Search Results (106)

Gastric cancer (GC) is the fifth most common cancer worldwide, with the highest incidence in East Asia. Although H. pylori is a well-known risk factor, carcinogenesis can occur independently of H. pylori infection, and approximately 43% of adults carry H. pylori as part of their native microbiota. This study aimed to identify potential oral and gastric microbial markers across different histological stages of GC in both H. pylori-positive and -negative patients. Buccal swabs and gastric mucosa samples were collected from patients with intestinal metaplasia, low-grade dysplasia, high-grade dysplasia, early GC, or advanced GC. Total DNA was extracted, and 16S rRNA gene amplicon sequencing was performed. Microbiome diversity generally remained stable across histological stages, with no directional shifts in community structure. Differential abundance analysis revealed higher relative abundances of Anaerostipes, Phocaeicola, and Collinsella in the gastric antrum of cancerous samples. Anaerostipes and Phocaeicola are typically enriched in the intestinal microbiota but are rarely observed in the stomach, suggesting their potential ecological and pathological relevance in gastric carcinogenesis. In H. pylori-negative patients, however, a different stage-associated abundance pattern was observed, in which Faecalibacterium, a genus predominantly associated with the intestinal environment, was less abundant in advanced gastric cancer samples than in earlier histological stages within the gastric body. These findings suggest that microbial changes during gastric cancer progression may follow different trajectories depending on H. pylori infection status. In oral samples, Haemophilus and Prevotella were more abundant in intestinal metaplasia than in low-grade dysplasia, and network analysis indicated links between Neisseria and Filifactor at oral and gastric sites. However, as the study population was limited to a single country and ethnicity, the applicability of these microbial markers should be carefully considered. Full article

Background and Objectives: Corpus atrophic gastritis (CAG) is associated with vitamin B₁₂ deficiency due to impaired gastric acid and intrinsic factor secretion. Untreated vitamin B₁₂ deficiency can lead to pernicious anemia, severe neurological consequences, and acute cardiocerebral-vascular events. Timely vitamin B₁₂ supplementation is relevant; however, the dosage of intramuscular (IM) vitamin B₁₂ supplementation has not been standardized to date. The objective was to assess the efficacy of a 1st and 2nd treatment schedule of IM-cyanocobalamin treatment in CAG patients with vitamin B₁₂ deficiency at long-term follow-up and to identify the predictors of increased cyanocobalamin requirement. Methods: This monocentric real-life cohort study included 213 CAG patients with vitamin B₁₂ deficiency. Inclusion criteria were adult age, histological diagnosis of CAG with vitamin B₁₂ deficiency (<220 pg/mL), and follow-up of more than 12 months. The 1st-treatment-schedule (TxA) was 5000 µg IM cyanocobalamin every 5 days for 3 times, followed by 5000 µg IM cyanocobalamin every 3 mos (20,000 µg/yr); the 2nd-treatment-schedule (TxB) was 5000 µg IM cyanocobalamin every 5 days for 3 times, followed by 5000 µg IM cyanocobalamin every 2 mos (30,000 µg/yr). The treatment endpoint was serum vitamin B₁₂ normalization. Clinical-biochemical follow-up was scheduled every 12 ± 6 mos: patients who satisfied the endpoint maintained the TxA, otherwise, TxB was prescribed. Results: Of the 213 CAG patients with vitamin B₁₂ deficiency, 48.3% had anemia, and 26.3% macrocytosis without anemia. TxA efficaciously corrected vitamin B₁₂ deficiency in 146 (68.5%) patients, maintaining efficacy until the longest available follow-up (42.2 ± 2.6 months). The remaining 67 patients (31.5%) were switched to TxB due to persistent vitamin B₁₂ deficiency observed at 12 (6–36) months and were maintained until the longest available follow-up (50.2 ± 4.1 months). At the longest available follow-up, a significant increase in Hb (TxA: 11.9 ± 0.2 to 13.1 ± 0.1 g/dL, p < 0.001; TxB: 12.2 ± 0.3 to 13.6 ± 0.2 g/dL, p = 0.003) and serum vitamin B₁₂ (TxA: 168 ± 7 to 402 ± 19 pg/mL, p < 0.0001; TxB: 157 ± 12 to 340 ± 24 pg/mL, p < 0.0001) was shown in both schedules. A significant decrease in MCV was shown in TxB only (p = 0.0003). In logistic regression, switching to TxB was significantly associated with severe corpus intestinal metaplasia (OR 11.0, 95% CI 2.8–43.7), macrocytosis at CAG diagnosis (OR 2.7, 95% CI 1.2–6.3), and male sex (OR 2.4, 95% CI 1.1–5.2). Conclusions: In this real-world setting, at long-term follow-up, nearly 70% of CAG patients with vitamin B₁₂ deficiency restored their vitamin B₁₂ levels with 20,000 µg/yr of cyanocobalamin, while the remaining 30% required 30,000 µg/yr. Male vitamin B₁₂-deficient CAG patients with advanced gastric damage and severe macrocytosis required higher dosages of cyanocobalamin. They should be carefully monitored to avoid suboptimal supplementation and potentially dangerous consequences of vitamin B₁₂ deficiency. Full article

