Search Results (344)

Background and Clinical Significance: Zolbetuximab, a claudin 18.2-targeted monoclonal antibody, has demonstrated efficacy in advanced gastric cancer. Hypoalbuminemia has emerged as a notable adverse effect, but its underlying mechanism remains unclear. Case Presentation: A 53-year-old male with unresectable advanced gastric cancer received zolbetuximab-based combination therapy, achieving tumor regression enabling conversion surgery. During six cycles of treatment, serum albumin levels decreased from 4.3 g/dL to 3.5-3.6 g/dL (grade 1 hypoalbuminemia). A histopathological examination of the surgical specimen revealed hypertrophic gastritis characterized by marked foveolar hyperplasia, increased mucus secretion, and pyloric gland metaplasia on the lesser curvature. These findings suggest that zolbetuximab-induced mucosal alterations may contribute to hypoalbuminemia through enhanced protein loss. Conclusions: This is the first pathological documentation of hypertrophic gastritis associated with zolbetuximab therapy. Clinicians should monitor albumin levels during treatment and consider nutritional support when indicated. These findings provide important insights for optimizing patient management and ensuring safe conversion surgery planning. Full article

Chronic gastritis (CG) is a prevalent digestive disorder. It progresses through multiple stages, has an insidious onset, and can lead to severe complications if untreated. Modern treatments primarily aim to eradicate Helicobacter pylori and relieve symptoms. However, drug resistance and adverse effects often limit their effectiveness. As a primary traditional Chinese medicine (TCM) therapy, acupuncture treats CG through multi-target mechanisms. This review systematically outlines the classification and pathology of CG. It also comprehensively analyzes animal and clinical studies on acupuncture for CG from the past decade. The study summarizes the mechanisms of acupuncture and related therapies for CG, covering gastric mucosal function, metabolism, intestinal flora, gastrointestinal hormones, apoptosis, inflammation, and oxidative stress. It further explores the relationships among diseases, interventions, acupoints, and molecular pathways. Additionally, it compares the therapeutic profiles of different external therapies. The review also examines the current state of clinical research, including the selection of acupoints, treatment duration, and outcome assessment. The results demonstrate that external therapies effectively alleviate common CG symptoms such as abdominal distension, acid reflux, and stomach pain. These treatments also improve gastric mucosal health and modulate serum levels of inflammatory factors, oxidative stress markers, and gastrointestinal hormones. In vivo experiments using chronic non-atrophic gastritis (CNAG) and chronic atrophic gastritis (CAG) models confirm these benefits, showing changes in key biomarkers and elucidating potential mechanisms. Nevertheless, future high-quality, large-sample clinical trials are still needed to firmly establish efficacy. Further mechanistic studies are also needed to validate the interconnections among relevant signaling pathways. Full article

The risk of Helicobacter pylori (H. pylori)-related gastric tumorigenesis is closely associated with the degree of chronic gastritis, although other gastric mucosa microbes may be relevant in this process. The morphological identification of the gastric mucosa associated with the cancer-promoting microbiome may have important implications for gastric cancer prevention. This study characterized gastric mucosa microbiome communities in relation to their mucosal morphologies. A total of 94 biopsies from non-neoplastic gastric bodies underwent 16S rRNA sequencing. Microbiome structures were characterized in relation to their mucosal morphologies, which were obtained using narrow-band imaging with magnifying endoscopy. H. pylori infection- and inflammatory mucosa-associated gastric mucosal morphologies exhibited decreased bacterial alpha diversity measures and an increase in the abundance of the Helicobacter genus, while the mucosal morphology associated with severely atrophic mucosa exhibited increased bacterial alpha diversity measures and a decrease in the abundance of the Helicobacter genus. This type of mucosal morphology was also associated with increased levels of well-known gastric cancer-related bacteria, e.g., Streptococcus. The microbial dysbiosis associated with gastric mucosa morphology also correlated well with the occurrence of gastric cancer and the DNA methylation status. Our results suggest that gastric microbiome communities correlate well with their premalignant condition-associated mucosal morphologies. 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

