Background Helicobacter pylori (H. pylori) eradication is one of the most well-established strategies for the prevention of gastric cancer and is recommended in several countries, particularly in high-risk countries. However, gastric cancer can still develop even after successful eradication. As H. pylori eradication has become more prevalent, characterizing gastric cancers that arise following eradication and surveillance and management strategies have emerged as important clinical challenges. Summary Gastric cancers that develop after H. pylori eradication predominantly arise from pre-existing precancerous lesions, such as atrophic gastritis or intestinal metaplasia, which often persist with irreversible histological, genetic, or epigenetic alterations. Although H. pylori eradication reduces the overall risk of gastric cancer, residual risk depends on the extent and severity of atrophy or intestinal metaplasia. Molecular changes, including persistent CpG island hypermethylation and aberrant miRNA expression, particularly within intestinal metaplasia, may persist after eradication. These cancers are mainly intestinal type and frequently present as small, depressed, gastritis-like appearance, or lesions covered by epithelium with low-grade atypia, making endoscopic diagnosis challenging. Risk prediction can be improved through endoscopic assessment of precancerous lesions, advanced high-resolution imaging endoscopy techniques and molecular biomarkers. Given the persistent risk, individualized, risk-based long-term surveillance strategies are essential, particularly for patients with extensive atrophy or intestinal metaplasia. Key Messages 1. Despite H. pylori eradication, the risk of gastric cancer persists in patients with atrophic mucosal changes and intestinal metaplasia. 2. Gastric cancers after H. pylori eradication exhibit distinct endoscopic and pathological features compared to those without prior eradication, making early diagnosis challenging. 3. Risk stratification based on endoscopic assessment, advanced imaging, and molecular biomarkers can refine surveillance strategies, emphasizing the importance of long-term, personalized follow-up after eradication.

Barrett's esophagus (BE) is the replacement of normal squamous epithelium in the distal esophagus by columnar epithelium. The prognosis of esophageal adenocarcinoma (EAC) depends largely on the stage at diagnosis. Advances in endoscopic imaging and quality standards have significantly improved the early detection of BE-associated neoplasia. This review summarizes current classification systems, sampling protocols, and adjunct tools for diagnosing early neoplasia in BE in Western practice. In Western practice, the diagnosis of Barrett's esophagus (BE) relies on consensus criteria requiring endoscopic evidence and histological confirmation of columnar epithelium proximal to the gastroesophageal junction. However, there are discrepancies regarding the minimum BE extent and the necessity of intestinal metaplasia for diagnosis. Detecting early neoplasia in BE is challenging due to the flat and subtle nature of dysplastic lesions. High-definition white light endoscopy (HD-WLE) is the standard modality for BE surveillance and is used to assess for characteristic features of neoplasia, including nodularity, surface irregularity, color changes, and demarcated areas. Image-enhancing techniques-such as virtual chromoendoscopy (e.g., Narrow-Band Imaging [NBI], Texture and Color Enhancement Imaging [TXI], Blue Light Imaging [BLI], Linked Color Imaging [LCI]), and acetic acid chromoendoscopy-have improved dysplasia detection when applied alongside validated classification systems. Despite technological advances, random four-quadrant biopsies (4QBs) remain the standard for dysplasia detection. Estimating lesion depth is based primarily on HD-WLE, with limited contribution from chromoendoscopy and ancillary imaging techniques (i.e. endoscopic ultrasound [EUS], confocal laser endomicroscopy [CLE], optical coherence tomography [OCT]). Early Barrett's neoplasia is challenging to detect. HD-WLE and image-enhancing techniques improve visualization, but random 4QBs remain central to the diagnostic process. Lesion depth is primarily assessed using endoscopic features and, to a limited extent, ancillary techniques.