Background/Objectives: Helicobacter pylori (H. pylori) is a well-established pathogen associated with chronic gastritis and gastric malignancies. Recent studies suggest that members of the Streptococcus anginosus group (SAG), particularly S. anginosus and S. constellatus, may also contribute to gastric mucosal damage, especially when co-infecting with H. pylori. This study aimed to evaluate the prevalence of these three bacterial species and their associations with gastric lesions in Vietnamese patients. Methods: A cross-sectional study was conducted on 200 adult patients with gastritis diagnosed by endoscopy and biopsy. PCR analysed gastric tissue samples from the antrum and corpus for H. pylori, S. anginosus, and S. constellatus. Gastric lesions were classified histologically, and associations with bacterial infections were assessed using odds ratios (OR) and 95% confidence intervals. Results: Infection rates were 62.5% for H. pylori, 62% for S. constellatus, and 48.5% for S. anginosus. Coinfections were frequent, with 25% of patients infected by all three bacteria. Atrophic gastritis was the most common lesion (80%) and was significantly associated with all three bacteria, particularly H. pylori (OR = 7.7), and in co-infections (e.g., H. pylori + S. constellatus, OR = 7.4, p < 0.0001). Triple infection was strongly linked to both atrophy (OR = 5.1) and intestinal metaplasia/dysplasia (OR = 3.4, p = 0.007). Conclusions: Polymicrobial infections involving H. pylori and SAG bacteria are common in Vietnamese patients with gastritis and are significantly associated with more severe gastric lesions. These findings highlight the need for broader microbial screening and integrated management strategies to improve gastritis treatment and gastric cancer prevention in high-prevalence settings. Full article

Background/Objectives: Gastric cancer is known to occur through a multistep process from gastric precancerous lesions, such as atrophic gastritis, intestinal metaplasia, and gastric dysplasia. Gastric precancerous lesions may have different risk factors for each stage, and it can be prevented by an anti-inflammatory diet. In this study, we examined the association between the dietary inflammatory index (DII) and the risk of gastric precancerous lesions among adults in a rural area. Moreover, we analyzed the interaction between the DII and H. pylori infection in relation to the risk of gastric precancerous lesion. Methods: Among 711 participants who had a gastroscopy in a community cohort study, 564 subjects were included in this analysis and were divided into three groups (233 in normal, 128 in atrophic gastritis, and 203 in intestinal metaplasia). Atrophic gastritis and intestinal metaplasia were diagnosed by endoscopy and histopathology in accordance with the Updated Sydney System. DII was derived from a food-frequency questionnaire and categorized into tertiles. H. pylori infection was determined by the Campylobacter-like organism test. Results: H. pylori infection was significantly associated with the increased risk of intestinal metaplasia (OR = 2.75, 95% CI = 1.76–4.27), but not with atrophic gastritis. The inflammation diet itself was not associated with both the risk of atrophic gastritis (OR = 0.93, 95% CI = 0.53–1.64) and intestinal metaplasia (OR = 1.32, 95% CI = 0.78–2.24). However, the risk of intestinal metaplasia was more increased in the inflammatory diet group with H. pylori infection (OR = 3.35, 95% CI = 1.54–7.30) compared to the anti-inflammatory diet group without H. pylori infection. Conclusions: This study found that H. pylori infection increased the risk of intestinal metaplasia, and this risk was further enhanced by a pro-inflammatory diet, suggesting that both diet and infection management are important for prevention of gastric precancerous lesions. Full article

