Autoimmune gastritis (AIG), distinct from Helicobacter pylori-associated atrophic gastritis (HpAG), is underdiagnosed due to limited awareness. This multicenter study aimed to develop a novel endoscopic artificial intelligence (AI) system for assisting in AIG diagnosis.

 Patients diagnosed with AIG, HpAG, or nonatrophic gastritis (NAG), were retrospectively enrolled from six centers. Endoscopic images with relevant demographic and medical data were collected for development of the AI-assisted system based on a multi-site feature fusion model. The diagnostic performance of the AI model was evaluated in internal and external datasets. Endoscopists' performance with and without AI support was tested and compared using Mann-Whitney U test. Heatmap analysis was performed to interpret AI model outputs.

 18 828 endoscopy images from 1070 patients (294 AIG, 386 HpAG, 390 NAG) were collected. On testing datasets, AI identified AIG with 96.9 % sensitivity, 92.2 % specificity, and area under the receiver operating characteristic curve (AUROC) of 0.990 (internal), and 90.3 % sensitivity, 93.1 % specificity, and AUROC of 0.973 (external). The performance of AI (sensitivity 91.3 %) was comparable to that of experts (87.3 %) and significantly outperformed nonexperts (70.0 %; P = 0.01). With AI support, the overall performance of endoscopists was improved (sensitivity 90.3 % [95 %CI 86.0 %-93.2 %] vs. 78.7 % [95 %CI 73.6 %-83.2 %]; P = 0.008). Heatmap analysis revealed consistent focus of AI on atrophic areas.

 This novel AI system demonstrated expert-level performance in identifying AIG and enhanced the diagnostic ability of endoscopists. Its application could be useful in guiding biopsy sampling and improving early detection of AIG.

Early-onset gastric cancer (EOGC) is a lethal malignancy. It differs from late-onset gastric cancer (LOGC) in clinical and molecular characteristics. The current strategies for EOGC detection have certain limitations in diagnostic performance due to the rising trend in EOGC.

We developed a liquid biopsy signature for EOGC detection.

We use a systematic discovery approach by analysing genome-wide transcriptomic profiling data from EOGC (n=43), LOGC (n=31) and age-matched non-disease controls (n=37) tissue samples. An extracellular vesicle-derived long non-coding RNA (EV-lncRNA) signature was identified in blood samples from a training cohort (n=299), and subsequently confirmed by qPCR in two external validation cohorts (n=462 and n=438), a preoperative/postoperative cohort (n=66) and a gastrointestinal tumour cohort (n=225).

A three EV-lncRNA (NALT1, PTENP1 and HOTTIP) liquid biopsy signature was developed for EOGC detection with an area under the receiver operating characteristic curve (AUROC) of 0.924 (95% CI 0.889 to 0.953). This EV-lncRNA signature provided robust diagnostic performance in two external validation cohorts (Xi'an cohort: AUROC, 0.911; Beijing cohort: AUROC, 0.9323). Furthermore, the EV-lncRNA signature reliably identified resectable stage EOGC patients (stage I/II) and demonstrated better diagnostic performance than traditional GC-related biomarkers in distinguishing early-stage EOGC (stage I) from precancerous lesions. The low levels of this biomarker in postsurgery and other gastrointestinal tumour plasma samples indicated its GC specificity.

The newly developed EV-lncRNA signature effectively identified EOGC patients at a resectable stage with enhanced precision, thereby improving the prognosis of patients who would have otherwise missed the curative treatment window.

Atrophic gastritis (AG) is a chronic inflammation where gastric glandular cells are replaced by intestinal-type epithelium. Gastric epithelial cell loss is often linked to multiple cell death signaling pathways. While Helicobacter pylori (H. pylori) infection is the main cause of AG, its role in inducing cell death goes beyond apoptosis and autophagy. Pyroptosis could promote development of inflammation related cancers, but its involvement in H. pylori-induced malignant transformation remains unclear.

The enrichment of pyroptosis signaling across pathological stages was assessed using immunohistochemistry and bioinformatic analysis. Gastric epithelial cells were co-cultured with VacA recombinant protein or VacA+H. pylori to investigate the role of VacA in pyroptosis, and its downstream targets. TNFAIP3 or TRAF1 was silenced/overexpressed in gastric epithelial cells to explore their impact on pyroptosis. Finally, the interaction between TNFAIP3 and TRAF1 was examined using Western Blot, immunofluorescence, co-immunoprecipitation and ubiquitin assays.

