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Liver stiffness measurement (LSM) is recommended for disease prognostication and monitoring. We evaluated if LSM, using transient elastography, and LSM changes predict decompensation and mortality in patients with alcohol-related liver disease (ALD). We performed an observational cohort study of compensated patients at risk of ALD from Denmark and Austria. We evaluated the risk of decompensation and all-cause mortality, stratified for compensated advanced chronic liver disease (cACLD: baseline LSM ≥10 kPa) and LSM changes after a median of 2 years. In patients with cACLD, we defined LSM changes as (A) LSM increase ≥20% ("cACLD increasers") and (B) follow-up LSM <10 kPa or <20 kPa with LSM decrease ≥20% ("cACLD decreasers"). In patients without cACLD, we defined follow-up LSM ≥10 kPa as an LSM increase ("No cACLD increasers"). The remaining patients were considered LSM stable. We followed 536 patients for 3,008 patient-years–median age 57 years (IQR 49–63), baseline LSM 8.1 kPa (IQR 4.9-21.7)–371 patients (69%) had follow-up LSM after a median of 25 months (IQR 17–38), 41 subsequently decompensated and 55 died. Of 125 with cACLD at baseline, 14% were "cACLD increasers" and 43% "cACLD decreasers", while 13% of patients without cACLD were "No cACLD increasers" (n = 33/246). Baseline LSM, follow-up LSM and LSM changes accurately predicted decompensation (C-index: baseline LSM 0.85; follow-up LSM 0.89; LSM changes 0.85) and mortality (C-index: baseline LSM 0.74; follow-up LSM 0.74; LSM changes 0.70). When compared to "cACLD decreasers", "cACLD increasers" had significantly lower decompensation-free survival and higher risks of decompensation (subdistribution hazard ratio 4.39, p = 0.004) and mortality (hazard ratio 3.22, p = 0.01). LSM by transient elastography predicts decompensation and all-cause mortality in patients with compensated ALD both at diagnosis and when used for monitoring. Patients at risk of alcohol-related liver disease (ALD) are at significant risk of progressive disease and adverse outcomes. Monitoring is essential for optimal disease surveillance and patient guidance, but non-invasive monitoring tools are lacking. In this study we demonstrate that liver stiffness measurement (LSM), using transient elastography, and LSM changes after a median of 2 years, can predict decompensation and all-cause mortality in patients at risk of ALD with and without compensated advanced chronic liver disease. These findings are in line with results from non-alcoholic fatty liver disease, hepatitis C and primary sclerosing cholangitis, and support the clinical utility of LSM, using transient elastography, for disease prognostication and monitoring in chronic liver diseases including ALD, as recommended by the Baveno VII. [Display omitted] • Liver stiffness (LSM) can be used to prognosticate and monitor alcohol-related liver disease. • Elevated baseline LSM (≥10 kPa) was associated with a 19-fold increased risk of decompensation. • LSM changes after a median of 2 years were associated with the risk of decompensation and death. • LSM increasers had lower decompensation-free survival and elevated risk of outcomes. [ABSTRACT FROM AUTHOR]

The risk of hepatocellular carcinoma (HCC) diminishes in patients with hepatitis C virus (HCV)-related advanced chronic liver disease after virological cure. However, despite viral clearance, HCV-induced epigenetic alterations, immune dysregulations, and hepatic parenchymal injuries remain, contributing to de novo HCC occurrence. While HCC incidence is low (0.45 - 0.5%) in patients with advanced fibrosis (F3), the presence of liver cirrhosis and clinically significant portal hypertension increases the HCC risk. The cost-effectiveness of lifelong HCC surveillance in patients with compensated advanced chronic liver disease (cACLD) has sparked debate, raising questions about the most reliable noninvasive tests and stratification models for predicting HCC in patients with sustained virological response (SVR). Furthermore, identifying cACLD patients who may not require long-term HCC surveillance after SVR remains crucial. Several HCC risk stratification scores have been suggested for patients with cACLD, and emerging evidence supports individualized care based on personalized risk assessments. This review focuses on revising the pretreatment and posttreatment predictors of HCC, as well as the indications for HCC surveillance in cACLD patients treated with direct-acting antivirals. