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 TGF-β signaling, reactive oxygen species (ROS) generation, and 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.

Medullary thyroid carcinoma (MTC) is a neuroendocrine malignancy arising from parafollicular C-cells with known variations in cytomorphologic and immunophenotypic features. New neuroendocrine markers pituitary homeobox 2 (PITX2), paired-like homeobox 2B (PHOX2B), and heart and neural crest derivatives expressed 2 (HAND2) have recently been introduced, but studies using these markers in MTC are limited. The aim of this study was to evaluate the expression and potential diagnostic utility of PITX2, PHOX2B, and HAND2 in primary and secondary MTCs and to compare their expression with chromogranin A, synaptophysin, insulinoma-associated protein 1 (INSM1), and calcitonin.

A total of 34 histologically confirmed cases of MTC with available cell blocks were included. Sixteen MTC samples were fine-needle aspirates from primary thyroid lesions, and eighteen were from secondary metastatic lesions. Twelve samples from thyroid carcinomas of follicular origin were included as controls.

PITX2 positivity was observed in 17 (50.0%) MTC samples and in 4 (33.3%) control samples (P = 0.502). PITX2 positivity was found in 43.8% of primary thyroid MTC lesions and in 55.6% of secondary MTC lesions (P = 0.366). Co-expression of PITX2 with chromogranin A, synaptophysin, INSM1, and calcitonin was observed. PHOX2B and HAND2 were negative in all MTC and control samples.

There were no significant differences in PITX2 expression between primary and secondary MTC samples. PITX2 did not show reliable utility in distinguishing MTC from thyroid carcinomas of follicular origin. PHOX2B and HAND2 were negative in all samples. These results suggest that these new markers do not offer diagnostic value for MTC as stand-alone markers or as additions to the diagnostic workup panel.

Early detection of gastric cancer is critical for reducing incidence and mortality, as well as for improving survival outcomes. Although gastroscopy remains the gold standard for gastric cancer screening and diagnosis, its invasiveness, discomfort during the procedure, and limited acceptability restrict population participation and screening coverage. Recently, rapid advances in liquid biopsy technologies have led to the discovery of numerous multi-omics biomarkers spanning genomics, transcriptomics, proteomics, and metabolomics, with promising diagnostic performance. However, their translational value for population-based gastric cancer screening and control remains insufficiently characterized. This review aims to provide a comprehensive overview of multi-omics biomarkers for gastric cancer screening and to evaluate their potential role in advancing population-level gastric cancer control. First, we synthesize multi-omics biomarkers with diagnostic and screening relevance across the continuum of gastric carcinogenesis, from chronic inflammation and atrophy to intestinal metaplasia, dysplasia, and early gastric cancer. Furthermore, we highlight the integrative value of multi-omics biomarkers, current limitations, translational challenges, and future opportunities for moving biomarkers from discovery to implementation in organized screening programs. In conclusion, multi-omics biomarkers have the potential to complement existing screening strategies by providing scalable, non-invasive, and risk-adapted approaches for early gastric cancer detection. Bridging the gap between biomarker discovery and real-world implementation will be essential for realizing their value in future gastric cancer screening programs.

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.

Myelodysplastic syndromes (MDS) are a group of hematopoietic disorders characterized by ineffective hematopoiesis, with manifestations of cytopenias in one, two, or three lineages. CD34+ micromegakaryocytes and giant platelets are very rarely seen in MDS patients but may lead to unnecessary treatments. Therefore, we report and follow up on an MDS case with such an unusual finding.

A 57-year-old male veteran with a history of MDS, alcoholic cirrhosis, and portal hypertension presented to the Emergency Department in 2020 for evaluation after a blackout, at which time peripheral blood samples and bone marrow biopsies were obtained. Flow cytometry analysis of his peripheral blood detected 8% CD34+ cells. This finding raised the possibility of acute leukemic transformation from MDS. Further studies revealed that these CD34+ cells represented dysplastic micromegakaryocytes and giant platelets rather than blasts. During his 4-year follow-up, the patient was alive and complained only of easy fatigability, lasting several weeks. His laboratory results showed pancytopenia and persistent iron-deficiency anemia.

The distinction between micromegakaryocytes and giant platelets versus megakaryoblasts is extremely important in patients with MDS. This distinction may prevent misdiagnosis of acute leukemia and unnecessary treatments such as chemotherapy.

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 GBD 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 chronic hepatitis B (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.

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.

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.

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.