Expression of pyroptosis components and pyroptosis enrichment score were upregulated in AG and gastric cancer tissues compared to normal or non-atrophic gastritis tissues. Upon incubation with VacA recombinant protein or VacA+H. pylori, pyroptosis and TNFAIP3/TRAF1 were elevated in gastric epithelial cells. TRAF1 promoted expression of downstream pyroptosis components and release of IL-1β/IL18. TRAF1 ablation could reverse pyroptosis activation caused by VacA. Finally, we proved TNFAIP3 as deubiquitinating enzyme to increase TRAF1 stability, further inducing pyroptosis.

The VacA/TNFAIP3/TRAF1 signaling cascade facilitates pyroptosis in H. pylori- infected tissue. Overactivation of Pyroptosis caused the atrophy-like morphological changes of gastric epithelium, further inducing sustainable malignant transformation.

The Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) are established classification systems used to evaluate atrophic gastritis and intestinal metaplasia, respectively.

We evaluated the association of OLGA and OLGIM scores and the risk of gastric cancer (GC) in only prospective cohort studies.

Systematic review and meta-analysis.

We systematically searched four databases for prospective cohorts that evaluated the use of OLGA and OLGIM staging systems in predicting the risk of GC. We primarily compared OLGA/OLGIM III-IV versus OLGA/OLGIM 0-II categories and GC events. Pooled risk ratios (RR) and absolute risk differences with their 95% confidence intervals (CIs) were calculated.

Eight studies were included (n = 12,526). The mean age of the patients ranged from 48.2 to 64.9 years. OLGA III-IV and OLGIM III-IV were associated with the development of GC in comparison to their 0-II categories (RR 32.31, 95% CI 9.14-114.21 and RR 12.38, 95% CI 5.75-26.65, respectively). OLGA III-IV and OLGIM III-IV were associated with an increase in the absolute risk of GC of 4% and 5%, respectively. The risk remained significant if we only included countries with high incidence of GC, and was greater if we excluded one study that included mostly patients with autoimmune gastritis. OLGA II and OLGIM II were associated with higher risk of high-grade dysplasia (HGD) and GC in comparison with OLGA 0-I and OLGIM 0-I, respectively.

Higher stages in OLGA and OLGIM systems are associated with a significantly increased risk of developing HGD and GC, validating these scoring systems for the assessment of GC risk and the design of endoscopic surveillance programs.

CRD42024565771.

Despite associated risk of anemia and gastric cancer, screening for autoimmune atrophic gastritis (AAG) is underperformed in subjects with type 1 diabetes mellitus (T1DM). We measured the predictive value of serum gastrin as a biomarker of gastric atrophy in subjects with T1DM and parietal cell autoantibodies (PCA).

PCA measurements were retrospectively retrieved in 1,425 consecutive subjects with T1DM between 2014 and 2018. Screening for AAG was conducted in PCA+ subjects by measuring blood counts, serum ferritin, vitamin B12 and gastrin; and by performing gastroduodenal fibroscopy, with fundic biopsies for histology and Helicobacter pylori. The performance of blood biomarkers of gastric atrophy was analyzed in comparison with the histopathological gold standard.

PCA were found in 185/1,425 subjects (13 %). PCA positivity was associated with female sex, older age, longer T1DM duration, and co-occurrence of anti-GAD and anti-thyroperoxydase autoantibodies. Of the 185 PCA+ subjects, 122 (66 %) participated in screening. AAG was found in 69/122 (57 %) subjects and Helicobacter pylori infection in 20/122 (16 %). Compared to PCA+ subjects without gastric atrophy, those with gastric atrophy had more frequently iron deficiency (65 % vs. 18 %, P < 0.0001), and/or vitamin B12 deficiency (57 % vs. 7 %, P < 0.0001); 44/69 (64 %) presented a pre-tumoral lesion and 6 % a tumor. Using a cut-off of 1.2-fold above the upper normal limit, serum gastrin concentration displayed 91 % sensitivity and 82 % specificity at predicting gastric atrophy.

In subjects with T1DM and PCA, serum gastrin is a reliable biomarker of gastric atrophy that can be used to select subjects requiring gastroduodenal fibroscopy.

