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SERUM Z POLYMER LEVELS AND FACTORS AFFECTING INCREASED LIVER FIBROSIS ARE ASSOCIATED WITH FUTURE SEVERE LIVER DISEASE OUTCOMES IN A PROSPECTIVE COHORT OF ADULTS WITH ALPHA-1-ANTITRYPSIN DEFICIENCY .

Read more about SERUM Z POLYMER LEVELS AND FACTORS AFFECTING INCREASED LIVER FIBROSIS ARE ASSOCIATED WITH FUTURE SEVERE LIVER DISEASE OUTCOMES IN A PROSPECTIVE COHORT OF ADULTS WITH ALPHA-1-ANTITRYPSIN DEFICIENCY .

<div>Background: Outcomes of adults with ZZ alpha-1-antitrypsin deficiency (AATD) liver disease is variable and unpredictable. There is a lack of prospective data, including on the utility of liver biopsy.

FIBROSIS IMPROVEMENT WITH PEGOZAFERMIN TREATMENT IN MASH PATIENTS WITH F4 FIBROSIS: ANALYSIS FROM A 24-WEEK RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED PHASE 2 TRIAL (ENLIVEN)

Read more about FIBROSIS IMPROVEMENT WITH PEGOZAFERMIN TREATMENT IN MASH PATIENTS WITH F4 FIBROSIS: ANALYSIS FROM A 24-WEEK RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED PHASE 2 TRIAL (ENLIVEN)

<div>Background: Metabolic dysfunction-associated steatohepatitis (MASH) patients who have developed stage F4 fibrosis (cirrhosis) are at risk of hepatic decompensation, hepatocellular carcinoma, liver transplant, cardiovascular events, liver and all-cause mortality. There are currently no approved therapies for non-cirrhotic or cirrhotic MASH.

MORTALITY, HEPATIC DECOMPENSATION, AND CARDIOVASCULAR OUTCOMES IN LEAN VS. NON-LEAN MASH CIRRHOSIS: A VETERANS AFFAIRS COHORT STUDY

Read more about MORTALITY, HEPATIC DECOMPENSATION, AND CARDIOVASCULAR OUTCOMES IN LEAN VS. NON-LEAN MASH CIRRHOSIS: A VETERANS AFFAIRS COHORT STUDY

<div>Background: Studies on incident liver and cardiovascular outcomes in lean (body mass index: BMI <25 kg/m2, or <23 kg/m2 for Asians) vs. non-lean individuals with metabolic dysfunction-associated steatohepatitis (MASH) have reported mixed results. We aimed to compare incident clinical outcomes and mortality between lean and non-lean individuals with compensated MASH cirrhosis in a large national cohort.

MULTI-ANCESTRY WHOLE GENOME SEQUENCING (WGS) AND META-ANALYSIS TO IDENTIFY LOCI ASSOCIATED WITH METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

Read more about MULTI-ANCESTRY WHOLE GENOME SEQUENCING (WGS) AND META-ANALYSIS TO IDENTIFY LOCI ASSOCIATED WITH METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

<div>Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of chronic liver disease in the US. Notably, disease prevalence differs greatly by race/ethnicity, with the highest prevalence in those of Hispanic and Asian ancestry, and the lowest prevalence in those of African ancestry. To date, studies have identified common variants associated with MASLD in predominantly European or American populations.

RELATIONSHIP OF NON-INVASIVE MEASURES WITH HISTOLOGICAL RESPONSE IN PATIENTS WITH NONALCOHOLIC STEATOHEPATITIS AND FIBROSIS: 52-WEEK DATA FROM THE PHASE 3 MAESTRO-NASH TRIAL

Read more about RELATIONSHIP OF NON-INVASIVE MEASURES WITH HISTOLOGICAL RESPONSE IN PATIENTS WITH NONALCOHOLIC STEATOHEPATITIS AND FIBROSIS: 52-WEEK DATA FROM THE PHASE 3 MAESTRO-NASH TRIAL

<div>Background: MAESTRO-NASH (NCT03900429) is an ongoing 54-month, randomized, double-blind, placebo-controlled Phase 3 trial evaluating the efficacy of resmetirom in patients with biopsy-confirmed nonalcoholic steatohepatitis (NASH) and fibrosis. 966 patients with biopsy-confirmed NASH were randomized 1:1:1 to resmetirom 80mg, resmetirom 100mg, or placebo administered once daily. Histologic endpoints were assessed after 52 weeks.

