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Baveno VI criteria for screening varices needing treatment (VNT) have not yet been validated in an exclusive pediatric and adolescent set of the population, in whom baseline parameters differ in relation to adults. Therefore, our primary objective was to validate Baveno VI and its expanded form in children below 18 years of age. The secondary aim was to elicit whether any revision of the above criteria with a target of not missing more than 5% VNT could be more accurate for this age group. The work was carried out in two medical institutes, over a span of 3 years. Consecutively enrolled patients below 18 years of age, with compensated cirrhosis confirmed by liver biopsy, were evaluated for related blood parameters, transient elastography (TE) and esophagogastroduodenoscopy. Out of the 33 recruited patients, five (15.15%) met the criteria for VNT. The sensitivity, specificity, PPV and NPV of Baveno VI and Expanded Baveno VI were observed as 60%, 92.3%, 60% and 92.3%, and 20%, 100%, 100% and 88%, respectively. We found that the Revised Baveno VI criteria with TE <19 kPa and platelet count of >175×10 cells/L, with sensitivity 100%, specificity 79%, PPV 45%, NPV 100% and accuracy of 82%, are more appropriate for this age group. We propose that further multicentrer studies with a larger sample size should be conducted before incorporating Revised Baveno VI criteria for high-risk varices in patients below 18 years in future guidelines.

Chronic liver disease (CLD), including non-alcoholic fatty liver disease (NAFLD) and its advanced form, non-alcoholic steatohepatitis (NASH), affects a significant portion of the population worldwide. NAFLD is characterised by fat accumulation in the liver, while NASH is associated with inflammation and liver damage. Osteosarcopenia, which combines muscle and bone mass loss, is an emerging clinical problem in chronic liver disease that is often underappreciated. The reductions in muscle and bone mass share several common pathophysiological pathways; insulin resistance and chronic systemic inflammation are the most crucial predisposing factors and are related to the presence and gravity of NAFLD and to the worsening of the outcome of liver disease. This article explores the relationship between osteosarcopenia and NAFLD/MAFLD, focusing on the diagnosis, prevention and treatment of this condition in patients with CLD.

Vitamin D is a crucial nutrient with many pleiotropic effects on health and various chronic diseases. The purpose of this review is to provide a detailed report on the pathophysiological mechanisms underlying vitamin D deficiency in patients with chronic liver disease, addressing the different liver etiologies and the condition of advanced chronic liver disease (cirrhosis) with related complications. To date, patients with liver disease, regardless of underlying etiology, have been shown to have reduced levels of vitamin D. There is also evidence of the predictive role of vitamin D values in complications and progression of advanced disease. However, specific indications of vitamin D supplementation are not conclusive concerning what is already recommended in the general population. Future studies should make an effort to unify and validate the role of vitamin D supplementation in chronic liver disease.

Purpose The mainstay of treatment for metabolic dysfunction-associated steatotic liver disease (MASLD) is weight loss. Endoscopic gastric remodeling (EGR) and glucagon-like peptide-1 receptor agonist (GLP-1RA) are effective weight loss therapies. This study aims to assess the effect of combining EGR with GLP-1RA on liver-related outcomes and weight profile. Materials and Methods This is a retrospective study of a prospectively collected registry of patients with MASLD and compensated advanced chronic liver disease (cACLD) who underwent EGR. Patients were categorized as (1) monotherapy: EGR alone and (2) combination therapy: GLP-1RA prescribed within 6 months prior to or after EGR. Outcomes included changes in noninvasive tests of hepatic fibrosis, weight profile, and insulin resistance status at 12 months. Results Thirty patients (body mass index 40.7 ± 9.3 kg/m 2 ) were included. Of these, 12 patients (40%) underwent EGR monotherapy, and 18 patients (60%) underwent EGR + GLP-1RA combination therapy. Combination therapy group experienced greater improvements in fibrosis compared to monotherapy group (alanine aminotransferase: reduction by 55 ± 23% vs 29 ± 22% ( p  = 0.008), NAFLD fibrosis score: reduction by 181 ± 182% vs 30 ± 83% ( p  = 0.04), liver stiffness measurement on transient elastography: reduction by 54 ± 12% vs 14 ± 45% ( p  = 0.05)). There were greater reductions in hemoglobin A1c and homeostatic model assessment for insulin resistance in combination therapy compared to monotherapy ( p  < 0.05). At 12 months, the combination therapy group experienced 18.2 ± 6.6% TWL, while monotherapy group experienced 9.6 ± 3.3% TWL ( p  = 0.004). Conclusions In patients with MASLD and cACLD, combination of EGR with GLP-1RA is associated with greater improvements in hepatic fibrosis, weight profile, and insulin resistance compared to EGR alone. Graphical Abstract