PurposeChronic atrophic gastritis (CAG) is a prevalent condition that can undergo precancerous lesions of gastric cancer (PLGC) and thus progression to gastric cancer. Weifuchun (WFC), a traditional Chinese herbal compound, is employed in CAG treatment and microbial homeostasis modulation. We aimed to explore the role of WFC in CAG from the perspective of gastrointestinal microbiota.MethodsPLGC rats were developed by N-methyl-N’-nitro-N-nitrosoguanidine treatment. Then, various doses of WFC were administered to the rats and WFC compositions were analyzed. The pathological changes and inflammatory markers of the rats were assessed. Key proteins in the interleukin (IL)-6/Janus Kinase 1/Signal Transducer and Activator of Transcription 3 (JAK1/STAT3) pathway were evaluated, alongside fecal microbial analysis through 16S ribosomal DNA sequencing.ResultsMost compounds identified from WFC were nucleosides, flavones, organic acids, phenylpropanoids and other components. WFC treatment alleviated intestinal metaplasia and dysplasia caused by atrophic gastritis in PLGC rats. WFC also reduced inflammatory marker levels, and inhibited the IL-6/JAK1/STAT3 pathway for PLGC rats. The higher the dose of WFC was administrated, the better the effects on the aforementioned results. Simultaneously, WFC improved the CAG gastrointestinal microbiota homeostasis. Interestingly, WFC increased Coprocuccus abundance, which was significantly correlated with proliferating cell nuclear antigen and IL-6 levels.ConclusionsWFC alleviated PLGC by regulating the balance of gastrointestinal microbiota and influencing the IL-6/JAK1/STAT3 pathway, revealing the potential connection between gastrointestinal microbiota and CAG progression. This study is the first to link gastrointestinal microbiota homeostasis and IL-6/JAK1/STAT3 pathway, providing novel insights into WFC’s multi-targeted therapeutic mechanism on CAG.

Objectives Oesophageal adenocarcinoma (OAC) has a poor prognosis as patients typically present with late-stage disease. Gastro-oesophageal reflux disease (GORD) can lead to Barrett’s oesophagus (BO), the only known precursor to OAC. Detecting patients with BO allows interventions to prevent development of late-stage OAC and improve survival. Non-endoscopic devices, such as EndoSign, coupled with biomarkers trefoil factor 3, atypia and p53 have demonstrated performance for diagnosis of BO. The CYTOPRIME 2 Study was designed to assess the feasibility of implementing this test in a real-world community care setting. Methods Patients with chronic GORD identified from general practitioner electronic records were invited to have a capsule sponge test (ie, EndoSign) in the community, of which 1815 completed the test. Results 266 (14.7%) had a subsequent endoscopy based on a positive test. 97 patients (5.3%) of the total group, or 36% of those endoscoped, had BO confirmed at endoscopy of whom 90 (93%) had intestinal metaplasia on histology and 3 had low-grade dysplasia (3%). In addition, 6 patients (0.3%), or 2.2% of those endoscoped, had cancer—4 with OAC, 1 squamous cell oesophageal tumour and 1 early stage gastric cancer. Patients’ and clinicians’ acceptability of the test was high. Conclusions Non-endoscopic capsule sponge testing can be used successfully in community settings to diagnose BO and minimally symptomatic oesophagogastric cancer in a target population of patients with GORD. Patients diagnosed with BO can be offered prospective surveillance to detect precancerous changes and allow endoscopic therapies to prevent late-stage oesophageal cancer.

Probe-based confocal laser endomicroscopy (pCLE) provides real-time, cellular-level "optical biopsy" during endoscopy. This review synthesizes the technology, diagnostic performance, clinical use, safety, costs, and future directions of pCLE across gastrointestinal indications. Targeted narrative review of randomized trials, meta-analyses, and observational studies on pCLE in Barrett's esophagus, gastric intestinal metaplasia (GIM), colorectal neoplasia, inflammatory bowel disease (IBD), and indeterminate biliary strictures. Outcomes included sensitivity/specificity, impact on biopsy yield and management, adverse events, and cost effectiveness. pCLE combines a fiber-optic probe and IV fluorescein with 488-nm excitation to generate optical sections (~1 µm lateral resolution; depth ~55-70 µm). In Barrett's esophagus, adding pCLE to high-definition endoscopy nearly doubled neoplasia detection sensitivity versus standard protocols. For GIM, pooled sensitivity and specificity reached 97% and 94%. For colorectal lesions, sensitivity 81-91% and specificity 75-91% allowed in vivo characterization and fewer unnecessary resections. In IBD surveillance, pCLE identified more neoplasia with fewer biopsies (up to ~4.7-fold increase) and pooled sensitivity/specificity of 87-100%/90-94%. In indeterminate biliary strictures, pCLE integrated with ERCP/EUS improved accuracy and achieved negative predictive values up to 100%. Safety is favorable; risks relate mainly to fluorescein. Limitations include superficial penetration, narrow field of view, operator dependence, image-interpretation variability, procedure time, and high capital and per-case costs. Current guidelines view pCLE as an adjunct rather than routine standard. Emerging AI-assisted interpretation and molecular/ multispectral probes may standardize reads, expand indications, and improve yield. pCLE strengthens endoscopic decision-making by enabling immediate, near-histologic assessment, targeted sampling, and earlier therapy. Broader adoption hinges on standardized training, validated image criteria, multicenter randomized trials with health-economic endpoints, and integration of AI and molecular imaging to reduce variability and cost.