Piwei Peiyuan (PWPY) prescription is a traditional Chinese medicine prescription and has been efficiently used in the clinics to treat chronic atrophic gastritis (CAG) for many years. However, the mechanism of action underlying PWPY for treating CAG remains elusive. A CAG rat animal and cell model was constructed in this study to explore the action mechanism of PWPY prescription in treating CAG. Here we show that PWPY attenuates the progression of CAG by eliciting MAPK10-mediated mitochondrial autophagy. Experimental model of CAG was introduced using N-methyl-n'-nitro-n-nitroguanidine (MNNG). Our histological analyses reveal that MNNG-induced CAG in rat undergoes classical morphological alterations judged by immunohistochemistry and serum level of PGⅠ, PGⅡ, and G17. Importantly, PWPY treatment prevents the progression of MNNG-induced CAG judged by serum level of PGⅠ, PGⅡ, and G17. Interestingly, PWPY treatment inhibits MAPK10 activity judged by biochemical assays and promotes mitochondrial autophagy judged by electron microscopic analyses. Thus, we conclude that PWPY attenuates the progression of MNNG-induced CAG and prevents precancerous lesions by harnessing MAPK10-elicited mitochondrial autophagy. The MNNG-induced experimental CAG model provides a robust platform for further delineating therapeutic targets underlying PWPY regimen.

Autoimmune gastritis (AIG) is a corpus-dominant atrophic gastritis in which patients are positive for antiparietal cell antibody (APCA) and/or anti-intrinsic factor antibody. The risk of developing gastric cancer in patients with AIG remains unclear, and reliable frequency data of AIG in patients with gastric cancer are lacking.

We included 624 Korean patients with gastric tumors (612 gastric cancers and 12 neuroendocrine tumors) who had APCA results and were available for AIG evaluation. In patients with positive APCA results, endoscopy and histology findings were reviewed to diagnose AIG.

Of the 624 patients, 37 (5.9%) tested positive for APCA, and ultimately, 11 (1.8%) met the diagnostic criteria for AIG (5 both endoscopy and histology findings, 4 endoscopy-only findings, 2 histology-only findings). The frequency of AIG in patients with gastric cancer was 1.3% (8/612), and that in patients with neuroendocrine tumors was 25.0% (3/12). Of the 11 patients with AIG, serum Helicobacter pylori antibody was positive in six patients (54.5%), all of whom had gastric cancer. Histologically, three patients showed pure AIG, four patients exhibited concurrent AIG and H. pylori gastritis, and the findings for four were indefinite for AIG. The pepsinogen (PG) I levels and PG I/II ratio were significantly lower in patients with gastric cancer with AIG than in patients with gastric cancer without AIG (p=0.042 and p=0.016, respectively).

The frequency of AIG in gastric cancer patients was very low compared to that in patients with neuroendocrine tumors. Rather, concurrent AIG and H. pylori gastritis was common in patients with AIG with gastric cancer.

Gastric premalignant conditions (GPMC) are common and include atrophic gastritis, gastric intestinal metaplasia, dysplasia, and certain gastric epithelial polyps. GPMC have an increased risk of progression to gastric adenocarcinoma. Gastric cancer (GC) in the United States represents an important cancer disparity because incidence rates are 2- to 13-fold greater in non-White individuals, particularly early-generation immigrants from regions of high GC incidence. The US 5-year survival rate for GC is 36%, which falls short of global standards and is driven by the fact that only a small percentage of GC in the US is diagnosed in the early, curable stage. This document represents the first iteration of American College of Gastroenterology guidelines on this topic and encompasses endoscopic surveillance for high-risk patients with GPMC, the performance of high-quality endoscopy and image-enhanced endoscopy for diagnosis and surveillance, GPMC histology criteria and reporting, endoscopic treatment of dysplasia, the role of Helicobacter pylori eradication, general risk reduction measures, and the management of autoimmune gastritis and gastric epithelial polyps. There is insufficient evidence to make a recommendation on upper endoscopic screening for GC/GPMC detection in US populations deemed high-risk for GC. Surveillance endoscopy is recommended for individuals at high risk for GPMC progression, as defined by endoscopic, histologic, and demographic factors, typically every 3 years, but an individualized interval may be warranted. H. pylori testing, treatment, and eradication confirmation are recommended in all individuals with GPMC. Extensive high-quality data from US populations regarding GPMC management are lacking, but continue to accrue, and the quality of evidence for the recommendations presented herein should be interpreted with this dynamic context in mind. The GPMC research and education agendas are broad and include high-quality prospective studies evaluating opportunistic endoscopic screening for GC/GPMC, refined delineation of what constitutes "high-risk" populations, development of novel biomarkers, alignment of best practices, implementation of training programs for improved GPMC/GC detection, and evaluation of the impact of these interventions on GC incidence and mortality in the US.