•Early clinical prognosis remains a challenge in advanced chronic liver disease (ACLD).•The Nutritional Prognostic Index (NPI) shows potential for nutritional assessment in ACLD.•An association between a NPI cutoff of <41 and mortality were observed in our ACLD population.•A total of 82.1% of the sample below cutoff experienced mortality within 12 mo.•NPI is a simple and effective tool which can aid in ACLD prognosis assessment. Early clinical prognosis and mortality reduction remains a challenge in chronic liver disease (CLD). The full potential of the Nutritional Prognostic Index (NPI) for nutritional assessment and management in CLD patients remains unexplored. The aim of this study was to establish an NPI cutoff point for the identification of nutritional risk in advanced CLD (ACLD) patients, as well as to assess the NPI's ability to predict ACLD-associated mortality. This ethically approved prospective cohort study investigated malnutrition risk using both the NPI and the Royal Free Hospital-Nutritional Prioritizing Tool (RFH-NPT) in patients hospitalized for ACLD. NPI reference values were determined using a receiver operating characteristic curve. Associations between nutritional risk identified by the RFH-NPT and the NPI were assessed using Fisher's exact test, and agreement between tools was assessed using the Kappa index. The association between NPI-defined nutritional risk and 12-mo mortality was examined using Pearson Chi-square test. The sample population consisted of 120 adults, comprising 84 (70%) male and 57 (50.9%) of alcoholic etiology and presenting as Child-Pugh A, B, or C at admission. The identified cutoff point for NPI was <41, identifying nutritional risk in 82.5% of patients. The NPI presented a statistically significant association with the RFH-NPT, with a substantial agreement coefficient of 0.34. An association between NPI <41 cutoff and mortality were observed, with 82.1% of the sample below cutoff experiencing mortality within 12 mo. The NPI is a valuable nutritional marker for the identification of nutritional risk in ACLD and is a simple and effective assessment tool that can aid in early CLD prognosis assessment. Validation, however, remains necessary in other CLD populations of different etiologies.

Patients with compensated advanced chronic liver disease (cACLD) have a significant risk of decompensation. Therefore, this study aimed to evaluate the predictive value of dynamic liver stiffness measurements (LSM) for decompensation risk, and their performance across different clinically significant portal hypertension (CSPH) risk stratification. This retrospective cohort study included 1409 patients with cACLD. Patients were divided into no CSPH, probable CSPH, and certain CSPH groups. Competing risk regression analysis was used to identify the independent predictors. The receiver operating characteristic curve and time-dependent area under the curve were used to evaluate the predictive performance. During follow-up, liver decompensation incidence increased with CSPH severity (22.2% with no CSPH, 37.5% with probable CSPH, and 64.9% with certain CSPH, p  < 0.001). Multivariate regression analysis identified age, basal LSM1, delta LSM/LSM1, delta LSM/delta year, spleen diameter, and international normalized ratio as independent risk factors for liver decompensation. In the no CSPH group, spleen diameter showed the best predictive ability (AUC = 0.710). For probable and certain CSPH groups, delta LSM/LSM1 showed superior predictive performance (AUC: 0.777 and 0.782, respectively). The predictive power of basal LSM1 was relatively limited across all groups (AUC: 0.554–0.639). Subgroup analysis revealed interactions between age, sex, different etiologies, and CSPH subgroups. The relative change rate of LSM outperformed basal LSM1 and annual change rate in predicting liver decompensation risk, particularly in patients with existing portal hypertension. Dynamic assessments and differentiated prediction strategies are essential for optimal patient managements.

