Gastrointestinal (GI) cancers account for approximately one-third of annual cancer-related deaths globally, while outcomes remain poor despite advances in surgery, chemotherapy, radiotherapy, and immunotherapy. Given the challenges of persistent resistance and treatment-related toxicities in current therapies, the pivotal roles of the gut microbiota and fecal microbiota transplantation (FMT) in GI cancer therapy are increasingly recognized. This review aims to explore the potential and mechanisms of FMT as a therapeutic adjuvant in the treatment of GI cancers. FMT may enhance antitumor treatment efficacy and reduce treatment-related toxicity through multiple mechanisms, including enhancing antigen presentation, reshaping the tumor microenvironment, and preserving intestinal barrier function. Preliminary clinical evidence indicates that FMT combined with immune checkpoint inhibitors, chemotherapy, or radiotherapy can improve treatment response rates in some trials and may reverse resistance and alleviate associated intestinal toxicities in selected cases. However, clinical application is hindered by donor microbiota functional heterogeneity, substantial interindividual variability in engraftment, and the absence of validated predictive models. To advance FMT toward precision intervention, we propose a functional screening framework: the Healthy Donor-derived Microbiota Xenograft model as a preclinical functional screening platform and its subsequent clinical application, Xenograft-screened FMT, which links donor-level functional validation with personalized microbiota delivery. By integrating mechanistic insights, emerging preclinical and clinical evidence, and a functional screening framework, this review contributes to advancing FMT from an empirical intervention toward a precision adjuvant strategy and offers insights into future clinical investigation of FMT as a therapeutic approach in GI oncology.

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.

Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasing rapidly, yet regional differences in burden and care quality remain unclear. This study aimed to compare regional incidence, mortality, and disability; evaluate care quality; identify key determinants; and project future incidence.

We analyzed the Global Burden of Disease 2023 estimates of MASLD incidence, deaths, and disability-adjusted life years from 1990 to 2023 by age, sex, country, and region. Age-standardized rates were assessed using joinpoint regression. A composite Quality of Care Index (QCI) was derived through principal component analysis. Gradient boosting models with SHapley Additive exPlanations interpretation identified key predictors, and Bayesian age–period–cohort models generated incidence projections.

In 2023, South and East Asia had the largest numbers of new cases, while North Africa and the Middle East and Andean Latin America recorded the highest age-standardized incidence, mortality, and disability rates. Eastern Europe and Andean Latin America showed sustained increases in mortality and disability despite moderate incidence growth. QCI values were lowest in South Asia, Western Sub-Saharan Africa, and Eastern Europe. High body mass index and fasting plasma glucose were prominent contributors in comparative risk attribution analyses, and machine learning models identified age and calendar year as the strongest predictors of modeled burden patterns. Incidence is projected to continue increasing through 2050, particularly in India and China.

MASLD burden and care quality vary widely across regions. Low-QCI regions show higher mortality and disability, unfavorable metabolic risk profiles, and delayed detection patterns. Strengthening prevention, early case finding, fibrosis assessment, and treatment access may slow MASLD progression.

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.

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.

Primary biliary cholangitis (PBC) significantly impairs health-related quality of life (HRQL), yet the impact of disease stage and fatigue on HRQL and psychological status remains insufficiently quantified. This study aimed to investigate differences in HRQL across disease stages and the impact of fatigue in patients with PBC.

This cross-sectional study recruited 219 patients with PBC from two Chinese tertiary hospitals (2011–2024). After excluding one preclinical case, 218 patients were analyzed. Quality of life was assessed using the validated Chinese versions of the SF-36 and Chronic Liver Disease Questionnaire (CLDQ); psychological status was assessed using the Self-Rating Anxiety Scale and Self-Rating Depression Scale. Between-group differences were quantified by mean differences (MDs) and odds ratios (ORs) with 95% confidence intervals (CIs). Baseline characteristics were balanced across stages (all P > 0.05).

Of the 218 patients (90.4% female; mean age, 57.2 ± 10.3 years), 41 were in the clinical stage, 75 in the fibrosis stage, and 102 in the cirrhosis stage. SF-36 scores were lowest in the cirrhosis stage (e.g., Physical Functioning MD, 17.26; 95% CI, 6.93–27.59 vs. clinical stage), with similar declines in CLDQ domains. Anxiety was highest in the clinical stage (58.5%; OR vs. cirrhosis, 4.13; 95% CI, 1.92–8.92), whereas depression was highest in the cirrhosis stage (55.9%; OR vs. clinical stage, 4.50; 95% CI, 1.95–10.38). Fatigue prevalence was 66.1% and increased with disease stage. Patients with fatigue had lower SF-36 scores in Physical Functioning, Bodily Pain, Vitality, Mental Health, and Physical Component Summary (e.g., Physical Component Summary MD, 38.22; 95% CI, 10.41–66.02).

HRQL declines progressively with PBC stage. Fatigue is strongly associated with impaired HRQL and is closely interrelated with anxiety and depression. Stage-specific psychological patterns suggest the need for tailored supportive interventions.

Nitric oxide (NO) is a crucial regulator of hepatic and systemic vascular tone. Abnormal distribution of NO in various anatomical locations is a pathogenetic characteristic of portal hypertension. Under normal portal pressure conditions, liver sinusoidal endothelial cells produce NO, which promotes both vasodilation and hepatic stellate cell relaxation. In portal hypertension, endothelial dysfunction, imbalance of asymmetric dimethylarginine levels, and production of superoxide result in impaired intrahepatic NO availability, leading to activation and contraction of hepatic stellate cells and worsening portal hypertension. Excess extrahepatic NO levels in the splanchnic vasculature result in systemic vasodilation, hyperdynamic circulation, and collateral vascular formation, worsening portal pressure. Abnormal clearance and production of NO can lead to extrahepatic complications, including hepatorenal syndrome and hepatopulmonary syndrome. Therapies including statins, phosphodiesterase-5 inhibitors, and midodrine have been developed to restore NO homeostasis but have achieved only partial success in modulating NO production, bioavailability, and distribution. The aim of this review is to update the understanding of the mechanisms and effects of NO dysregulation in cirrhosis as they relate to current and future therapeutic options.