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. Full article

Background/Objectives: Gastric intestinal metaplasia (GIM) is a recognized premalignant condition for gastric cancer (GC), but long-term outcomes and predictors of progression remain incompletely understood. This study aimed to evaluate the progression of GIM and identify factors associated with malignant transformation. Methods: In this retrospective single-center study, 1204 adult patients with histologically confirmed GIM and at least 12 months of follow-up after esophagogastroduodenoscopy (EGD) were analyzed. Clinical and pathological variables, including GIM extent, Helicobacter pylori status, family history of GC, demographic factors, and residence in endemic regions, were assessed. Patients were stratified into high- and low-risk groups according to established criteria, and progression to GC or other neoplasms was recorded. Results: During a mean follow-up of 38.6 months, 49.1% of patients had no detectable GIM at the end of follow-up, 48.7% remained unchanged, and 2.2% showed disease progression. Among progressed cases, adenocarcinoma accounted for 66.7%, dysplasia for 29.6%, and SCC for 3.7%. Progression was significantly more common among males, older patients, and those with antrum + corpus involvement. The overall progression rate from GIM to adenocarcinoma was 1.5% (approximately 0.45% per patient-year). No significant difference in progression or survival was observed between high- and low-risk groups. Conclusions: The long-term malignant transformation rate of GIM is low. Male sex and extensive gastric involvement were associated with higher progression rates, while H. pylori was not predictive of malignant transformation. These findings support individualized surveillance strategies for patients with GIM, while routine surveillance of antrum-limited GIM may provide minimal benefit but increase healthcare burden. Full article

Chronic infection with Helicobacter pylori is the leading environmental cause of gastric carcinogenesis, yet the molecular pathways remain incompletely defined. This review links H. pylori-derived outer membrane vesicles (OMVs) and host epithelial exosomes through their shared cargo of heat shock protein 60 (GroEL/Hsp60). We proposed the concept of the “muco-microbiotic layer” as a fifth, functionally distinct layer of the gastric wall, where bacterial and host extracellular vesicles (EVs) interact within the mucus–microbiota interface. In this compartment, OMVs carrying bacterial GroEL and exosomes containing human Hsp60 engage in bidirectional communication that may promote chronic inflammation and epithelial transformation, with putative participation of molecular mimicry. The high structural homology between microbial and human Hsp60 enables repeated immune exposure to trigger cross-reactive responses—potentially leading to autoimmune-driven tissue damage, immune tolerance, and immune evasion in pre-neoplastic lesions. This vesicular crosstalk aligns with the evolution from non-atrophic gastritis to atrophy, from intestinal metaplasia to dysplasia, and lastly adenocarcinoma. Therapeutically, targeting EV-mediated Hsp60/GroEL signaling might offer promising strategies: EV-based biomarkers for early detection, monoclonal antibodies against extracellular Hsp60/GroEL, modulation of vesicle release, and probiotic-derived nanovesicles to restore mucosal balance. Hence, recognizing the muco-microbiotic layer and its vesicle-mediated signaling provides a new framework for understanding the infection–inflammation–cancer axis and for developing diagnostic and therapeutic approaches in H. pylori-associated gastric cancer. Full article

