Porto-sinusoidal vascular disease (PSVD) is a non-cirrhotic vascular liver disorder characterized by portal and sinusoidal microvascular lesions and is frequently complicated by portal hypertension. Accurate assessment of portal pressure is essential for diagnosis, risk stratification, therapeutic decision-making, and prognostic evaluation in PSVD. However, unlike cirrhosis, portal hypertension in PSVD is predominantly presinusoidal, making hepatic venous pressure gradient measurement prone to underestimating true portal pressure. Recent advances have promoted a transition from conventional invasive assessment toward a multimodal and precision-oriented strategy integrating non-invasive and minimally invasive techniques. Ultrasound elastography, computed tomography, and magnetic resonance imaging—particularly radiomics-based approaches—provide valuable tools for differentiating PSVD from cirrhosis and estimating the severity of portal hypertension. Endoscopic ultrasound-guided portal pressure gradient measurement has emerged as a promising minimally invasive technique for direct hemodynamic assessment and prognostic stratification. In addition, laboratory biomarkers, digital modeling, and artificial intelligence-assisted analysis may further improve individualized risk prediction and dynamic monitoring. This review summarizes current advances in portal pressure assessment in PSVD, critically discusses the strengths and limitations of existing approaches, and highlights future directions toward non-invasive, digital, and precision-guided management.

The Asia-Pacific region accounts for a larger share of the hepatitis B burden than any other regions of the world, presenting a challenge to meeting the World Health Organization (WHO) 2030 elimination targets. In this study, we aimed to quantify the burden of chronic hepatitis B (CHB) and project its trends through 2030 using the Global Burden of Disease 2023 framework, thereby identifying gaps and priorities for the Asia-Pacific region to achieve WHO 2030 targets.

Using data from the Global Burden of Disease Study 2023, we analyzed CHB prevalence, mortality, and disability-adjusted life years. We evaluated temporal trends (1990–2023) using average annual percent changes and projected the 2024–2030 burden using Bayesian age-period-cohort models.

In 2023, the Asia-Pacific region accounted for 63% of global CHB cases (178.0 million), 66% of deaths (259.1 thousand), and 65% of disability-adjusted life years (8.4 million). Regional prevalence and mortality rates exceeded global averages, although childhood (<5 years) prevalence was comparatively lower (590.3 vs. 1,325.3 per 100,000). East Asia bore the highest absolute burden (99.2 million cases), and South Asia had the largest pediatric caseload. Between 1990 and 2023, Western Asia showed the steepest decline in adult prevalence (−1.99%), whereas Southeast and Central Asia exhibited upward mortality trends. Projections indicate that the Asia-Pacific region is off track to meet the WHO 2030 disease elimination targets, as the prevalence rate in children under five years remains above the 0.1% target threshold and absolute mortality is projected to increase.

The Asia-Pacific region continues to contribute the largest share of the global CHB burden and now faces persistent gaps despite progress. Although substantial progress has been made in reducing prevalence through immunization, the region is currently off track to meet the WHO 2030 targets for both incidence and mortality.

Lipid metabolism reprogramming drives malignant proliferation and invasiveness in hepatocellular carcinoma (HCC). Beyond supplying energy and membrane components, lipids function as signaling molecules that modulate tumor cell epigenetics and the microenvironment. Accumulating research has clarified the implications of these metabolic alterations in HCC, providing a rationale for targeted therapies. This review summarizes key alterations in lipid metabolism within HCC and explores their mechanistic contributions to tumor progression. It further examines how lipid metabolic shifts in immune and stromal cells of the tumor microenvironment promote HCC advancement. Finally, we discuss the therapeutic potential of targeting lipid metabolism in liver cancer treatment.

