid homeostasis.To study the structure of the intestinal microbiota and its function in bile acid homeostasis in alcoholic patients based on the severity of alcoholic liver disease.In this prospective study, we included four groups of active alcoholic patients (N = 108): two noncirrhotic, with (noCir_AH, n = 13) or without alcoholic hepatitis (noCir_noAH, n = 61 (...) ), and two cirrhotic, with (Cir_sAH, n = 17) or without severe alcoholic hepatitis (Cir_noAH, n = 17). Plasma and faecal bile acid profiles and intestinal microbiota composition were assessed.Plasma levels of total bile acids (84.6 vs 6.8 μmol/L, P < 0.001) and total ursodeoxycholic acid (1.3 vs 0.3 μmol/L, P = 0.03) were higher in cirrhosis with severe alcoholic hepatitis (Cir_sAH) than Cir_noAH, whereas total faecal (2.4 vs 11.3, P = 0.01) and secondary bile acids (0.7 vs 10.7, P < 0.01) levels were

2018 Alimentary Pharmacology & Therapeutics

177. A Validated Score Predicts Acute Kidney Injury and Survival in Patients with Alcoholic Hepatitis: A Multicentric International Prospective Cohort Study. Full Text available with Trip Pro

A Validated Score Predicts Acute Kidney Injury and Survival in Patients with Alcoholic Hepatitis: A Multicentric International Prospective Cohort Study. Identifying patients at high risk for acute kidney injury (AKI) during hospitalization among patients admitted with severe alcoholic hepatitis (AH) is an unmet clinical need. We performed a multicentric prospective cohort study using data from 4 different cohorts on well-characterized patients hospitalized with severe AH. Data collected on 773 (...) AH patients from 4 cohorts across the globe were randomly split into test (n = 390) and validation (n = 383) cohorts. We found that 32% of the patients developed inpatient AKI in the test cohort. Approximately 60% of patients met criteria for systemic inflammatory response syndrome (SIRS) at admission. Hepatic encephalopathy, SIRS, and Model for End-Stage Liver Disease score at admission predicted inpatient AKI with odds ratios of 3.86, 2.24, and 1.14, respectively. The AKI risk score developed

2018 Liver Transplantation

178. Survey of Liver Transplantation Practices for Severe Acute Alcoholic Hepatitis. Full Text available with Trip Pro

Survey of Liver Transplantation Practices for Severe Acute Alcoholic Hepatitis. Liver transplantation (LT) has a demonstrated survival benefit in select patients with severe acute alcoholic hepatitis (SAH) who do not respond to steroids, but prior studies suggest low adoption among US LT centers. Our study explored current perceptions and practice patterns of LT for SAH in the United States. We administered a Web-based survey to medical directors of US LT centers between May and October of 2017 (...) psychiatric disorder (91.3%), and official psychosocial evaluation (87.0%). Reported posttransplant survival of SAH patients was excellent, with 17 (73.9%) centers reporting 1-year posttransplant survival exceeding 90%. Among centers that had not performed LT for SAH, the most commonly cited reason was perceived high risk of alcohol relapse. In conclusion, our data demonstrate that LT is increasingly adopted as a therapeutic intervention for patients with SAH and that careful selection allows

2018 Liver Transplantation

179. Effect of prebiotics, probiotics and symbiotic on the treatment of non alcoholic fat hepatic disease:a systematic review

Effect of prebiotics, probiotics and symbiotic on the treatment of non alcoholic fat hepatic disease:a systematic review Print | PDF PROSPERO This information has been provided by the named contact for this review. CRD has accepted this information in good faith and registered the review in PROSPERO. The registrant confirms that the information supplied for this submission is accurate and complete. CRD bears no responsibility or liability for the content of this registration record, any

2020 PROSPERO

180. Outcomes After Hepatic Resection for Hepatocellular Carcinoma in Non-Alcoholic Fatty Livers. A Systematic Review and Meta-Analysis

Outcomes After Hepatic Resection for Hepatocellular Carcinoma in Non-Alcoholic Fatty Livers. A Systematic Review and Meta-Analysis Print | PDF PROSPERO This information has been provided by the named contact for this review. CRD has accepted this information in good faith and registered the review in PROSPERO. The registrant confirms that the information supplied for this submission is accurate and complete. CRD bears no responsibility or liability for the content of this registration record

2020 PROSPERO

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