Gastric cancer (GC) often presents a poor prognosis due to its asymptomatic phenotype at early stages. Upper endoscopy, which is the current gold standard to diagnose GC, is invasive with limited sensitivity for detecting gastric preneoplasia. Non-invasive biomarkers, such as blood circulating proteins, offer a promising alternative for the early detection of gastric lesions. In this prospective study, we identified plasma protein biomarkers for gastric preneoplasia and cancer using mass spectrometry-based proteomics in an exploratory cohort (n = 39). Fifteen promising protein candidates emerged to distinguish patient categories and were further confirmed by enzyme-linked immunosorbent assays (ELISA) in plasma samples from a validation cohort of 138 participants. Our predictive models demonstrated high classification performance with a minimal set of biomarkers. A four-protein panel (ARG1, CA2, F13A1, S100A12) achieved 94.1–98.2% AUROC (95% CI) for distinguishing cancer from non-cancer cases, while a five-protein panel (ARG1, CA2, HPT, MAN2A1, LBP) reached 97.3–99.5% AUROC (95% CI) for distinguishing cancer or preneoplasia from healthy or non-atrophic gastritis cases on the full cohort. Leveraging simple blood sampling, this strategy holds promise to detect high-risk gastric lesions, even at asymptomatic stages. Such an approach could significantly improve early detection and clinical management of GC, offering direct benefit for patients. Full article

Optical imaging technologies expand gastrointestinal endoscopy beyond white-light endoscopy (WLE), improving visualization of mucosal, vascular, and subsurface features. They are applied to the detection of neoplastic and premalignant lesions, inflammatory diseases, and small bowel and pancreatic disorders, though their validation and readiness for routine practice vary. This review critically evaluates both guideline-endorsed and investigational optical imaging techniques across major gastrointestinal indications, highlighting diagnostic performance, level of validation, current guideline recommendations, and practical challenges to adoption. In Barrett’s esophagus, narrow-band imaging (NBI) is guideline-endorsed, while acetic acid chromoendoscopy is validated in expert centers. For gastric intestinal metaplasia and early gastric cancer, magnifying NBI achieves diagnostic accuracies exceeding 90% and is guideline-recommended, with acetic acid chromoendoscopy aiding in margin delineation. In inflammatory bowel disease, dye-spray chromoendoscopy is the reference standard for dysplasia surveillance, with virtual methods such as NBI, FICE, and i-SCAN serving as practical alternatives when dye application is not feasible. In the colorectum, NBI supports validated optical diagnosis strategies (resect-and-discard, diagnose-and-leave), while dye-based chromoendoscopy improves detection of flat and serrated lesions. Capsule endoscopy remains the standard for small bowel evaluation of bleeding, Crohn’s disease, and tumors, with virtual enhancement, intelligent chromo capsule endoscopy, and AI-assisted interpretation emerging as promising adjuncts. Pancreaticobiliary applications of optical imaging are also advancing, though current evidence is still preliminary. Investigational modalities including confocal laser endomicroscopy, optical coherence tomography, autofluorescence, Raman spectroscopy, and fluorescence molecular imaging show potential but remain largely restricted to research or expert settings. Guideline-backed modalities such as NBI and dye-based chromoendoscopy are established for clinical practice and supported by robust evidence, whereas advanced techniques remain investigational. Future directions will rely on broader validation, integration of artificial intelligence, and adoption of molecularly targeted probes and next-generation capsule technologies, which together may enhance accuracy, efficiency, and standardization in gastrointestinal endoscopy. Full article

