Eosinophilic esophagitis (EoE) is characterized by esophageal dysfunction and ≥15 eosinophils/high-power field on biopsy. The specific clinicopathologic characteristics and therapeutic outcomes of patients with concurrent gastric Helicobacter pylori infection and EoE remain poorly defined. This observational cohort study reexamines this relationship and evaluates the clinicopathologic features and outcomes of patients with concurrent diseases.

We retrospectively reviewed esophageal and gastric biopsies obtained between January 1, 2022, and December 30, 2025. Patients with a first-time diagnosis of EoE and concurrent treatment-naive gastric H. pylori infection were identified and confirmed by morphology and immunohistochemistry. Patients with a history of prior H. pylori eradication therapy or eosinophilic gastrointestinal disease were excluded. Clinical, pathologic, and follow-up data were analyzed.

Among 5,443 patients undergoing concurrent esophageal and gastric biopsy evaluation, 197 (3.6%, 95% confidence interval [CI], 3.1–4.1%) met the diagnostic criteria for EoE, and 286 (5.3%, 95% CI, 4.7–5.9%) had gastric H. pylori infection. Twenty-eight patients with concurrent EoE and gastric H. pylori infection were initially identified, corresponding to an H. pylori prevalence of 14.2% (28/197) among patients with EoE. A significant association was identified between EoE and H. pylori infection (odds ratio, 3.20; 95% CI, 2.11–4.87; Fisher’s exact test, P < 0.001). After exclusion of 1 patient with eosinophilic gastrointestinal disease and 3 patients with prior H. pylori treatment, 24 patients met the study inclusion criteria for the subsequent clinicopathologic analysis. Among these 24 patients (M:F = 7:1; mean age, 29.5 years; range, 8–82 years), 8 (33%) were children. The most common presentations (n = 18, 75%) were abdominal pain in children and dysphagia in adults. Atopy was present in 7 (29%) patients. Histologically, 5 (21%) cases exhibited classic features, while 19 (79%) showed nonclassic features with lower eosinophil density and a more uniform distribution of eosinophils within the epithelium. Among 10 patients with follow-up, 3/10 (30%) achieved resolution of both H. pylori infection and EoE after H. pylori eradication therapy with or without steroids; 5/10 (50%) had persistent H. pylori infection and persistent or recurrent EoE; 2(20%) achieved H. pylori-negative status but had persistent EoE; and fungal infection developed in 2 of 4 patients (50%) treated with steroids.

H. pylori infection may be associated with a nonclassic pattern of EoE. Recognition of this pattern may have implications for diagnosis and management.

Biliary atresia (BA) is the leading cause of pediatric obstructive cholestasis and a major indication for liver transplantation in infants. Organoid models are increasingly used to investigate BA pathogenesis and therapeutic responses, but incomplete methodological and clinical reporting may limit cross-study comparison and translational interpretation. This study aimed to map the landscape of BA-related organoid research, identify major reporting gaps, and propose Biliary Atresia Minimum Reporting Standard (BA-MRS) as a preliminary framework for improving reporting completeness.

PubMed, Scopus, and Web of Science Core Collection were searched on March 8, 2026, in accordance with the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) and the 2024 Joanna Briggs Institute (JBI) Manual for Evidence Synthesis. Reporting completeness was assessed using a 36-item BA-MRS across six domains, scored as fully reported, partially reported, not reported, or not applicable.

Twenty-six studies published between 2020 and 2026 were included. Fibrosis and epithelial–mesenchymal transition were the most frequently studied themes, whereas only one study linked organoid findings to post-Kasai outcomes. BA case/model definition, ethics approval, and differentiation protocols were fully reported in all applicable studies (100%). In contrast, contamination monitoring (3.8%), core biliary function assays (34.6%), and clinical outcome linkage (26.3%) were poorly reported. Culture System and Sample Acquisition showed the lowest domain-level fully reported rates (58.1% and 63.2%, respectively).

BA organoid research has progressed beyond early model development, but reporting remains insufficient for robust comparison, reproducibility, and clinically meaningful interpretation. BA-MRS may serve as a preliminary framework for improving standardized reporting in future studies.