Liver fibrosis is a central pathological process driving the progression of chronic liver disease, yet effective antifibrotic therapies remain limited. Increasing evidence has identified the mineralocorticoid receptor (MR), a ligand-activated nuclear receptor, as a key regulator of intrahepatic homeostasis and fibrogenesis. MR is expressed across multiple hepatic cell types, including hepatocytes, hepatic stellate cells, macrophages, and liver sinusoidal endothelial cells, where it integrates metabolic, inflammatory, and microvascular signaling. Under pathological conditions, MR activation—mediated by both aldosterone-dependent and ligand-independent mechanisms such as hypoxia and oxidative stress—amplifies core profibrotic pathways, including transforming growth factor-β (TGF-β) signaling, reactive oxygen species (ROS) generation, and nuclear factor-kappa B (NF-κB)–driven inflammation. These molecular mechanisms are executed in a cell-type–specific manner, promoting hepatic stellate cell activation, macrophage-mediated inflammation, hepatocyte metabolic dysfunction, and liver sinusoidal endothelial cell capillarization, thereby forming a self-reinforcing fibrogenic network. Preclinical studies consistently demonstrate that mineralocorticoid receptor antagonists attenuate fibrosis by targeting these interconnected pathways. However, clinical evidence remains limited, with only early-phase trials in metabolic dysfunction-associated steatohepatitis and indirect support from cardiorenal studies. Nonsteroidal mineralocorticoid receptor antagonists, particularly finerenone, exhibit improved receptor selectivity and safety profiles, highlighting their therapeutic potential. Future research should focus on disease-specific patient stratification, validated antifibrotic endpoints, and rigorous safety evaluation to enable effective clinical translation of MR-targeted therapies in liver fibrosis.

Disorders of gut–brain interaction (DGBIs) encompass some of the most common gastrointestinal disorders and affect up to 40% of the general population. Despite their inherent heterogeneity and diverse clinical manifestations, many of the underlying pathophysiological mechanisms overlap among different DGBIs. Activation of the gastrointestinal mucosal immune system at a low level (“low-grade inflammation”) and impairments in gut epithelial barrier structure and function have been reported to play a key role in the pathophysiology of multiple DGBIs, but these alterations cannot be detected using routine clinical testing. Confocal laser endomicroscopy (CLE) is an established, readily available technology that can be added to standard gastrointestinal endoscopy, enabling “real-time” microscopic evaluation of the gastrointestinal surface epithelium. CLE has been found to be capable of identifying gastrointestinal mucosal abnormalities that are reflective of epithelial barrier impairment and/or low-grade immune activation. Over the past several years, multiple intriguing studies have utilized CLE as a clinically applicable tool to evaluate the intestinal mucosa in patients with various DGBIs. The aim of this narrative review is to summarize the available literature on the role of CLE in patients with DGBIs and to provide a perspective on the use of this technology in DGBIs.

The gut microbiota engages in a complex, bidirectional dialogue with the liver via the gut–liver axis, and its dysbiosis plays a central role in the initiation and progression of various liver diseases. This review comprehensively integrates recent advances in the common features and etiology-specific patterns of gut microbial dysbiosis in liver diseases, signal decoding of key microbial metabolite axes, gut–liver immune crosstalk mechanisms, the accelerating role of gut barrier disruption, and recent progress in the use of the microbiome as diagnostic and prognostic biomarkers. We focus on analyzing the common patterns of reduced diversity, depletion of beneficial bacteria, and enrichment of pathogenic bacteria associated with gut flora dysbiosis across different liver diseases, ranging from nonalcoholic fatty liver disease and alcoholic liver disease to cirrhosis and hepatocellular carcinoma, as well as their unique etiology-related characteristics. Core findings reveal that microbial metabolites act as key chemical messengers that precisely drive liver disease progression by modulating host metabolic, immune, and inflammatory pathways. Meanwhile, the translocation of microbes and their products resulting from disruption of gut barrier integrity serves as a key accelerator, exacerbating liver injury and related complications. Based on these mechanisms, this review further explores ecological niche remodeling strategies targeting the gut microbiota, including the existing evidence and limitations of fecal microbiota transplantation and probiotics/prebiotics, as well as the prospects of emerging precision interventions such as phage therapy, microbial enzyme inhibitors, and engineered bacteria. Finally, we emphasize the potential and personalized implementation pathways of synergistically integrating microbiota modulation with existing therapies such as antivirals, antifibrotics, immunotherapy, and metabolic surgery. Future research must focus on promoting the translation of microbiome research from association studies to clinical applications through multi-omics integration and prospective clinical trials, ultimately achieving precise prevention and treatment of liver diseases based on gut–liver axis regulation.

