RISK AND PREDICTORS OF HEPATIC DECOMPENSATION IN GREY ZONE PATIENTS BY THE BAVENO VII CRITERIA: A COMPETING RISK ANALYSIS

<div><p><b>Background: </b>Baveno VII was proposed for non-invasive identification of clinically significant portal hypertension. However, a substantial proportion of patients is classified in the grey zone (i.e., liver stiffness 15-24.9 kPa and/or platelet count &lt;150 &#215;10<sup>9</sup>/L). We aimed to evaluate the risk and predictors of hepatic decompensation in grey zone patients and determine the prognostic role of spleen stiffness measurement (SSM).</p>

SAFETY AND EFFICACY OF DAPAGLIFLOZIN IN RECURRENT ASCITES: A PILOT STUDY

<div><p><b>Background:<a href="The pathophysiology of ascites in cirrhosis entails vasodilatation with the consequential activation of sympathetic nervous system and renin-angiotensin-aldosterone system, leading to retention of sodium and water. Dapagliflozin, a sodium glucose linked transporter-2 inhibitor, induces natriuresis and is beneficial in patients with heart failure. We hypothesised that a similar natriuretic effect may improve mobilization of ascites in patients with cirrhosis.

IMMUNOLOGICAL PROFILE ASSOCIATED WITH SEX DISPARITY OF CHOLESTATIC LIVER INJURY IN Mdr2-/- MICE

<div><p><b>Background: </b>Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterized by inflammation, bile duct proliferation, and hepatic fibrosis, with a high risk for liver cancer. Multi-drug resistance 2-deficient (Mdr2<sup>-/-</sup>) mice have been widely used as a PSC model. These mice spontaneously develop fibrosis as early as 6-8 weeks and liver tumors at 10-12 months.

TARGETING OF INFLAMMATORY MONOCYTES VIA CCL2/CCR2 SIGNALING AS A THERAPEUTIC STRATEGY AGAINST AUTOIMMUNE HEPATITIS BY USING MACROPHAGE-DERIVED EXTRACELLULAR VESICLES

<div><p><b>Background: </b>Autoimmune hepatitis is a serious chronic liver disease with immune disorders, histological lesions and liver dysfunction, with a gradually increasing prevalence. Yet the cellular and molecular mechanisms of immune dysregulation in AIH are poorly understood.</p>

DEEP PHENOTYPING OF TM6SF2 TO CHARACTERIZE HEPATIC STEATOSIS, PLASMA LIPID TRAITS, AND METABOLIC RISK FACTORS USING A GENOME-FIRST APPROACH

<div><p><b>Background: </b>An unbiased ‘genome-first’ approach has the potential to expand the understanding of common coding and predicted loss-of-function (pLOF) variants associated with non-alcoholic fatty liver disease (NAFLD). Utilizing this approach, we aimed to uncover the functionality of pathogenic variants in <em>TM6SF2</em>.</p>

ANALYSIS OF IMMUNE-RELATED ADVERSE EVENTS AND TIME-TO-TREATMENT DISCONTINUATION OF ATEZOLIZUMAB AND BEVACIZUMAB IN PATIENTS WITH HEPATOCELLULAR CARCINOMA: A MULTICENTER COHORT STUDY

<div><p><b>Background:</p> </b><p>Pragmatic endpoints, such as time-to-treatment discontinuation (TTD), defined as the duration from starting a medication to the date of treatment discontinuation or death, have been proposed as a potential efficacy endpoint for real-world practice. This study aims to analyze the frequency and severity of immune-related adverse events (irAEs) and TTD in patients with hepatocellular carcinoma (HCC) receiving Atezolizumab and Bevacizumab (A+B) treatment.</p>

DAILY ASPIRIN THERAPY FOR THE TREATMENT OF METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE: A RANDOMIZED CONTROLLED TRIAL

<div><p><b>Background: </b>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic, progressive disease with substantial morbidity and mortality and no approved treatments. Observational studies have linked aspirin use to reduced prevalence and progression of MASLD. However, the efficacy and safety of aspirin for reducing hepatic steatosis, inflammation, and fibrosis in patients with MASLD are unknown.</p>

MITOCHONDRIAL Ca2+ UNIPORTER (MCU) IN HEPATOCYTES BUT NOT IN KUPFFER CELLS PROMOTES LIVER INJURY INDUCED BY ACETAMINOPHEN (APAP)

<div><p><b>Background: </b>Iron-catalyzed formation of reactive oxygen species (ROS) increases after APAP overdose and triggers the mitochondrial permeability transition (MPT). Previous studies show that iron translocation from lysosomes into mitochondria by MCU in hepatocytes promotes the MPT after APAP. Kupffer cells are liver resident macrophages that are involved in uptake, processing, and export of iron. Here, our Aim was to investigate and compare the roles of MCU in hepatocytes and Kupffer cells in APAP hepatotoxicity. </p>

HUMAN-CORRELATED GENETIC HCC MODELS IDENTIFY COMBINATION THERAPY FOR PRECISION MEDICINE

<div><p><b>Background:</p> </b><p>Hepatocellular carcinoma (HCC) is a major cause of mortality worldwide. Providing precision medicine to patients is a key unmet need. Preclinical models, when accurately reflecting human disease, offer an opportunity to understand varying therapeutic responses between different patient groups.</p>

PRELIMINARY OFF-TREATMENT RESPONSES FOLLOWING 48 WEEKS OF VEBICORVIR, NUCLEOS(T)IDE REVERSE TRANSCRIPTASE INHIBITOR, AND AB-729 COMBINATION IN VIROLOGICALLY SUPPRESSED PATIENTS WITH HEPATITIS B E ANTIGEN NEGATIVE CHRONIC HEPATITIS B: ANALYSIS FROM AN OPEN

<div><p><b>Background:</p> </b><p>This open-label study assessed the safety and efficacy of vebicorvir (VBR)+AB-729+nucleos(t)ide reverse transcriptase inhibitor (NrtI) in virologically suppressed (VS) patients (pts) with hepatitis B e antigen (eAg) negative chronic hepatitis B infection (NCT04820686). VBR is a 1st-generation core inhibitor and AB-729 is a single trigger GalNAc-siRNA targeting all HBV RNA transcripts. Initial end of treatment (EOT) responses were previously described.

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