Celiac disease remains underdiagnosed despite an established diagnostic pathway, reflecting phenotypic heterogeneity, delayed recognition, and dependence on resource-intensive testing. This narrative review synthesizes evidence on artificial intelligence and phenomics in celiac disease (CD) across four operational layers: electronic health record phenotyping, Human Phenotype Ontology-based semantic encoding, machine-learning pre-screening from routine clinical data, and deep-learning-assisted histopathology. A targeted literature search of PubMed/MEDLINE, Embase, and Google Scholar covered publications from January 2010 through December 2025, using combinations of CD/coeliac disease with artificial intelligence, machine learning, deep learning, phenomics, Human Phenotype Ontology, computable phenotype, electronic health records, and natural language processing, supplemented by targeted searches and citation chaining. We present a curated minimum viable CD phenome and discuss clinical actionability, age-specific considerations, and current pediatric validation gaps. Selected models have demonstrated promising CD detection or pre-screening performance in specific datasets, but prospective, multicenter evidence with external validation remains insufficient to establish clinical utility. Artificial intelligence should augment expert clinical care rather than replace it.

Anal canal melanoma (ACM) is a rare, aggressive malignancy with an ominous prognosis. However, its associated factors are largely unknown. Therefore, we investigated potential independent associations of sex and self-reported race with ACM and physiological anal canal pigmentation.

Two case-control cohorts from a single institution in Miami, Florida, were evaluated. The biopsy cohort comprised 117 sequential patients evaluated prospectively for melanocytic cells/pigment and anal intraepithelial neoplasia (AIN)/squamous intraepithelial lesion (SIL) in anal transitional zone biopsies between January 2021 and August 2022. The melanoma cohort consisted of 28 patients diagnosed with ACM between January 2003 and August 2021 and 116 of the patients in the pigmentation cohort. Multivariable logistic regression analysis was conducted to examine independent factor associations.

In the biopsy cohort, anal transitional melanocytic cells/pigment were identified in 48% (26/54) of Black patients compared to 17% (10/59) of White patients. Multivariable analysis demonstrated that White race was inversely associated with mucosal pigmentation (odds ratio (OR) = 0.19, 95% confidence interval (CI): 0.08–0.48, P < 0.001). Conversely, White race was associated with ACM (OR = 6.25, 95% CI: 2.07–18.81, P = 0.001). Male sex was also inversely associated with ACM (OR = 0.18, 95% CI: 0.07–0.47, P < 0.001). No significant correlations were observed between mucosal pigmentation and AIN/SIL or human immunodeficiency virus status.

Anal transitional zone pigmentation is more prevalent in self-reported Black individuals but is not associated with neoplastic squamous cell precursors. White (versus Black) individuals and female (versus male) individuals both have a significant association with ACM.

Although hepatitis B surface antigen (HBsAg)-specific B cells have been partially characterized in chronic hepatitis B (CHB), the role of Naïve B cells and their potential relevance to functional cure remain insufficiently explored. Here, we aimed to characterize the naïve B-cell subsets between cured and uncured patients with CHB.

In this retrospective study, we applied single-cell RNA sequencing to compare peripheral B-cell profiles between cured and uncured CHB patients. Key findings were validated by flow cytometry in an independent cohort and further supported in a nucleos(t)ide analog monotherapy cohort stratified by HBsAg levels.

Single-cell RNA sequencing characterized two Naïve B-cell subsets, designated IL-4R+SELL+ and IL-4R−SELL− Naïve B cells, which were differentially distributed between functionally cured and uncured patients. Cured patients showed higher frequencies of total B cells and IL-4R+SELL+ Naïve B cells than uncured patients. In contrast, uncured patients exhibited persistent hyperactivation of type I interferon signaling in both Naïve and memory B cells. The IL-4R+SELL+ subset showed a transcriptional signature associated with germinal center biology and exhibited stronger ligand–receptor interactions with CD40LG+CD4+ T cells. Notably, the frequency of the IL-4R+SELL+ subset was inversely correlated with HBsAg levels. Consistently, patients with lower HBsAg levels also exhibited significantly higher frequencies of IL-4R+SELL+ Naïve B cells compared with those with high HBsAg levels.