This narrative review provides a detailed and comprehensive examination of hemoadsorption therapy and its role in treating severe poisoning. First, the global problem of suicidal and nonsuicidal self-injury is described, with regional differences in the types of poisons used noted. Lower- and middle-income countries are disproportionately affected by pesticides compared to high-income countries. Organophosphates often constitute the majority of pesticide poisoning in many of these countries. Next, we review the history of hemoadsorption therapy from its early origins to its current evolution. The key physical and chemical principles underlying extracorporeal therapy and its effectiveness are described. A review of the literature examining the evidence for the efficacy of hemoadsorption therapy in poisoning is presented. Current evidence-based guidelines are summarized, including toxin types, clinical indications, and the extracorporeal therapies recommended. Emerging evidence regarding the use of hemoadsorption therapy for severe organophosphate and calcium channel blocker poisoning is also considered. A care pathway for considering hemoadsorption in poisonings where formal guidelines are lacking is proposed. Both the hemoadsorption strategies used and the potential adverse effects of this therapy are discussed. For this narrative review, the PubMed/Medline was searched from inception to April 30, 2025, using the terms (“hemoperfusion” OR “hemadsorption”) AND (“poisoning”). Clinical trials, randomized controlled trials, and meta-analyses were included, along with additional relevant studies identified through a manual review of references. The role of modern resin bead hemoadsorption therapy for severe poisoning is expanding to include removal of commonly encountered poisons that are protein-bound and have a large volume of distribution. Using a multicycle approach, hemoadsorption therapy has shown improved outcomes for both calcium channel blockers and organophosphate poisoning.

Antimitochondrial antibody (AMA)-negative primary biliary cholangitis (PBC) is a rare presentation of PBC that comprises 5%–10% of all PBC patients. The pathogenesis of AMA-negative PBC appears to be similar to that of AMA-positive PBC. AMA-negative PBC presents similarly to AMA-positive PBC, with symptoms of cholestasis, fatigue, and pruritus most commonly reported. Defective bicarbonate production, resulting in acidification of bile and bile acids, has been proposed as the primary mechanism of damage to bile ducts and hepatocytes and is reflected in elevations of alkaline phosphatase and aminotransferases. Chronic damage can lead to the development of cirrhosis. The diagnosis is made by the finding of AMA negativity by ELISA or assays of similar sensitivity and a positive PBC-specific antinuclear antibody (ANA; anti-glycoprotein 210 and anti-speckled 100 kDa protein) test. In cases in which anti-glycoprotein 210 and anti-speckled 100 kDa protein assays are also negative, a liver biopsy is required to make the diagnosis after exclusion of other causes of cholestasis by magnetic resonance cholangiopancreatography or endoscopic retrograde cholangiopancreatography. Treatment for AMA-negative PBC is the same as for AMA-positive cases, with ursodeoxycholic acid as the first-line treatment. Current treatment is most effective in early stages, where it slows but does not eliminate progression. Risk stratification by validated tools such as the GLOBE and UK-PBC scores remains useful in AMA-negative PBC.

Autoimmune pancreatitis (AIP) is a rare immune-mediated form of chronic pancreatitis. It may affect multiple organs, and its heterogeneous clinical manifestations complicate diagnosis and management. Based on the Chinese Guidelines for the Diagnosis and Management of Autoimmune Pancreatitis (Shanghai 2012 Draft), together with the latest domestic and international guidelines and research advances, the present guideline provides 20 recommendations covering four aspects: diagnosis, treatment, follow-up, and prognosis. The aim is to improve the diagnosis and management of AIP in China and ultimately improve patient outcomes.