(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. Full article

Background/Objectives: Age-related changes in the gastric mucosa remain incompletely understood. We aimed to assess and compare clinical, endoscopic and histologic changes in the gastric mucosa associated with aging, and to explore whether gastric aging is associated with a distinct histological pattern. Methods: Single-center observational study. Younger (18–45 years) and older (≥70 years) adults undergoing elective upper endoscopy were included and underwent gastric biopsies. The clinical, endoscopic and histologic features were analyzed and compared. Results: A total of 100 patients were included (45 men/55 women), 50 with 18–45 years and 50 with ≥70 years. Dyspepsia, gastro-esophageal reflux disease and peptic ulcer disease were the most common indications for upper endoscopy. Gastric lesions (erythema, erosions, ulceration and polyps) were more common in older patients (80% vs. 50%, p = 0.003), as well as histologic changes such as chronic gastritis (56% vs. 38%, p = 0.004), chronic atrophic gastritis (CAG; 28% vs. 4%, p < 0.001) and intestinal metaplasia (28% vs. 4%, p < 0.001). These findings persisted after adjusting for Helicobacter pylori (H. pylori) status and proton pump inhibitor intake on the multivariate analysis. Prevalence of H. pylori was similar between both groups (28% vs. 32%, p = 0.189). Conclusions: Aging is associated with clinical, endoscopic and histologic changes in the gastric mucosa including CAG and metaplasia, independent of the presence of H. pylori. These findings may result from several aging-related pathophysiological processes and decades of cumulative gastric injury and support the hypothesis of an aging stomach phenotype, underscoring the need for an age-adjusted interpretation of gastric biopsies. Full article

Background/Objectives: This study was designed to investigate the potential clinical, biochemical, haematological, and pathological associations of carpal tunnel syndrome through a multidisciplinary approach encompassing the fields of internal medicine, gastroenterology, and neurology. Methods: The study group (CTS-positive) comprised 265 patients who presented with dyspeptic complaints and underwent upper gastrointestinal endoscopy, gastric antrum biopsy, electromyography, and comprehensive biochemical and haematological analyses. A control group of 265 patients with similar symptoms but without CTS was selected for comparison. A comparative analysis was conducted on clinical findings, gastric biopsy results, and biochemical and haematological parameters. Results: There were no significant differences in age, gender distribution, or gastric biopsy findings (Helicobacter pylori, intestinal metaplasia, atrophy, and dysplasia) between the CTS-positive and CTS-negative groups. However, significant biochemical differences were identified, including elevated calcium and reduced magnesium levels in CTS-positive patients. Haematological evaluations revealed higher lymphocyte, eosinophil, basophil, erythrocyte, haemoglobin, and haematocrit levels, along with reduced neutrophil-to-lymphocyte ratios and red blood cell distribution widths in the CTS-positive group. Further analysis in the form of correlation and logistic regression analyses provided further confirmation of the association of elevated calcium, haemoglobin, and lymphocyte levels with increased risk of CTS. Conclusions: This multidisciplinary study identifies significant associations between CTS and specific biochemical and haematological parameters, notably calcium-magnesium imbalance and erythrocyte indices. These findings suggest underlying biological interactions that may guide future diagnostic and therapeutic strategies for patients with carpal tunnel syndrome. Full article

Background: Gastric cancer (GC) is the fifth most common malignancy worldwide. Early detection of precancerous conditions—atrophic gastritis (AG), intestinal metaplasia (IM), and dysplasia—is vital for surveillance. Objectives: To assess the accuracy of single high-quality endoscopy (HQE) in detecting advanced GPCs and to identify risk factors for AG, IM, and dysplasia. Methods: A retrospective review of 442 gastroscopies (2017–2022) at a single center. Endoscopic findings were compared with histology, including OLGA/OLGIM staging, dysplasia, and Helicobacter pylori (H. pylori) status. Results: The study population comprised 319 women (72.17%) and 123 men (27.83%), with a mean age of 59 years (SD: 12.53). AG, as defined by OLGA and OLGIM staging, was identified in 90 patients (20.36%) and 50 patients (11.31%), respectively. A total of 44 cases of de novo gastric dysplasia were observed, while HP infection was confirmed in 37 individuals (8.37%). We observed similar low sensitivity for detection of advanced OLGA (32.5%), OLGIM (40%), and dysplasia (19.7%) with relatively high specificity (~89%). Advanced AG and IM peaked at ages 51–53. Risk factors for advanced OLGIM included male sex (OR 2.26; p < 0.001) and presence of dysplasia (OR 2.09; p = 0.02). Dysplasia was positively associated with AG (OR 2.03; p < 0.001) and IM (OR 2.21; p < 0.001) but inversely associated with a family history of GC (OR 0.44; p < 0.001). Conclusions: A single HQE can help exclude advanced GPCs, but due to low sensitivity, gastric mapping biopsies remain crucial. Males are at increased risk of extensive IM. Family history of GC was linked to lower OLGA/OLGIM stages. Full article