Helicobacter pylori is a gastric pathogen that induces chronic gastritis, which may progress to neutrophilic activity, glandular atrophy, intestinal metaplasia, and gastric carcinoma. The aim of this study was to evaluate H. pylori-induced tissue damage. A total of 602 gastric biopsy samples were collected, categorized, and analyzed using hematoxylin and eosin and Giemsa staining, followed by molecular confirmation through PCR targeting the species-specific 16S rRNA gene. H. pylori density and histopathological features were evaluated and graded according to the updated Sydney classification system. H. pylori was detected in 55% (n = 334) of cases, and the antrum (50.83%, p < 0.00001) was the predominant site. A slightly higher prevalence was observed in females, accounting for 56.9% compared to males at 43.1%, which was attributed to sociocultural exposure differences. Individuals aged 11–40 years accounted for 58.3% (n = 195), highlighting early-age acquisition of infection. H. pylori infection was significantly linked to moderate-to-severe inflammation (63.2%, p < 0.00001) and neutrophilic activity (53.3%, p < 0.00001). Intestinal metaplasia and atrophy were infrequent, present in 0.6% (95% CI, 0.02, p = 0.149) and 0.9% (95% CI, 0.05, p = 0.430) of individuals. H. pylori infection causes chronic inflammation and neutrophilic infiltration of the stomach mucosa. Early identification and histopathological examination are essential in assessing H. pylori-related gastric pathology.

Abstract Introduction/Objective Epstein-Barr virus-associated gastric carcinoma (EBVaGC) typically arises in intestinalized mucosa, with EBV infection considered a late event. Its role in precursor lesions remains poorly understood. Methods/Case Report An 82-year-old male with remote Billroth II surgery underwent endoscopic evaluation for a pancreatic mass. Incidentally, a 25 mm gastric body lesion was identified and resected by endoscopic submucosal dissection. Histology revealed foveolar-type dysplasia and adjacent intramucosal adenocarcinoma. Both components were strongly EBV-positive by EBER in situ hybridization (EBER-ISH). The dysplasia showed MUC5AC positivity with a gastric phenotype (CK7 patchy, CDX2−), while the carcinoma exhibited loss of MUC5AC and increased p53 expression with a wild-type pattern. Background mucosa lacked intestinal metaplasia, Helicobacter pylori, and enterochromaffin-like cell hyperplasia, consistent with post-surgical atrophic body-type mucosa. Results NA Conclusion This case demonstrates EBV-positive foveolar-type dysplasia progressing to carcinoma in non-metaplastic gastric mucosa, challenging the conventional sequence of EBVaGC development. The findings support EBV as an early and sufficient oncogenic driver, independent of intestinal metaplasia or H. pylori, and highlight an underrecognized gastric pathway. Awareness of this alternate route may impact diagnostic classification, early detection, and surveillance strategies.

Indications for combining remnant resection in a primary Roux-N-Y gastric bypass: Preliminary results.

Should we subtype gastric intestinal metaplasia in gastric biopsies, a single institution's experience.

