IDENTIFICATION OF A REGULATORY VARIANT IN A LONG NONCODING RNA THAT INFLUENCES EXPRESSION OF EXOC3L4 AS A RISK FACTOR FOR CHOLESTATIC-MIXED DRUG-INDUCED LIVER INJURY

<div><p><strong>Background</strong>: Genetic factors associated with DILI susceptibility have been observed to be largely drug specific. The aim of this study was to identify novel risk factors for Cholestatic-Mixed Drug Induced Liver Injury (CM-DILI).</p>

FOUR-YEAR OVERALL SURVIVAL UPDATE FROM THE PHASE 3 HIMALAYA STUDY OF TREMELIMUMAB PLUS DURVALUMAB IN UNRESECTABLE HEPATOCELLULAR CARCINOMA

<div><p><b>Background:</p> </b><p>In the primary analysis (data cut-off: 27 August 2021) of the phase 3 HIMALAYA study (NCT03298451) in unresectable hepatocellular carcinoma (uHCC), STRIDE (Single Tremelimumab Regular Interval Durvalumab) significantly improved overall survival (OS) and demonstrated a durable long-term survival benefit versus sorafenib; durvalumab monotherapy was noninferior to sorafenib (Abou-Alfa et al. <em>NEJM Evid</em> 2022). Here, we report an updated 4-year OS analysis of HIMALAYA.</p>

SERUM PROTEOMICS REVEALS UNIQUE ASSOCIATION OF CCL24 WITH DISEASE-RELATED PATHWAYS AND SIGNATURES IN PRIMARY SCLEROSING CHOLANGITIS

<div><p><b>Background: </b>Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by inflammation and fibrosis of the bile ducts.<strong> </strong>CCL24 (Eotaxin-2) is a chemokine that promotes inflammation and fibrosis and is overexpressed in the liver of patients with PSC, particularly in areas with biliary injury. Previous studies showed that blocking CCL24 interferes with core pathways that contribute to PSC pathophysiology in preclinical models.

Addition of rifaximin to broad-spectrum antibiotics has no beneficial role in critically ill cirrhosis patients with acute overt hepatic encephalopathy- A double-blind, randomized controlled trial

<div><p><b>Background: </b>Critically ill cirrhosis (CIC) patients admitted to the intensive care unit (ICU) are usually on broad-spectrum intravenous antibiotics due to suspected infection or as a protocol. Few reports have suggested rifaximin to be beneficial in acute overt hepatic encephalopathy (OHE). However, the role of rifaximin in patients on broad-spectrum antibiotics admitted to ICU is still unclear. Therefore, we aimed to assess the efficacy of addition of rifaximin to broad-spectrum antibiotics for CIC patients admitted to ICU for OHE.</p>

ER-ASSOCIATED PROTEIN DEGRADATION AS A POTENTIAL ANTI-FIBROTIC TARGET IN HEPATIC STELLATE CELLS

<div><p><b>Background: </b>Liver injury activates hepatic stellate cells (HSCs) which drive fibrosis through secreting extracellular matrix proteins. Proteins destined for secretion are cotranslationally translocated into the endoplasmic reticulum (ER), folded, and exported for secretion. Activated HSCs exhibit increased protein translation leading to ER stress, which is sensed by ER membrane proteins Activating transcription factor 6 (ATF6α), Inositol-requiring enzyme 1 (IRE1α), and Protein kinase R-like ER kinase (PERK).

POSITIVE RESULTS FROM THE ALPINE 4 STUDY: A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED, MULTICENTER, PHASE 2b TRIAL EVALUATING MULTIPLE DOSES OF THE FGF19 ANALOGUE ALDAFERMIN IN PATIENTS WITH COMPENSATED CIRRHOSIS DUE TO NONALCOHOLIC STEATOHEPATITIS

<div><p><b>Background: </b>Patients with<strong> </strong>cirrhosis are at increased risk of liver decompensation and HCC which can result in liver transplant or death. There is no available therapy and previous clinical trials have failed to show a benefit in patients with NASH and cirrhosis. Aldafermin, an engineered analog of the human hormone FGF19, improved liver histology in previous non-cirrhotic, phase 2 trials.

GENETIC ABLATION OF CD4 T CELLS IN MICE ATTENUATES LIVER INJURY, INFLAMMATION, AND FIBROSIS IN NONALCOHOLIC STEATOHEPATITIS

<div><p><strong><b>Background:</strong> </b>Nonalcoholic steatohepatitis<strong> </strong>(NASH) is a progressive condition characterized by excessive inflammation, which may lead to fibrosis. To date, the contribution of T cells to NASH remains largely unexplored. Our unpublished data suggest that CD4 T cells with pathogenic Th1 phenotype accumulate in murine NASH livers. Therefore, we investigated the role of CD4 T lymphocytes in NASH development.</p>

SINGLE-CELL ANALYSIS OF LIVER FINE NEEDLE ASPIRATES REVEALS DIFFERENCES IN GENE EXPRESSION BETWEEN CHRONIC HBV-MONOINFECTED VERSUS HBV/HIV-COINFECTED ADULTS

<div><p><b>Background: </b>HIV infection accelerates the natural history of HBV-related liver disease. The <span>mechanisms by which this occurs </span>are incompletely understood due to limited access to comparable groups of people living with HBV with/without HIV and lack of access to the liver compartment.

SIMULTANEOUS LIVER TRANSPLANT AND SLEEVE GASTRECTOMY IS A SAFE SURGICAL OPTION THAT IMPROVES METABOLIC SYNDROME AND REDUCES ALLOGRAFT STEATOSIS

<div><p><b>Background: </b>The prevalence of obesity and metabolic syndrome (MS) is rising dramatically among liver transplant (LT) candidates, many of whom have NASH. Following LT, untreated MS often causes recurrent NAFLD and NASH. Several small case series describe bariatric surgery pre-, post-, or concurrently with LT as a treatment for MS. We reviewed our experience with LT and concurrent sleeve gastrectomy (LTSG) with aims to determine long-term safety, efficacy, and impact on progression of MS and liver disease after transplantation.</p>

LOW ANTIVIRAL TREATMENT RATE FOR PATIENTS WITH HEPATITIS C (HCV)-RELATED HEPATOCELLULAR CARCINOMA (HCC)– A REAL-WORLD NATIONWIDE U.S. STUDY

<div><p><b>Background: </b>All-oral interferon-free direct-acting antiviral agents (DAAs) for treatment and cure of hepatitis C virus (HCV) became available in 2013-2014. Our primary objective is to determine the proportion of patients with HCV-related HCC who received DAA after 2014 and factors associated with treatment receipt. We also evaluated DAA treatment impact on the overall survival in this population as a secondary outcome.</p>

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