Helicobacter pylori infection represents a well-established risk factor for the development of gastric carcinogenesis, yet reliable clinical or endoscopic predictors of infection remain poorly defined. Identifying non-invasive or endoscopic markers of this infection could improve early detection, which is crucial for effective prevention and clinical management. This single-center study included 737 patients who underwent upper gastrointestinal endoscopy. We compared clinical, laboratory, and endoscopic features between H. pylori-positive and H. pylori-negative individuals. A total of 263 with H. pylori-positive gastric biopsies and 474 with H. pylori-negative biopsies were enrolled in our study. Cerebrovascular disease (9.51% vs. 5.51%, p = 0.04, OR = 1.80), type 2 diabetes mellitus (T2DM—22.05% vs. 15.86%, p = 0.04, OR 1.5), and alcohol consumption (18.96% vs. 9.3%, p = 0.00, OR = 2.28) were significantly more prevalent among H. pylori-positive patients. Heartburn was more commonly reported in H. pylori-negative individuals (23.77% vs. 15.38%, p = 0.01, OR = 0.58). Laboratory parameters showed no significant differences between groups. Regarding endoscopic findings, corporal erythema (26.92% vs. 16.17%, p = 0.00, OR = 1.91), corporal erosions (11.54% vs. 5.32%, p = 0.00, OR = 2.32), and submucosal hemorrhages (20.91% vs. 11.6%, p = 0.00, OR = 2.01) were associated with H. pylori infection. In the multivariate logistic regression models, alcohol consumption and corporal lesions remained independent predictors of H. pylori-associated gastritis, even after adjusting for age, sex, and PPI use. This study identifies alcohol consumption and specific corporal mucosal changes as novel, independent predictors of H. pylori infection. Heartburn was negatively associated with active H. pylori infection, while the rest of the symptoms did not predict infection or mucosal lesions. The laboratory parameters did not differ significantly between groups. These findings underscore the potential of targeted endoscopic evaluation and risk-based screening (particularly among T2DM and alcohol-consuming populations) to enhance early detection and management of H. pylori-associated disease. Full article

Equine gastric ulcer syndrome (EGUS) refers to mucosal gastric disease in horses, including equine squamous gastric disease (ESGD) and equine glandular gastric disease (EGGD), which present as two distinct disease entities differing in pathophysiology and approach to disease management. Both diseases are a source of pain in affected horses, partly explaining why EGUS continues to receive substantial attention in the equine medical, welfare and equitation research sectors. There is a complex interplay between EGUS and a variety of physical and psychological stressors. Horses with EGUS are often presented to veterinarians with a history of problem behaviors, some of which resolve following gastroprotectant therapy. However, problem behaviors persist in some cases, despite gastroscopic resolution of disease. Some of these horses have pain-related learnt, anticipatory behavior, even after the original source of pain has resolved. Such cases, as well as chronic or refractory EGUS cases, can benefit from a behavioral medicine approach. This includes the management of any underlying diseases, environmental modification, behavior modification, and, in select cases, behavior-modifying medication. This commentary, based on the authors’ clinical experiences and current literature, explores how behavioral medicine can be integrated with traditional pharmacologic, nutraceutical, and husbandry strategies for the multi-modal management of EGUS, with a focus on managing the horse’s experience to improve case outcome. 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

Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by progressive destruction of gastric parietal cells driven by autoreactive CD4⁺ T-cells, epithelial stress pathways, and microbial factors. Parietal cell loss results in achlorhydria, intrinsic factor deficiency, and vitamin B12 malabsorption, ultimately leading to pernicious anemia. Compensatory hypergastrinemia promotes enterochromaffin-like (ECL) cell hyperplasia and contributes to the development of type 1 gastric neuroendocrine neoplasms (gNENs). These clinical consequences are well recognized, yet the cellular and molecular mechanisms driving mucosal atrophy and neoplastic transformation remain incompletely defined. Recent advances highlight the role of endoplasmic reticulum stress, impaired autophagy, innate immune effectors, and dysbiosis in perpetuating inflammation and epithelial injury. The frequent coexistence of AIG with other autoimmune disorders further adds to its clinical complexity. Therapeutic options remain limited, spanning vitamin B12 replacement and endoscopic management to emerging targeted approaches. Netazepide, a gastrin/CCK2 receptor antagonist, is the only agent tested in clinical trials, whereas interventions targeting ER stress, autophagy, immune tolerance, or microbiome composition are still in the preclinical stage. Clarifying these mechanisms is crucial to improve biomarker development, optimize surveillance, and identify targeted therapies to prevent neoplastic transformation. Full article