BackgroundGastric cancer progression involves complex interactions among tumor cells, immune components, and stromal elements within the tumor microenvironment. However, a comprehensive understanding of cellular heterogeneity, spatial organization, and cell-cell communication in gastric cancer remains incomplete.MethodsSingle-cell RNA sequencing was performed on 252, 399 cells from six tissue types, spanning gastritis, intestinal metaplasia, primary tumors, adjacent normal tissue, and metastatic lesions. Integration with spatial transcriptomics enabled spatial mapping of cellular interactions. Pseudotime, cell-cell communication, and transcriptional heterogeneity analyses were conducted. Tumor stage-associated gene modules were identified using Weighted Gene Co-expression Network Analysis (WGCNA) of The Cancer Genome Atlas (TCGA) data. Finally, a deep learning-based prognostic model was developed and externally validated.ResultsOur analysis revealed dynamic remodeling of the tumor microenvironment during gastric cancer progression, characterized by the expansion of dysfunctional CD8+ T cells, pro-tumorigenic fibroblasts (e.g., ITGBL1+, PI16+, and ITLN1+), and altered myeloid populations. Stromal-immune crosstalk, particularly fibroblast-driven immunosuppressive signaling, was prominent. Spatial transcriptomics revealed the colocalization of immune and stromal cells, supporting spatially organized cellular interactions. WGCNA identified a gene module (657 genes) associated with T cell, myeloid, and stromal alterations, as well as tumor stage. A deep learning model based on this gene set accurately stratified patients according to survival in both TCGA and independent validation cohorts. Risk scores were correlated with clinical features, including tumor stage and therapeutic response.ConclusionsOur integrative single-cell, spatial, and computational analysis provides a high-resolution map of gastric cancer microenvironment remodeling. We identified key stromal and immune subpopulations, extensive cellular communication networks, and spatial structures that collectively drive tumor progression and metastasis. The derived gene signature and prognostic model have the potential for clinical risk stratification and therapeutic targeting in gastric cancer.

BackgroundThe association between gastric intestinal metaplasia severity grades, histological subtypes, and oncogenic potential remains unclear. This study explored gastric intestinal metaplasia (GIM) subtypes and c-Myc protein expression across mild, moderate, and severe GIM cases.MethodsA total of 180 paraffin-embedded gastroscopy biopsy samples from patients diagnosed with atrophic gastritis were selected, with 60 cases each of mild, moderate, and severe GIM. Alcian blue-Periodic acid-Schiff (AB-PAS) and high iron diamine (HID) staining were used to classify GIM into types I-III. Immunohistochemistry was performed to assess c-Myc expression, with low, moderate, and high expression defined as the percentage of c-Myc-positive cells in the GIM area of <15%, 15–40%, and ≥ 40%, respectively. Spearman and Kruskal–Wallis tests were used to analyze the correlation between GIM severity, GIM subtype, and c-Myc expression.ResultsGIM was predominantly diagnosed in middle-aged and elderly individuals. Regarding the subtype, 53.89% were type II, 25.56% were type III, and 20.56% were type I. Low c-Myc expression was present in 47.78% of cases, moderate expression in 36.67%, and high expression in 15.56%. Neither the severity of GIM nor its subtype or c-Myc expression level was correlated with age or sex. Type III GIM accounted for approximately 10% of mild-to-moderate cases, whereas > 50% of severe GIM cases were type III. A positive correlation was found between GIM severity and subtype (rs = 0.376, P < 0.05). There was no significant correlation in c-Myc expression across different GIM severities. From type I to type III GIM, the proportion of low c-Myc expression increased and that of high expression decreased, whereas that of moderate expression remained almost unchanged. A negative correlation was observed between the GIM subtype and c-Myc expression (rs = −0.148, P < 0.05).ConclusionGIM incidence increases with age; however, the histological severity of GIM (as defined by the extent of mucosal gland involvement) within a single biopsy sample does not show a corresponding increase with age. The more severe the GIM is, the greater the proportion of type III GIM cases present. c-Myc expression did not correlate with GIM severity. Conversely, as the GIM subtype becomes more advanced (from type I to type III), c-Myc expression decreases.

In the context of dysbiosis, chronic inflammation, and carcinogenesis, non-Helicobacter pylori bacteria are becoming more widely acknowledged as significant contributors to stomach diseases. The stomach contains a variety of bacterial communities, including Fusobacterium nucleatum, Streptococcus species, Lactobacillus species, Prevotella species, Veillonella species, and Propionibacterium acnes, according to studies employing next-generation sequencing. Because of adaptation processes like urease activity, acid-tolerant metabolism, and biofilm development, these organisms can survive in acidic environments. While some, like Lactobacillus, can create metabolites like lactic acid that may impact carcinogenic nitrosation reactions, others, including F. nucleatum and Streptococcus, cause inflammation through immune activation and cytokine production. A known stomach carcinogen, N-nitroso compound, may be formed more frequently if nitrate-reducing bacteria proliferate. Following H. pylori eradication, dysbiosis frequently involves elevated abundance of these taxa, which may impact stomach cancer risk and mucosal integrity. The need for more comprehensive microbiome-targeted therapeutic approaches is highlighted by mounting evidence that non-H. pylori bacteria interact either antagonistically or synergistically with H. pylori and host factors, causing intestinal metaplasia, gastritis, and tumour progression, even though causality is still being investigated.