Collectively, these findings indicate that the IL-4R+SELL+ Naïve B-cell subset is characterized by germinal center-related responses and enhanced T-cell-mediated help and may serve as an immunological component associated with functional cure in CHB.

Upper gastrointestinal precancerous lesions are important targets for cancer screening and prevention. This study evaluated the diagnostic accuracy of artificial intelligence (AI)-assisted endoscopy for upper gastrointestinal precancerous lesions.

PubMed, Embase, MEDLINE, Cochrane Library, and IEEE Xplore were searched from inception to March 31, 2026. Studies reporting sensitivity and specificity, or sufficient data for their calculation, were included. Two reviewers independently extracted data. Pooled sensitivity, specificity, and the area under the receiver operating characteristic curve were estimated using a bivariate random-effects model.

Fifteen studies comprising 24 datasets and 19,578 records were included. Pooled sensitivity and specificity were 0.930 (95% confidence interval (CI): 0.886–0.958) and 0.944 (95% CI: 0.906–0.967), respectively; the diagnostic odds ratio was 223.79 (95% CI: 92.24–542.94), and the area under the receiver operating characteristic curve was 0.9661. Substantial heterogeneity was observed (bivariate I² = 73%). Among the variables formally evaluated by meta-regression, imaging modality was associated with heterogeneity (global test P = 0.005); image-enhanced endoscopy had higher sensitivity than white-light endoscopy (0.960 vs. 0.875). No significant publication bias was detected by Egger’s test (P = 0.833), Begg’s test (P = 0.641), or Deeks’ funnel plot asymmetry test (P = 0.053).

AI-assisted endoscopy shows high diagnostic accuracy for upper gastrointestinal precancerous lesions. Multicenter prospective studies are needed for validation.

Metabolic dysfunction-associated steatotic liver disease affects roughly 38% of adults, yet approved agents do not correct the upstream redox-metabolic perturbations—a depressed nicotinamide adenine dinucleotide (NAD+/NADH) ratio, saturated lipid excess, and endoplasmic reticulum (ER) stress—that drive hepatocyte injury. Cytochrome b5 reductase 3 (CYB5R3) couples NADH oxidation to fatty acid desaturation, nuclear factor erythroid 2-related factor 2 (NRF2)-linked antioxidant and cholesterol-handling pathways, NAD+/sirtuin signaling, and ER-phagy, and is the sole electron input to mitochondrial amidoxime-reducing component 1 (mARC1). This review grades every link in the axis across the steatosis–cirrhosis–hepatocellular carcinoma spectrum, reporting effect estimates with sample sizes and test statistics alongside a study-level appraisal of clinical relevance. The common MTARC1 p.A165T variant protects against all-cause cirrhosis (odds ratio, 0.91; 95% CI, 0.89–0.94; P = 2.3 × 10−11; 12,361 cases, 790,095 controls), with lower hepatic fat, liver enzyme levels, and low-density lipoprotein cholesterol levels. Germline mARC1 deletion reduces picrosirius red fibrosis area by 24–50% depending on diet, without altering histological disease activity, whereas partial protein reduction confers no protection. Critically, therapeutic hepatocyte-directed knockdown loses its anti-fibrotic effect when started at higher disease burden and in the choline-deficient model: efficacy depends on the depth, compartment, and timing of inhibition. Deep, hepatocyte-restricted mARC1 inhibition by GalNAc-conjugated oligonucleotides—which also avoids a male-predominant cardiac liability—is therefore the most credible near-term strategy, only in pre-cirrhotic F2–F3 disease. CYB5R3 activation, and its combination with mARC1 inhibition, remain unproven, and no clinical trial of this axis has been reported. Falsifiable in vivo and pharmacodynamic biomarker roadmaps are proposed, together with the efficacy, delivery, and safety uncertainties specific to advanced cirrhosis and a non-invasive pharmacodynamic framework.