Background/Aim: The present study aimed to develop detailed parameters for prediction of prognosis for patients with unresectable hepatocellular carcinoma (uHCC) receiving Atezolizumab plus Bevacizumab (Atez/Bev). Methods: Between September 2020 and January 2023, the patients treated with Atez/Bev were enrolled (n=719, males 577, median age 74 years). Factors involved in overall survival (OS) were extracted and a prognostic scoring system based on hazard ratio (HR) was created. OS and progression-free survival (PFS) were examined retrospectively, and the prognostic ability of the newly system was compared to CRAFITY score using concordance index (c-index) and Akaike Information Criterion (AIC) results. Results: Cox-hazards multivariate analysis showed BCLC classification C/D (HR 1.4; 1 point), AFP ≥100 ng/mL (HR 1.4; 1 point), mALBI 2a (HR 1.7; 1 point), mALBI 2b/3 (HR 2.8; 2 points), and DCP ≥100 mAU/mL (HR 1.6; 1 point) as significant factors. The assigned points were added and used for IMnunotherapy with AFP, BCLC staging, mALBI, and DCP evaluation (IMABALI-De) scoring. For IMABALI-De scores of 0/1/2/3/4/5, OS was not applicable (NA)/NA/26.11/18.79/14.07/8.32 months (P<0.001; AIC 2788.67, c-index 0.699), while for CRAFITY scores of 0/1/2, OS was 26.11/20.29/11.32 months (p<0.001; AIC 2864.54, c-index 0.606). PFS for those IMABALI-De scores was 21.75/12.89/9.18/8.0/5.0/3.75 months (P<0.001; AIC 5203.32, c-index 0.623) and for the CRAFITY scores was10.32/7.68/3.57 months (p<0.001; AIC 5246.61, c-index 0.574). IMABALI-De score had better AIC and c-index results as compared to CRAFITY score for both OS and PFS. Conclusion: The proposed IMABALI-De score may have a favorable prognostic predictive ability for uHCC patients with Atez/Bev.

Objective: To develop a novel non-invasive model for CSPH, and investigate whether carvedilol could reduce the risk of decompensation in patients with high-risk CSPH stratified by the novel model. Methods: International multicenter observational study with a median follow-up time of 38 months. Three cohorts were included in study from 6 countries. In this study, a total of 1,304 patients were fulfilled diagnosis of liver cirrhosis. Patients were treated with carvedilol in longitudinal carvedilol-treating cohort. The primary outcome was the development of the first hepatic decompensation . Results: Six studies from the meta-analysis were involved (n=819), and LSM and platelet count (PLT) were identified as independent risk factors of CSPH, with pooled risk ratios of 1.10 (95% confidence interval [CI] 1.06-1.15) and 0.99 (95% CI 0.98-0.99). A novel model was established. In HVPG cohort (n=151), the areas under the receiver operating characteristic curve (AUC) of the novel model, ANTICIPATE model, and Baveno VII criteria for CSPH were 0.91 (95% CI 0.86-0.95), 0.80 (95% CI 0.73-0.87), and 0.83 (95% CI 0.77-0.89). The novel model narrows down the grey zone to 22.5%, significantly lower than 50.3%, using Baveno VII criteria (p<0.001). In follow-up cohort (n=1,102), the cumulative incidences (1.7% vs 2.5% vs 15.8%) of decompensation events were significantly different by using the novel model cutoff values of >0, 0 to -0.68 (medium-risk), and <-0.68 (p<0.001). In the carvedilol-treating cohort, the patients with high-risk CSPH stratified by the novel model (treating cohort, n=51) had significantly lower rates of decompensation than those of NSBBs untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=102 after PSM, all p<0.05). Conclusion: A novel model provides stratification for CSPH and decompensation in patients with liver cirrhosis. Treatment with carvedilol significantly reduces the risk of decompensation among high-risk CSPH patients stratified by the novel model.

Background and aims: The causal relationship between sarcopenia and sleep disorder in patients with chronic liver disease (CLDs) is unclear. We aimed examine the influence of sarcopenia-related factors (grip strength (GS) and muscle mass) on the progression of sleep disorder in patients with chronic liver disease (n=182, 46 cirrhotic cases, median age=64 years). Methods: Sleep quality was evaluated by the Japanese version of Pittsburgh Sleep Quality Index (PSQI-J). PSQI-J >6 points was defined as sleep disorder. In all analyzed patients, evaluation using PSQI-J questionnaire was performed twice or more during the follow-up period. Time interval from the date of baseline PSQI-J and the first confirmed date of elevation of PSQI-J score was calculated. Our primary endpoint was the elevation of PSQI-J score compared to the baseline PSQI-J score. GS decline was diagnosed with a GS of <26 kg for male and <18 kg for female. Loss of muscle mass was diagnosed by a skeletal muscle index of <7.0 kg/m2 for male and <5.7 kg/m2 for female on bioelectrical impedance analysis. Results: The median PSQI-J score was 5. PSQI-J >6 points at baseline was found in 83 patients (45.6%). In patients with GS decline (n=48), the 3-year cumulative elevation rate of PSQI-J score was 82.4%, while in patients with GS non-decline, that was 36.2% (P<0.0001). In patients with SMI decline (n=64), the 3-year cumulative elevation rate of PSQI-J score was 60.6%, while in patients with SMI non-decline, that was 43.4% (P=0.1822). On the multivariate analysis of factors associated with the elevation of PSQI-J score, only GS decline (P=0.0002) was a significant factor. Conclusions: Reduced GS rather than loss of muscle mass is independently associated with an elevated risk for the progression of sleep disorder in CLD patients.