Background. Barrett’s esophagus is the only known histological precursor of esophageal adenocarcinoma. Combining mo­dern endoscopic treatment methods with the capabilities of artificial intelligence can significantly improve treatment outcomes, increase diagnostic accuracy, and enable a personalized approach to the management of Barrett’s esophagus. Objective: to improve methods for the diagnosis, monitoring, and treatment of Barrett’s esophagus through the application of artificial intelligence. Materials and me­thods. A prospective study was conducted involving 96 patients with Barrett’s esophagus combined with hiatal hernia, 52 males and 44 females. Their mean age was 54.4 ± 12.3 years. Particular attention was paid to clinical prediction in detecting dysplasia, as well as to the efficacy of endoscopic argon plasma coagulation (APC) for different types of Barrett’s esophagus, utilizing artificial intelligence. Results. Reflux esophagitis was diagnosed in 71.1 % of cases, most commonly LA grade A (30.9 %). Type I hiatal hernia was found in 45.8 % of patients, type III in 50 %, and type IV in 4.2 %. Morphological analysis revealed intestinal metaplasia with low-grade dysplasia in 45.26 % of cases, high-grade dysplasia in 4.21 %, and high-grade dysplasia combined with Abrikosov tumor in 1.05 %. Endoscopic treatment included conventional APC in 30 patients and hybrid APC in 65. Single-stage conventional APC was performed in 36.7 % of cases, while two-stage treatment was used in 63.3 %. Hybrid APC was applied in a single stage in 78.8 % of patients and in two stages in 21.2 %. Postoperative complications occurred less frequently after hybrid APC. Conclusions. Hybrid argon plasma coagulation, compared to conventional treatment methods, is the preferred option for endoscopic management of Barrett’s esophagus due to its high safety profile and effective eradication of metaplastic epithelium. The use of artificial intelligence enables the selection of individualized treatment strategies, which enhances clinical effectiveness, reduces complication rates, and optimizes the economic aspect of care.

Accurate localization of early gastric cancer (EGC) remains challenging due to its morphological resemblance to gastritis. This study presents an artificial intelligence (AI)-assisted bedside diagnostic system to enhance EGC detection by visualizing gastric mucosal acidity. The ATPase H+/K+ transport β subunit (ATP4B), a key regulator of acid secretion, is progressively downregulated in gastric mucosal atrophy and intestinal metaplasia, and significantly reduced in EGC. A surface-enhanced Raman scattering (SERS) microarray is developed to map mucosal pH in 50 patient specimens (1,516 points), with founding compared to pathological images. A multi-model neural network is trained and validated internally on data from 40 patients (1,127 points) and externally validated on 10 patients (389 points). Using an optimal pH threshold of 6.845, the system achieved a strong correlation (R2 = 0.79) and low error (SSE = 71.83). External validation demonstrated 87.79% sensitivity, 85.04% specificity, 86.89% accuracy, and a κ score of 0.71. This system detected mild pH shifts in atrophic gastritis with intestinal metaplasia, but marked increases with EGC onset, and is able to predict inflammation prior to pathology confirmation. By integrating pH mapping with morphological features, this approach enables precise EGC localization, improves guidance for endoscopic submucosal dissection (ESD), and reduces false-positive diagnoses.

Gastric cancer is a leading cause of cancer-related mortality and highlights the need for early detection of gastric cancer and Helicobacter pylori (HP) infection, which is a major risk factor. Early non-invasive and convenient diagnostic tools capable of capturing the dynamic molecular alterations during carcinogenesis and HP infection is needed. In this study, we use Raman spectroscopy and machine learning algorithms to detect different gastric lesions and HP infection condition with gastric juice samples. 133 patients from Peking University Third Hospital were involved and categorized into groups based on histopathological diagnosis: early gastric cancer (EGC), dysplasia (DYS), intestinal metaplasia (IM), and chronic superficial gastritis (CSG), with further classification based on HP infection. The stacked machine learning model demonstrated high diagnostic performance, achieving 90% accuracy, 90% sensitivity, and 97% specificity in distinguishing pathological stages, along with 96% accuracy, 96% sensitivity, and 96% specificity in HP detection. The multilayer perceptron (MLP) model based on gastric juice Raman spectroscopy showed excellent discrimination capability, with an AUC of 0.98 for differentiating controls from patients with DYS and EGC. Additionally, Raman spectroscopy achieved an AUC of 0.95 in distinguishing control gastric mucosa from precancerous lesions (IM, DYS) and EGC. The approach offers a rapid, accurate, and minimally invasive diagnostic tool, demonstrating significant potential for clinical application in rapid and accurate detection of precancerous lesions, early gastric cancer, and HP infection.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-20270-9.

