James S. Park

Background and Aims: Chronic hepatitis B virus (HBV) infection remains a major cause of hepatocellular carcinoma (HCC). Although antiviral therapy reduces cirrhosis and liver failure, HCC may still develop in patients with HBV, including in non‐cirrhotic livers. This review aimed to evaluate current HCC surveillance strategies in HBV infection, focusing on risk stratification and advances in early detection. Methods: English‐language literature published in PubMed and the Cochrane Database was comprehensively reviewed. This narrative review assessed the effectiveness of HCC surveillance strategies in HBV‐infected patients, with emphasis on recent advances in early‐stage HCC detection. Results: This review summarizes viral, host and environmental factors associated with HCC susceptibility and evaluates current surveillance using ultrasound with or without alpha‐fetoprotein (AFP). Surveillance eligibility should follow guideline‐defined risk criteria: patients with an estimated annual HCC risk below 0.2% generally do not require routine surveillance and should undergo periodic risk reassessment, whereas patients meeting surveillance criteria should undergo ultrasound with or without AFP every 6 months. Risk‐prediction scores can refine assessment but should be distinguished from early‐detection tests. GALAD, HES 2.0, multi‐target blood tests, and abbreviated magnetic resonance imaging are promising early‐detection approaches, but much of the supporting evidence derives from mixed‐aetiology or non‐HBV cohorts and prospective HBV‐specific validation remains limited. Conclusion: A risk‐adapted approach should separate estimation of future HCC risk from surveillance and early‐detection testing. Guideline‐eligible patients should undergo surveillance every 6 months, while emerging biomarker, imaging and artificial‐intelligence approaches remain adjunctive or investigational pending further HBV‐specific validation.

Revamping hepatitis C global eradication efforts: towards simplified and enhanced screening, prevention, and treatment

Achieving a sustained virologic response (SVR) through direct-acting antivirals for hepatitis C virus (HCV) infection significantly reduces the long-term risk of hepatocellular carcinoma (HCC), particularly in patients with advanced fibrosis (F3) or cirrhosis (F4). However, despite this improvement, the risks associated with HCC and the optimal surveillance strategies for patients who have achieved SVR remain topics of debate. This controversy is compounded by challenges in reliably staging liver fibrosis non-invasively, especially at advanced fibrosis (F3), and the unclear cost-effectiveness, modality, frequency, and duration of HCC surveillance in individuals with SVR but without cirrhosis. These factors contribute to significant variations in surveillance guidelines recommended by different professional societies. Therefore, there is a pressing need for an optimal surveillance strategy that is both simplified and cost-effective to facilitate wider adoption by clinicians. This review article evaluates the existing data, addresses ongoing controversies, and aims to provide new perspectives on HCC surveillance strategies for patients who have achieved SVR from HCV.

Alcohol withdrawal syndrome (AWS) is characterized by neuronal hyperexcitability, autonomic dysregulation, and severe negative emotion. The nucleus tractus solitarius (NTS) likely plays a prominent role in the neurological processes underlying these symptoms as it is the main viscerosensory nucleus in the brain. The NTS receives visceral interoceptive inputs, influences autonomic outputs, and has strong connections to the limbic system and hypothalamic-pituitary-adrenal axis to maintain homeostasis. Our prior analysis of single neuronal gene expression data from the NTS shows that neurons exist in heterogeneous transcriptional states that form distinct functional subphenotypes. Our working model conjectures that the allostasis secondary to alcohol dependence causes peripheral and central biological network decompensation in acute abstinence resulting in neurovisceral feedback to the NTS that substantially contributes to the observed AWS. We collected single noradrenergic and glucagon-like peptide-1 (GLP-1) neurons and microglia from rat NTS and measured a subset of their transcriptome as pooled samples in an alcohol withdrawal time series. Inflammatory subphenotypes predominate at certain time points, and GLP-1 subphenotypes demonstrated hyperexcitability post-withdrawal. We hypothesize such inflammatory and anxiogenic signaling contributes to alcohol dependence via negative reinforcement. Targets to mitigate such dysregulation and treat dependence can be identified from this dataset.

Background A critical aspect of liver transplantation in hepatitis B patients is to prevent graft reinfection with hepatitis B virus. The use of hepatitis B immune globulin after transplant was a significant milestone, which allowed prolonged graft and patient survival by controlling hepatitis B reinfection in liver grafts. The development of anti-viral treatments with oral nucleos(t)ide analogues, led to a further reduction in graft reinfection and improvement in patient survival. The combination of the aforementioned two therapies has been widely used in hepatitis B-associated liver transplants. Aim To address the post-transplant management of hepatitis B and provide updates on preventing graft reinfection. Methods We performed a literature search on Ovid and PubMed for RCTs or cohort studies in English, which investigated the effectiveness of hepatitis B immune globulin and anti-viral therapy on hepatitis B-associated transplants (1/2000-1/2020). Studies that met pre-established criteria were reviewed. Results Based on currently available evidence, an algorithm for post-transplant management with anti-viral therapy is proposed. Also, the management of recipients who received grafts from hepatitis B core antibody-positive donors is discussed. Conclusions The development of hepatitis B immune globulin and anti-viral treatments led to substantial improvement in graft and patient survival. The prevention of hepatitis B graft reinfection is complex and involves a broad interdisciplinary team.