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.

The clinical spectrum from cirrhosis to hepatocellular carcinoma (HCC) reflects interactions among hepatic dysfunction, systemic inflammation, and tumor burden. Whether circulating biomarkers add value beyond clinical parameters remains uncertain. This study aimed to evaluate an exploratory Model for End-Stage Liver Disease (MELD)–neutrophil-to-lymphocyte ratio (NLR)-based clinical–inflammatory phenotyping framework for discriminating advanced HCC features and to determine whether circulating hsa_circ_101555 provides incremental discriminatory value beyond this framework.

This single-center cross-sectional study included 92 consecutive patients (30 with cirrhosis without HCC and 62 with HCC). Patients were classified into three exploratory clinical–inflammatory phenotypes using a hierarchical MELD–NLR algorithm (Phenotype I, n = 25; II, n = 33; III, n = 34). Circulating hsa_circ_101555 was quantified by reverse transcription quantitative polymerase chain reaction. Receiver operating characteristic analysis evaluated Barcelona Clinic Liver Cancer stage C among patients with HCC (n = 62; events = 28). Internal validation used bootstrap resampling.

Higher-risk phenotypes included progressively larger proportions of patients with HCC and greater frequencies of advanced tumor characteristics. The combined MELD–NLR model showed the highest discrimination (the area under the receiver operating characteristic curve (AUC) 0.90; 95% confidence interval 0.82–0.97), with 85.7% sensitivity, 82.4% specificity, and 83.9% accuracy. This performance exceeded that of NLR alone (AUC, 0.80) and MELD alone (AUC, 0.77). Circulating hsa_circ_101555 was associated with smaller tumors and an earlier Barcelona Clinic Liver Cancer stage but showed modest discrimination (AUC, 0.69) and did not improve the MELD–NLR model (ΔAUC = 0.002; DeLong P = 0.79).

The exploratory MELD–NLR-based clinical–inflammatory framework identifies patient groups with differing frequencies of advanced HCC features. Circulating hsa_circ_101555 provides no incremental discriminatory value beyond routinely available clinical–inflammatory parameters and requires external validation before clinical use.

Hepatitis B virus (HBV) vertical transmission remains a major health challenge, and the characteristics of the placental immune microenvironment in chronic infection remain unclear. This study aimed to use mass cytometry to comprehensively analyze phenotypic changes in placental immune cell subsets.

We collected placental tissues from 20 pregnant women (6 healthy controls and 14 with chronic HBV infection). CD45+ leukocytes were detected using a 35-marker antibody panel. Unsupervised clustering identified 14 clusters, of which 13 immune clusters were analyzed.

HBV mainly caused functional remodeling of placental immune cells rather than changes in cell composition (P > 0.05 for all subsets). In natural killer (NK) cells, CD38 (P = 0.015) and CD16 (P = 0.0020) were notably upregulated and strongly correlated (ρ = 0.872, P < 0.001), suggesting potentially enhanced ADCC function. T cells showed upregulation of CD27, CD38, and CXCR5. Basophils exhibited the most pronounced changes: 9 differential markers (including chemokine receptors CCR4 and CCR7) were consistently downregulated. Classical monocytes showed an M1 polarization tendency (CD38↑, CD163↓). All P-values were raw; no markers remained significant after false discovery rate correction at an FDR threshold of < 0.1, indicating nominal significance. In addition, the coordinated expression patterns of markers within multiple cell subsets were weakened after infection.

These exploratory findings suggest that HBV may reshape placental immunity through enhanced NK cell activation, broad basophil suppression, and disrupted marker coordination. The sample size was limited (n = 20), so the results need to be validated in larger cohorts. These findings provide new perspectives for understanding the mechanisms of mother-to-child transmission.

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.