Background and objectivesSex steroid hormones have been hypothesized to be associated with the risk of gastric cancer (GC); however, it has not been widely validated in prospective studies. We aimed to investigate the associations between sex steroid hormone metabolites and the risk of gastric cancer and precancerous lesions in a prospective cohort of Chinese men.MethodsUsing liquid chromatography-tandem mass spectrometry (LC-MS/MS) and electrochemical luminescence immunoassay, we examined 20 sex steroid hormone metabolites and sex hormone-binding globulin (SHBG) in serum from 470 eligible men, including high-grade lesions or GC (n = 32), intestinal metaplasia (IM, n = 146), and 1:2 matched normal participants (n = 292) from 2007 to 2012. IM and normal participants were further followed up until December 2021, during which 32 new GC cases were identified with a median follow-up of 11.8 years. Associations between baseline sex steroid hormone metabolites and IM, high-grade lesions and gastric cancer were assessed using logistic regression, and associations between sex steroid hormone metabolites and incident GC risk were assessed using Cox proportional hazards regression in the prospective analysis.ResultsIn the cross-sectional analysis, androstenedione levels were potentially associated with IM risk and significantly associated with high-grade lesions or GC risk (ORcontinuous = 2.45, 95% CI: 1.01–5.95). Higher concentrations of 17α-hydroxypregnenolone (ORcontinuous = 2.35, 95% CI: 1.13–4.88), progesterone (ORcontinuous = 2.68, 95% CI: 1.09–6.61), and estrone (ORcontinuous = 5.36, 95% CI: 1.28–22.52) were also associated with an increased risk of high-grade lesions or GC. Furthermore, significant positive associations between GC risk and serum levels of SHBG (HRcontinuous = 2.57, 95% CI: 1.04–6.36), epitestosterone (HRcontinuous = 2.10, 95% CI: 1.07–4.15) and pregnenolone (HRcontinuous = 1.30, 95% CI: 1.03–1.63) were identified in the follow-up study focusing on participants diagnosed as normal or IM. Notably, the subgroup analyses stratified by H. pylori status revealed similar associations between androstenedione, 17α-hydroxypregnenolone, progesterone, estrone, SHBG, pregnenolone, and GC risk.ConclusionsSeveral sex hormone metabolites were significantly associated with gastric cancer and its precancerous lesions, indicating a role for sex hormones in gastric carcinogenesis and potentially providing novel biomarkers for the identification of high-risk populations and risk prediction for GC.

(1) Background: Gastric cancer continues to pose a significant public health challenge, with its incidence influenced by various factors, including Helicobacter pylori (H. pylori) infection. In Lebanon, data on H. pylori prevalence and its associated risk factors remain limited. This study aimed to determine the prevalence of H. pylori infection among Lebanese outpatients presenting with gastrointestinal symptoms undergoing gastroscopy, to explore correlations between the infection and demographic and clinical variables, and to evaluate the prevalence of associated conditions such as gastritis, duodenitis, and intestinal metaplasia. (2) Methods: Using a retrospective design, data from 786 patients admitted at a hospital in Beirut over a three-year period were extracted from records. (3) Results: The prevalence of H. pylori infection was 29.6% despite 91.5% of patients showing signs of gastritis on endoscopy. The infection showed significant associations with erosive gastritis, non-erosive gastritis, mosaic gastritis, as well as with both erosive and non-erosive duodenitis. No significant relationships were observed between H. pylori and demographic factors, atrophic, or nodular gastritis. (4) Conclusions: These findings underscore the importance of targeted testing and early eradication of H. pylori to manage gastritis effectively and reduce the risk of progression to more serious gastric conditions in the Lebanese population.