Background: Necrotizing enterocolitis (NEC) is a life-threatening condition characterized by necrosis of the gastrointestinal tract caused by hypoperfusion and hypoxia-induced inflammation. Surgical treatment often requires resection, with high morbidity and mortality. Intestinal tissue engineering using absorbable biomaterials represents a potential alternative. Small intestinal submucosa (SIS) is a biodegradable extracellular matrix (ECM) scaffold that may facilitate regeneration of the native tissue. Objectives: The aim of our study is to investigate the regenerative potential of SIS in a rat model with multiple gastrointestinal defects. Methods: In rats, after a midline laparotomy, an approximately 1 cm full-thickness incision was performed on the anterior gastric wall, on the antimesenteric side of the small and large intestine, each covered with an SIS patch. After three weeks, the graft sites and adjacent fragments were harvested and fixed in 10% neutral buffered formalin. Cross-sections of the grafted area were processed and stained with hematoxylin and eosin for histologic analysis. Results: Among the fifteen Wistar rats used in the study, the survival rate was 80% (12/15). Macroscopic examination of the abdominal cavity after the second surgery showed no complications. Adhesions were present in 92% (11/12). Histological examination demonstrated complete mucosal coverage in all stomach samples, nine of the small intestine, and ten of the large intestine. Mild fibrosis with minimal inflammatory infiltrates predominated. Ulceration with granulation tissue replacement was observed in three small intestine samples. Foreign body reactions were restricted to suture sites. Conclusions: In this multifocal injury model, SIS integrated effectively and supported early regenerative healing across gastric, small-intestinal, and colonic sites at 3 weeks. These data support further studies with longer follow-up, quantitative histology and functional assessment, and evaluation in neonatal-relevant large animal models to determine translational potential for NEC surgery. Full article

The gastrointestinal (GI) tract is increasingly recognized as an important regulator of energy balance and metabolism, extending beyond its traditional digestive functions. This review synthesizes current research on how modifications to the GI tract, particularly those induced by metabolic bariatric surgery (MBS), influence hormonal and physiological processes involved in glucose regulation and appetite control. MBS procedures, such as Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG), induce significant and sustained weight loss, but also elicit adaptive morphological and functional changes within the intestines. These alterations include intestinal hypertrophy, increased mucosal surface area, changes in nutrient transit time, and modifications in enzyme activity. Such changes enhance the secretion of key gut hormones, including glucagon-like peptide 1 (GLP-1) and peptide YY (PYY), which play vital roles in promoting insulin secretion, suppressing appetite, and improving blood glucose regulation. The benefits stem from the exposure of undigested nutrients to different intestinal segments, which stimulates enteroendocrine activity and positively influences systemic metabolism. These hormonal adaptations contribute significantly to the metabolic improvements observed post-surgery, independent of weight loss alone. Understanding how gut structural and functional changes drive hormonal responses provides valuable insights into the mechanisms underlying the success of MBS. Moreover, elucidating these processes may facilitate the development of less invasive therapies that mimic the metabolic benefits of surgery. Ultimately, this research advances our understanding of gut-mediated regulation of energy and glucose homeostasis and holds promise for improving treatment strategies for obesity and related metabolic disorders. Full article

