Background and Aim: Age and biological sex are risk factors for hepatocellular carcinoma (HCC) occurrence, but their impact on overall survival (OS) is a matter of debate. This study aims to investigate how sex and age at diagnosis, along with other associated factors (i.e., comorbidities, etiologies, therapy) impact OS in the HCC population. Method: Data from two HCC cohorts—a prospective registry from the University Hospital of Bern, Switzerland, and a retrospective registry from General Hospital Vienna, Austria—were combined and analyzed. Clinical and laboratory data were reviewed, and OS was compared using Kaplan-Meier curves and the log-rank test. Cox regression models with penalized splines were applied to examine how age at diagnosis influenced OS. Results: Of 1547 HCC patients, 1284 (84.1%) were male. Females were older (67 vs. 63 years, p < 0.001) and had lower rates of liver cirrhosis (p < 0.001), cardiac comorbidities (p < 0.001), and diabetes (p < 0.001). No significant difference in median OS between men and women was observed (18 months vs. 16 months, p = 0.304). Mortality risk increased with age, particularly between 60 and 70 years. However, after adjusting for treatment, the age effect became non-significant (p = 0.171). Conclusions: After controlling the model for therapy, neither age nor sex independently influenced OS in HCC patients, underscoring the impact of therapy on survival.

Introduction: The use of direct-acting antivirals (DAAs) has drastically changed the management of HCV-infected patients by achieving a 95–98% sustained virologic response (SVR) and reducing morbidity and mortality in this population. However, despite their effectiveness, controversy exists concerning the occurrence of oncologic events following DAA therapy. Aims and Methods: A retrospective analysis was conducted on data from the Swiss Hepatitis C Cohort Study, a prospective cohort involving patients with positive HCV viremia upon inclusion, enrolled in various Swiss centers from September 2000 to November 2021. To examine potential differences in the risk of intrahepatic tumor (IHT) occurrence and death among patients treated with direct-acting antivirals (DAAs), untreated patients, and those receiving interferon (IFN)-based therapy, a semiparametric competing risk proportional hazards regression model was used. Results: Among 4082 patients (63.1% male, median age 45 years; genotype 1: 54.1%; cirrhosis: 16.1%), 1026 received exclusive treatment with IFN-based regimens, and 1180 were treated solely with DAAs. Over a median follow-up of 7.8 years (range: 3.8–11.9), 179 patients (4.4%) developed intrahepatic tumors (IHT), and 168 (4.1%) experienced extrahepatic tumors (EHT). The 5-year cumulative incidence of IHT was 1.55% (95% CI 0.96–2.48) for IFN-based therapy, 4.27% (95% CI 2.93–6.2) for DAA and 0.89% (95% CI 0.4–1.99) for untreated patients. There was no statistically significant difference in the risk of developing IHT (HR = 1.34; 95% CI = [0.70; 2.58]; p = 0.380) or death (HR = 0.66; 95% CI = [0.43; 1.03]; p = 0.066) between patients treated with DAAs and those treated with IFN. Conclusions: The DAAs reduced the risk of death and were not associated with an increased risk of extrahepatic tumors (EHT). In the adjusted model, accounting for cirrhosis and high liver stiffness, the DAA treatment was associated with a higher risk of IHT occurrence compared with untreated patients, emphasizing the relevance of implementing standardized hepatocellular carcinoma (HCC) screening post-DAA treatment.

Background & Aim: Sustained‐virological‐response (SVR) after direct‐acting‐antiviral (DAA) therapy improves outcomes in patients with HCV‐related compensated‐advanced‐chronic‐liver‐disease (cACLD). However, it remains unclear whether absolute post‐SVR LSM or LSM reduction better predicts prognosis after SVR. This study evaluated the prognostic performance of absolute‐values‐LSM versus dynamic‐change for predicting liver‐related‐events after SVR. Methods: We retrospectively analysed patients with HCV‐related cACLD treated with DAA between December 2014 and March 2022. Baseline and post‐SVR non‐invasive tests (LSM, FIB‐4 and APRI) were assessed. Predictive performance for liver‐related events was evaluated using time‐dependent receiver operating characteristic analysis. Associations between Baveno‐VII criteria for clinically significant LSM improvement and clinical outcomes were assessed using Fine–Grey competing‐risk models. Results: During a median of 60 months (95%; CI 52–69), 11/135 patients (8%) developed liver‐related events. Patients who developed events had higher baseline LSM than those who remained event‐free (24 vs. 18 kPa, p = 0.049), and higher follow‐up LSM values (20 vs. 12 kPa, p = 0.043). Follow‐up LSM showed good discriminative ability for liver‐related events within the first 3 years after SVR (tAUC at 2 years: 0.86 [95% CI 0.75–0.97]; tAUC at 3 years: 0.82 [0.71–0.93]). Follow‐up LSM was significantly superior to ΔLSM and percentage ΔLSM at both 2 and 3 years (all p ≤ 0.028). In competing‐risk analysis, only follow‐up LSM > 20 kPa was significantly associated with liver‐related events (subdistribution hazard ratio 5.61, p = 0.007), whereas Baveno‐VII criteria for LSM regression were not (SHR 0.33, p = 0.097). Conclusions: Absolute post‐treatment‐LSM provides stronger prognostic information than dynamic changes from baseline. These findings support repeated post‐SVR LSM assessment for risk stratification suggesting the relevance of residual liver disease in predicting liver‐related outcomes.

Background/Objectives: The prevalence and management options of bland (non-neoplastic) portal vein thrombosis (PVT) in patients with hepatocellular carcinoma (HCC) are poorly characterized and data remain limited. Methods: We performed a retrospective analysis of a prospectively collected single-center cohort of 638 patients with HCC. Bland PVT was identified at baseline or during follow-up. Treatment exposure was modeled as time-varying to account for differences in timing of anticoagulation initiation. Results: Bland PVT was identified in 39 patients (25 at baseline and 14 during follow-up). Patients with PVT showed features of more advanced portal hypertension (lower platelet count and higher prevalence of ascites) and had a higher tumor burden (more often outside the Milan criteria; higher AFP). A total of 30 patients received anticoagulation. Anticoagulation was associated with partial or complete recanalization in 30% of cases at three months and with decrease in bilirubin, but was not associated with improved 1 year survival. Bleeding events occurred in four anticoagulated patients (13.3%). Conclusions: Bland PVT in HCC is associated with more severe liver disease. Our data indicate that anticoagulation in patients with HCC and concomitant bland PVT was generally well-tolerated and was associated with thrombus regression in one-third of cases. However, we did not observe an improved survival in patients on anticoagulation.

Biometric authentication based on physiological signals offers promising potential for enhancing security in mobile patient monitoring. ‘Intelligent medical devices’, which check the identity of a patient before usage to address safety risks from device-patient mix-ups, do not yet exist. In this project, an AI-based identification system that uses vital signs for biometric authentication will be realized in order to enable the identification on the basis of biometric patterns. By integrating this component into a patient monitoring platform, a seamless and reliable method for verifying patient identity before device use is established, supporting safer and more efficient clinical workflows.