The etiology of obesity, which is considered a pandemic, is influenced by several factors. According to the literature, gastric cells in obese patients have not been examined by silver-stained nuclueolus organizing regions (AgNOR) staining. This study investigated the relationship between obesity, nucleolus organizing region (NOR) protein synthesis, and histopathological findings. Nonobese patients undergoing gastric biopsy for various reasons and patients undergoing bariatric surgery were included. Histopathological findings, mean AgNOR count, and total AgNOR area/nuclear area ratio (TAA/NA) were evaluated for each case. In the study, 30 nonobese patients who underwent gastric biopsy and 28 patients who underwent bariatric surgery were included. Additionally, no significant differences were found in the TAA/NA ratios with respect to the presence or absence of histological activity, intestinal metaplasia, or Helicobacter pylori infection (P = .686, P = .588, and P = .069, respectively). However, a statistically significant difference in the TAA/NA ratio was observed between the patients with and without lymphocytic infiltration (P < .013). This study suggests that NOR protein synthesis is associated with lymphocytic infiltration in patients with treatment-resistant obesity. These findings may contribute to a better understanding of the underlying etiology of obesity, and should be supported by further comprehensive studies.

Deoxycholic acid (DCA), a microbial-derived secondary bile acid, plays a multifunctional role in gastrointestinal (GI) carcinogenic through various molecular and cellular mechanisms. Mechanistically, DCA causes disruption of epithelial barrier function by occludin, downregulation of claudin-5, and disruption of ERK signaling, increasing permeability and inflammation. DCA initiates DNA damage by reactive oxygen species (ROS), production of hydroxyl radicals, and degradation of p53, triggering Poly (ADP-ribose) polymerase (PARP)-mediated DNA repair signals. DCA triggers pro-oncogenic signaling such as β-catenin, M3 muscarinic receptor (M3R) transactivation of Epidermal Growth Factor Receptor (EGFR), and Nuclear factor kappa B (NF-κB), promoting cell proliferation, synthesis of Mucin 2 (MUC2), and pro-inflammatory cytokine release (e.g., Interleukin-8 (IL-8), Interferon gamma (IFN-γ)). DCA also inhibits antitumor immunity by blocking Ca2⁺-Nuclear factor of activated T-cell (NFAT) 2 signaling in CD8⁺ T cells, thus disrupting cytotoxicity. DCA causes intestinal metaplasia and trans-differentiation in gastric and esophageal epithelial cells via KLF Transcription Factor 5 (KLF5)-caudal-related homeobox transcription factor 2 (CDX2) signaling. While acute levels of DCA induce apoptosis by mitochondrial membrane depolarization and caspase-9 activation, chronic accumulation leads to tumorigenesis through chronic inflammation, disruption of barrier function, and immune escape. DCA-heparin conjugates are antiangiogenic and chemo-sensitizing and offer new therapeutic windows. Taken together, these data provide evidence for the dualistic action of DCA and its central position as a microbial metabolite linking diet, barrier function, immunity, and GI carcinogenesis.

This study aimed to assess perspectives and practices among expert gastroenterologists regarding the screening, diagnosis, and management of BE. Significant variability in the management of Barrett's esophagus (BE) persists among physicians despite the development and dissemination of several clinical practice guidelines. An online survey was conducted with 38 expert gastroenterologists specializing in BE management. The 38-question survey evaluated demographics, medical management, and attitudes toward endoscopic treatment, with responses analyzed for trends and variations. Of the 38 experts, 34 (89%) responded. Respondents were primarily male (85%), with 82% affiliated with academic hospitals and 53% clinically focused on BE. Half discussed BE risks during initial consultations for gastroesophageal reflux disease (GERD). Most (61.8%) agreed BE should be considered in women with chronic GERD, and 88.2% regularly used narrow-band imaging (NBI). However, 44% were neutral or disagreed with diagnosing BE based solely on community gastroenterologist biopsies, and acceptance of Wide-Area Transepithelial Sampling with 3D Analysis (WATS-3D) for Barrett's esophagus diagnosis and surveillance was limited. Fifty-three percent recommended ablation for nondysplastic BE. Fifty-two percent recommended indefinite daily PPI therapy after complete eradication of intestinal metaplasia (CEIM), regardless of symptoms. When encountering cardia intestinal metaplasia after endoscopic eradication, 38% recommended ablation, while 47% continued surveillance. This study highlights substantial variations in the management of BE among expert gastroenterologists, despite the existence of updated guidelines. Identifying these discrepancies is crucial for optimizing care. Further efforts are needed to standardize practices and enhance the implementation of evidence-based guidelines in clinical settings.