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.

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.