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is a major cause of morbidity and mortality in patients with advanced chronic liver disease (ACLD) caused by chronic hepatitis C who have achieved sustained virologic response (SVR). We developed risk stratification algorithms for de novo HCC development after SVR and validated them in an independent cohort. We evaluated the occurrence of de novo HCC in a derivation cohort of 527 patients with pre-treatment ACLD and SVR to interferon-free therapy, in whom alpha-fetoprotein (AFP) and non-invasive surrogates of portal hypertension including liver stiffness measurement (LSM) were assessed pre-/post-treatment. We validated our results in 1,500 patients with compensated ACLD (cACLD) from other European centers. During a median follow-up (FU) of 41 months, 22/475 patients with cACLD (4.6%, 1.45/100 patient-years) vs. 12/52 decompensated patients (23.1%, 7.00/100 patient-years, p < 0.001) developed de novo HCC. Since decompensated patients were at substantial HCC risk, we focused on cACLD for all further analyses. In cACLD, post-treatment-values showed a higher discriminative ability for patients with/without de novo HCC development during FU than pre-treatment values or absolute/relative changes. Models based on post-treatment AFP, alcohol consumption (optional), age, LSM, and albumin, accurately predicted de novo HCC development (bootstrapped Harrel's C with/without considering alcohol: 0.893/0.836). Importantly, these parameters also provided independent prognostic information in competing risk analysis and accurately stratified patients into low- (~2/3 of patients) and high-risk (~1/3 of patients) groups in the derivation (algorithm with alcohol consumption; 4-year HCC-risk: 0% vs. 16.5%) and validation (3.3% vs. 17.5%) cohorts. An alternative approach based on alcohol consumption (optional), age, LSM, and albumin (i.e. , without AFP) also showed a robust performance. Simple algorithms based on post-treatment age/albumin/LSM, and optionally, AFP and alcohol consumption, accurately stratified patients with cACLD based on their risk of de novo HCC after SVR. Approximately two-thirds were identified as having an HCC risk <1%/year in both the derivation and validation cohort, thereby clearly falling below the cost-effectiveness threshold for HCC surveillance. Simple algorithms based on age, alcohol consumption, results of blood tests (albumin and α-fetoprotein), as well as liver stiffness measurement after the end of hepatitis C treatment identify a large proportion (approximately two-thirds) of patients with advanced but still asymptomatic liver disease who are at very low risk (<1%/year) of liver cancer development, and thus, might not need to undergo 6-monthly liver ultrasound. [Display omitted] • We studied de novo HCC development in patients with cACLD after SVR in a derivation cohort (n = 475) and validation cohort (n = 1,500). • Algorithms based on post-treatment age/albumin/LSM, and optionally, AFP and alcohol consumption, accurately stratified de novo HCC risk. • Approximately two-thirds of patients were identified as having an HCC risk <1%/year. • In these patients, HCC-surveillance might not be cost-effective. [ABSTRACT FROM AUTHOR]

Introduction: Nonalcoholic fatty liver disease (NAFLD) patients can progress to cirrhosis. In these, there is a compensated stage in which esophageal varices can exist. However, no more than 20% of these patients have varices needing treatment (VNT). Objective: Evaluate the accuracy of non-invasive models to predict esophageal varices, as well as their performance to avoid esophagogastroduodenoscopy (EGD) with a risk of missing VNT of less than 5%, in Brazilian patients with compensated advanced chronic liver disease (cACLD) secondary to NAFLD. Methods: Twenty-one patients with biopsy-proven cACLD secondary to NAFLD were submitted to liver stiffness measurement (LSM) by transient elastography (TE), and data were collected to measure platelet count/spleen diameter ratio (PSR), LSM-spleen diameter to platelet ratio score (LSPS), varices risk score (VRS), Baveno VI, Expanded Baveno VI and NAFLD cirrhosis criteria. Results: The mean age was 61 (±6.6) years, and 81% were female; 14% presented VNT. For detection of VNT, LSPS and VRS performed excellently, with an area under receiver operating characteristic (AUROC) of 0.961 for both. LSM presented an AUROC of 0.889 and a cutoff point of 21.8 kPa. LSPS and VRS enabled sparing 75-80% of EGDs for VNT, with no risk of missing varices. Expanded Baveno VI enabled sparing 71% of EGDs, with 4.8% risk of missing VNT. Conclusion: LSPS and VRS performed excellently in both predicting VNT and sparing EGD, and Expanded Baveno VI showed good performance in sparing EGDs, with acceptable risk of missing VNT. An LSM cutoff point was established and had good performance. [ABSTRACT FROM AUTHOR]