Chronic atrophic gastritis and intestinal metaplasia (IM) are gastric precancerous conditions (GPCs) associated with an increased risk of gastric cancer. Early detection and accurate characterization of GPC are therefore crucial for risk stratification and the implementation of preventive strategies. In the absence of clear mucosal changes observed through white-light imaging (WLI) or virtual chromoendoscopy, endocytoscopy can help unveil the presence of GPC by enabling in vivo assessment of nuclear and cellular structures at ultra-high magnification. Endocytoscopy is typically performed using WLI following dye-based staining of the mucosa. In this case, we demonstrate that combining endocytoscopy with the texture and color enhancement imaging (TXI) mode substantially improves the assessment of the gastric mucosa. In a 61-year-old man undergoing esophagogastroduodenoscopy, WLI showed multifocal erythema in the stomach, without clearly visible lesions on either WLI or narrow-band imaging. Conventional endocytoscopy revealed multiple small spots of IM with characteristic changes in glandular structures, which were even more evident when using the TXI mode. Histological analysis of targeted biopsies confirmed small foci of IM in both the antrum and corpus. The patient was enrolled in a surveillance program because of his clinical background. The combination of endocytoscopy with the TXI mode significantly enhances the delineation of mucosal and cellular architecture, supporting a more accurate optical diagnosis. Full article

Background: Gastric cancer (GC) remains a major global health challenge, with rising incidence among patients post-Helicobacter pylori (H. pylori) eradication, particularly those with persistent intestinal metaplasia (IM). Current risk stratification tools are limited in this high-risk population. Aim: To develop, validate, and externally test a machine learning-based prediction model—termed the Early Gastric Cancer Model (EGCM)—for identifying early gastric cancer (EGC) risk in H. pylori-eradicated patients with IM, and to implement it as a web-based clinical tool. Methods: This retrospective, dual-center study enrolled 214 H. pylori-eradicated patients with histologically confirmed IM from 900 Hospital and Fujian Provincial People’s Hospital. The dataset was split into a training cohort (70%) and an internal validation cohort (30%), with an external test cohort from the second center. A total of 21 machine learning algorithms were screened using cross-validation and hyperparameter optimization. Boruta and SHAP analyses were employed for feature selection, and the final EGCM was constructed using the top five predictors: atrophy range, xanthoma, map-like redness (MLR), MLR range, and age. Model performance was evaluated via ROC curves, precision–recall curves, calibration plots, and decision curve analysis (DCA), and compared against conventional inflammatory biomarkers such as NLR and PLR. Results: The CatBoost algorithm demonstrated the best overall performance, achieving an AUC of 0.743 (95% CI: 0.70–0.80) in internal validation and 0.905 in the external test set. The EGCM exhibited superior discrimination compared to individual inflammatory markers (p < 0.01). Calibration analysis confirmed strong agreement between predicted and observed outcomes. DCA showed the EGCM yielded greater net clinical benefit. A web calculator was developed to facilitate clinical application. Conclusions: The EGCM is a validated, interpretable, and practical tool for stratifying EGC risk in H. pylori-eradicated IM patients across multiple centers. Its integration into clinical practice could improve surveillance precision and early cancer detection. Full article