PNPLA3 GENOTYPES ARE SIGNIFICANTLY ASSOCIATED WITH LIVER-RELATED OUTCOMES IN INDIVIDUALS WITH BIOPSY-PROVEN NONALCOHOLIC FATTY LIVER DISEASE (NAFLD)

Read more about PNPLA3 GENOTYPES ARE SIGNIFICANTLY ASSOCIATED WITH LIVER-RELATED OUTCOMES IN INDIVIDUALS WITH BIOPSY-PROVEN NONALCOHOLIC FATTY LIVER DISEASE (NAFLD)

<div>Background: The effect of PNPLA3 rs738409 I148M variant (G allele) on the clinical course of adults with biopsy-proven nonalcoholic fatty liver disease (NAFLD) has not been prospectively investigated. We examined (1) the association between PNPLA3 G allele and clinical outcomes and (2) how relationships among PNPLA3 G allele, age, and type 2 diabetes mellitus (T2DM) impact clinical outcomes in patients with biopsy-proven NAFLD.

MICROBIAL MONOTHERAPY WITH LEUCONOSTOC SP. LB-P8 IMPROVES INFLAMMATION AND FIBROSIS IN MOUSE MODELS OF PRIMARY SCLEROSING CHOLANGITIS.

Read more about MICROBIAL MONOTHERAPY WITH LEUCONOSTOC SP. LB-P8 IMPROVES INFLAMMATION AND FIBROSIS IN MOUSE MODELS OF PRIMARY SCLEROSING CHOLANGITIS.

<div>Background: PSC is an archetypical example of a disease with an impaired gut-liver axis and PSC patients with or without inflammatory bowel disease exhibit enteric microbial dysbiosis. Gut microbiota produce diverse metabolic products but how microbes influence PSC disease progression is unclear. By screening bacterial species (sp.) in a transwell gut-liver axis model, we identified novel Leuconostoc sp. (LB-P8) that may have anti-fibrotic properties via inhibition of TGF-β/SMAD signaling.

ALBUMIN IS INTERNALIZED BY PRIMARY MONOCYTES USING CLATHRIN-INDEPENDENT ENDOCYTOSIS WHICH IS REQUIRED FOR ITS ANTI-INFLAMMATORY EFFECT.

Read more about ALBUMIN IS INTERNALIZED BY PRIMARY MONOCYTES USING CLATHRIN-INDEPENDENT ENDOCYTOSIS WHICH IS REQUIRED FOR ITS ANTI-INFLAMMATORY EFFECT.

<div>Background: Albumin has been shown to modulate systemic inflammation in patients with decompensated liver cirrhosis receiving infusions of this protein as therapy. Although the anti-inflammatory effect of albumin has been described to be secondary to its internalization into mononuclear leukocytes, the cell type and the mechanism by which albumin is internalized by these immune cells are at present unknown.

ETHANOL-INDUCED REDUCTION IN THE INTESTINAL METHYLATION POTENTIAL PROMOTES TIGHT JUNCTION DISRUPTION: PROTECTION BY BETAINE TREATMENT

Read more about ETHANOL-INDUCED REDUCTION IN THE INTESTINAL METHYLATION POTENTIAL PROMOTES TIGHT JUNCTION DISRUPTION: PROTECTION BY BETAINE TREATMENT

<div>Background: The gut-liver interaction has emerged as a critical component in alcohol-associated liver disease (ALD) pathogenesis. The central mediators are the gut luminal antigens, especially endotoxins that translocate to the liver. This occurs because of (i) compromised gut barrier integrity due to epithelial tight junction (TJ) disruption; and (ii) qualitative/quantitative gut microbiota changes and increased production of pathogenic antigens.

NOVEL MECHANISMS UNDERLYING GUT LEAKINESS AND SYSTEMIC ENDOTOXEMIA IN PROMOTING LIVER FIBROSIS VIA THE GUT-LIVER AXIS AND THE MECHANISTIC PROTECTION OF MELATONIN

Read more about NOVEL MECHANISMS UNDERLYING GUT LEAKINESS AND SYSTEMIC ENDOTOXEMIA IN PROMOTING LIVER FIBROSIS VIA THE GUT-LIVER AXIS AND THE MECHANISTIC PROTECTION OF MELATONIN

<div>Background: Liver fibrosis is the consequence of chronic liver diseases that can progress to cirrhosis and liver failure. However, the role and mechanism of gut leakiness in liver fibrosis are poorly understood, and there is no FDA-approved drug to treat liver fibrosis.

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