Background and AimsAssessment of clinically significant portal hypertension (CSPH) non-invasively using a combination of liver stiffness measurement (LSM) and platelet counts is proposed as an alternative to hepatic venous pressure gradient (HVPG) estimation. Utility of these criteria in compensated advanced chronic liver disease (cACLD) patients of different etiologies including nonalcoholic steatohepatitis (NASH) with BMI  >  30 kg/m2 was studied in a large cohort.MethodsConsecutive patients of cACLD with available anthropometric and laboratory details, LSM, and HVPG were included in a retrospective analysis. A LSM of ≥ 25 kPa alone and LSM ≤ 15 kPa plus platelets ≥  150 × 109/L were evaluated as non-invasive rule-in and rule-out criteria for CSPH, respectively. The NASH-ANTICPATE model (composite of BMI, platelets, and LSM) was evaluated in patients with obese NASH.ResultsPatients with cACLD (n = 626) (mean age: 50.8 ± 12.4 years, 74.2% males) with alcohol (ALD, 30.3%), NASH (26.4%), hepatitis C (HCV, 16.6%), hepatitis B (HBV,10.2%) etiology were included. The prevalence of CSPH was  >  80% across all etiologies except in HBV (62.5%) and in obese non-NASH (71–72%). The rule-in criteria had a PPV  >  90% for all etiologies except in HBV (80.8%). The rule-out criteria had a negative predictive value (NPV) of 65%, 53%, and 40% in ALD, HCV, and NASH, respectively. The NASH-ANTCIPATE model had specificity of 100% and NPV of 33% to detect CSPH in obese NASH (n = 62).ConclusionsLSM ≥ 25 kPa predicted CSPH in most etiologies except HBV. A significant proportion of patients have CSPH despite satisfying the rule-out criteria. The NASH-ANTICIPATE model is specific but fails to exclude CSPH in nearly two-third patients with obesity and NASH. There is a need for precise disease-specific non-invasive models for detecting CSPH.

Advanced chronic liver disease (ACLD) is associated with a wide spectrum of immune dysfunction. The clinical impact of SARS-CoV-2 on the development of decompensation and immune response in unvaccinated outpatients has not as yet been clearly defined. This study aimed to evaluate the clinical and immunological impact of SARS-CoV-2 on outpatients with ACLD. This is an observational case–control study, in which ACLD outpatients were included prospectively and consecutively and classified into two groups: SARS-CoV-2 infected and non-infected. Patients’ baseline characteristics and infection data were collected and analyzed. Immunoglobulin G (IgG) levels against Spike 1 were evaluated. The primary endpoint was risk of liver decompensation during follow-up, assessed after propensity score matching and adjusted by Cox regression. Between October 2020 and July 2021, ACLD outpatients (n = 580) were identified, and 174 patients with clinical follow-up were included. SARS-CoV-2 infection incidence was 7.6% (n = 44). Risk of liver decompensation was significantly higher after infection (HR = 2.43 [1.01–5.86], p = 0.048) vs. non-infection. The time of IgG evaluation was similar in all patients (n = 74); IgG concentrations were significantly higher in compensated vs. decompensated patients (1.02 ± 0.35 pg/mL vs. 0.34 ± 0.16 pg/mL, p < 0.0001) and correlated with hemoglobin levels. The dysregulation of the innate immune response in patients with decompensated liver disease increased the risk of further decompensation following SARS-CoV-2, mainly due to a worsening of ascites.

The concept of ‘cirrhosis’ is evolving and it is now clear that compensated and decompensated cirrhosis are completely different in terms of prognosis. Furthermore, the term ‘advanced chronic liver disease (ACLD)’ better reflects the continuum of histological changes occurring in the liver, which continue to progress even after cirrhosis has developed, and might regress after removing the etiological factor causing the liver disease. In compensated ACLD, portal hypertension marks the progression to a stage with higher risk of clinical complication and requires an appropriate evaluation and treatment. Invasive tests to diagnose cirrhosis (liver biopsy) and portal hypertension (hepatic venous pressure gradient measurement and endoscopy) remain of crucial importance in several difficult clinical scenarios, but their need can be reduced by using different non-invasive tests in standard cases. Among non-invasive tests, the accepted use, major limitations and major benefits of serum markers of fibrosis, elastography and imaging methods are summarized in the present review.