Background/Objectives: Gastric mucosal lesions represent a significant health burden, with Helicobacter pylori infection being the primary cause of chronic gastritis worldwide. However, the role of modifiable lifestyle factors in modulating the severity of gastric lesions remains incompletely characterized, particularly in Eastern European populations. This study aimed to analyze the relationship between dietary behaviors, smoking, alcohol consumption, and the severity of endoscopic gastric lesions in Romanian patients. Methods: We conducted a cross-sectional study including 361 patients who underwent upper gastrointestinal endoscopy at Târgu Mureș County Clinical Emergency Hospital between 2019 and 2025. Endoscopic lesion severity was classified on an ordinal scale (0 = normal; 1 = edema/erythema; 2 = erosions; 3 = ulcer/bleeding). Dietary intake was assessed using a validated food frequency questionnaire, with foods classified as pro-inflammatory or protective. Ordinal logistic regression models were used to examine associations between lifestyle factors and the severity of gastric lesions, adjusted for age, sex, and H. pylori status. Results: Among participants (median age 65 years, 46.5% male), 45.2% had clinically significant lesions (≥2). H. pylori infection was present in 31.6% of participants. Current smoking (15.2% of participants) showed a trend toward increased severity of gastric lesions (fully adjusted OR 1.59, 95% CI 0.93–2.71, p = 0.092), though not statistically significant. Among current smokers, 52.7% had clinically significant lesions versus 43.8% among non/former smokers. The smoking–alcohol interaction was not statistically significant (interaction OR = 1.19, 95% CI: 0.34–4.17, p = 0.780). Dietary balance score showed no association with the severity of gastric lesions (OR = 1.061 per 10-unit increase, p = 0.355). NSAID use emerged as the strongest predictor (OR = 1.68, 95% CI 1.01–2.78, p = 0.044). The number of cumulative risk factors correlated significantly with clinically significant lesions (Spearman r = 0.107, p = 0.042), with prevalence increasing from 34.5% in patients with 0–1 factors to 83.3% with 6+ factors. Conclusions: Current smoking showed a trend toward increased severity of gastric lesions in this Romanian cohort, though not reaching statistical significance. NSAID use was the only significant independent predictor. The dose–response relationship between cumulative risk factors and the severity of lesions emphasizes the importance of comprehensive risk assessment and multi-factorial interventions in gastric disease prevention. However, as a cross-sectional study, these associations cannot establish causality and should be confirmed in prospective cohorts. Full article

Despite the frequent gastrointestinal involvement, no studies have described the ultrasonographic appearance of the stomach in dogs with acute kidney injury (AKI) or acute-on-chronic kidney disease (ACKD). This retrospective study aimed to characterize the ultrasonographic features of gastropathy in such patients. Dogs diagnosed with AKI or ACKD and showing gastric abnormalities on ultrasound between January 2014 and January 2024 were included. A total of 113 dogs met the inclusion criteria. Gastric wall thickening was observed in all cases. Mucosal and/or submucosal abnormalities were present in 86.7% of dogs. Mucosal changes alone were found in 54.9%, including hyperechoic band or stripe and diffusely increased echogenicity, suggestive of possible mucosal mineralization. The most common mucosal finding was a hyperechoic band (48.4%), associated with higher calcium–phosphorus product levels. Submucosal changes alone were seen in 20.3% of dogs, typically as thickening with decreased echogenicity, consistent with possible submucosal edema. Both mucosal and submucosal abnormalities were present in 11.5% of cases. Mucosal changes were more frequent in ACKD, while submucosal alterations were more common in AKI. This study provides the first detailed description of gastric ultrasonographic features in dogs with AKI and ACKD. Full article

Gastric subepithelial tumors (SETs) are commonly identified during routine endoscopy. Most SETs are asymptomatic and small (<2 cm) and exhibit benign behavior over time. Various histopathological types exist, including benign lesions, such as lipomas and heterotopic pancreas, and malignant lesions, such as gastrointestinal stromal tumors (GISTs). Endoscopic ultrasound (EUS) plays a critical role in evaluating the lesion size, layer of origin, border characteristics, and internal echogenicity. Approximately 4–15% of gastric SETs increase in size over ~5 years. The risk factors for the growth and malignant potential of SETs include initial tumor size, irregular or heterogeneous EUS features, mucosal ulceration, and confirmed GIST diagnosis. While lesions ≥2 cm in size or those with high-risk features are typically subjected to resection, small and low-risk SETs are managed with periodic EUS or endoscopic surveillance. Tissue acquisition via EUS-guided biopsy or endoscopic resection is warranted for indeterminate or suspicious cases. A risk-stratified approach minimizes unnecessary interventions while enabling timely detection of clinically significant lesions. Surveillance protocols should be tailored according to characteristics of SETs, patient comorbidities, and diagnostic confidence. This review highlights the long-term outcomes of gastric SETs, evaluates established risk factors for their growth and malignant potential, and discusses evidence-based strategies for surveillance and management. Full article

Background and Objectives: Early gastric cancer (EGC) has an excellent prognosis when detected, yet miss rates during endoscopy remain high. Narrow-band imaging (NBI) enhances mucosal and vascular visualization and is increasingly used, but its benefit over white-light imaging (WLI) in high-risk patients is uncertain. This study aimed to compare NBI with WLI for the detection of gastric neoplasia in patients undergoing gastroscopy. Materials and Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs), registered in PROSPERO (CRD42025649908) and reported according to PRISMA 2020 guidelines. PubMed, Scopus, and CENTRAL were searched up to October 2024. Eligible RCTs randomized adults undergoing gastroscopy for cancer surveillance or red-flag symptoms to NBI or WLI. Data extraction and risk of bias assessment were performed independently by two reviewers. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated using a random-effects model, and certainty of evidence was graded with GRADE. Results: From 21 records, 3 RCTs comprising 6003 patients were included. NBI did not significantly increase gastric neoplasm detection compared with WLI (2.79% vs. 2.74%; RR = 0.98; 95% CI: 0.66–1.45; I² = 22%). Focal gastric lesion detection rates (14.73% vs. 15.50%; RR = 1.05; 95% CI: 0.72–1.52; I² = 87%) and positive predictive value (29.56% vs. 20.56%; RR = 1.29; 95% CI: 0.84–1.99; I² = 61%) also showed no significant differences. Risk of bias was high for blinding, and overall evidence certainty was low. In practical terms, both NBI and WLI detected gastric cancers at similar rates, indicating that while NBI enhances visualization, it does not increase the likelihood of finding additional cancers in high-risk patients. Conclusions: NBI did not significantly improve gastric neoplasm detection compared with WLI in high-risk patients, though it remains valuable for mucosal and vascular assessment. Larger, multicenter RCTs across diverse populations are required to establish its role in surveillance strategies. Full article

Background and Objectives: Perioperative enteral and parenteral nutrition have been increasingly used to treat malnutrition in patients with gastric cancer. Immunonutrients have been suggested to reduce postoperative inflammatory responses and enhance immune function compared to conventional nutritional formulas. However, the insufficiency of evidence and unclear specific mechanism limit the recommendation level of immunonutrients in clinical guidelines. This study aimed to investigate the effects of immunonutrients on intestinal barrier function and to explore potential mechanisms through gut microbiota modulation. Methods: A total of 58 patients who underwent gastric cancer surgery participated in this randomized controlled trial. The immunonutrients group (n = 29) was additionally supplemented with 282 mg of omega-3 fatty acids, 1.2 g of arginine, and 128 mg of nucleotides per 100 kilocalories compared to the standard nutrients group (n = 29). Perioperative serum immune, nutritional parameters, and intestinal barrier markers (diamine oxidase, D-lactate, endotoxin) were evaluated. Fecal microbiota structure and functional pathways were analyzed via metagenomic sequencing. Results: Postoperative immune and nutritional parameters showed no statistically significant intergroup differences, though mean value curves suggested a protective trend in the immunonutrients group. The immunonutrients group exhibited significantly lower postoperative diamine oxidase (p = 0.043) and endotoxin levels (p = 0.043), alongside a substantial increase in microbiota α-diversity (p = 0.0005). Probiotic genera such as Akkermansia (3.26%) and Bifidobacterium longum (2.31%) were enriched in the immunonutrients group. Functional pathway analysis suggested that immunonutrients enhanced intestinal barrier protection. Conclusions: Immunonutrients may attenuate surgery-induced intestinal barrier damage in gastric cancer patients by modulating gut microbiota diversity, enriching beneficial taxa, and suppressing pathogenic bacteria. Full article