Gastric cancer remains a leading cause of cancer-related mortality worldwide. In the United States, gastric cancer incidence and mortality are substantially higher among non-White racial and ethnic groups and new immigrants from high-incidence countries. This is in large part related to the higher prevalence of Helicobacter pylori-associated gastric premalignant changes in these populations. Apart from primary prevention, early detection of gastric cancer is the principal strategy to reduce gastric cancer mortality and improve survival. Extensive evidence in Asian countries has demonstrated the benefits of endoscopic screening in detecting early-stage gastric cancer and reducing gastric cancer-related mortality. By contrast, direct, high-quality US-based data, such as from large clinical trials or observational studies, on important outcomes of gastric cancer screening are still lacking. In this review, we evaluate and summarize the latest global evidence on the epidemiology and predisposing factors of gastric cancer as well as the efficacy, benefits vs. risks, and cost-effectiveness of gastric cancer screening. We further discuss the critical knowledge gaps and challenges in promoting gastric cancer screening in the United States. Dedicated research is urgently needed to enrich the US-based data on gastric cancer primary and secondary prevention to inform clinical practice and reduce gastric cancer-related morbidity and mortality in a cost and resource efficient manner.

Atrophic gastritis-the end stage of chronic gastritis-is an asymptomatic disease due to Helicobacter pylori infection causing decreased vitamin B12 and folate absorption, which may lead to severe haematological and neuropsychological disorders including Alzheimer's disease. The diagnosis requires endoscopy and biopsies from symptomatic patients, explaining why its true prevalence in the population is not well-known.

We aimed to evaluate the prevalence of various stages of chronic gastritis in an autopsy series most closely representing the general population.

Gastric mucosa samples were collected prospectively from out-of-hospital deaths included in the Tampere Sudden Death Study (n = 70, mean age 63, age range 22-91 years). Antrum and corpus samples were stained with a H. pylori antibody and staged histopathologically.

Chronic gastritis with or without atrophic changes was detected in 40% of the cases. The proportion of healthy mucosa decreased age-dependently from 71.4% among individuals aged <50 years to 43.5% among the oldest individuals (>70 years), and that of chronic non-atrophic gastritis from 21.4% to 8.7%. In contrast, the prevalence of atrophic gastritis was 27.1% and increased in the age groups from 7.1% to 47.8% (P = .019) among the oldest individuals, showing a strong association (P < .0001) with H. pylori immunopositivity.

Atrophic gastritis is a common feature of the ageing stomach, which is observed in every second individual aged 70+ years, showing a strong association with H. pylori immunopositivity. Atrophic gastritis may be a more common risk factor in old age for diseases associated with low serum B12 and folate levels than has been previously known.

Stomach cancer is one of the leading causes of cancer death, and its epidemiologic characteristics are regionally heterogeneous worldwide. The BRICS nations (Brazil, Russian Federation, India, China, and South Africa) have markedly increasing influences on the international stage. We aim to investigate time trends in stomach cancer mortality among the BRICS countries from 1982 to 2021.

Data for this study were obtained from the Global Burden of Disease (GBD) 2021 public dataset to investigate the deaths, all-age mortality rate, and age-standardized mortality rate (ASMR) of stomach cancer. The age-period-cohort (APC) model was employed to estimate net drift, local drift, age-specific curves, and period (cohort) relative risks, and the Bayesian generalized linear model was employed to evaluate the relationship between food intake and mortality rate.

In 2021, there were approximately 572,000 stomach cancer deaths across the BRICS, accounting for 59.9% of global death. Russian Federation exhibited the most significant reduction in ASMR of stomach cancer among the BRICS. In contrast, China continued to report the highest number of stomach cancer deaths. The risk of mortality associated with stomach cancer exhibited a marked increase with advancing age, both within these countries and at the global level. PUFA, sodium, calcium and trans fat may have an impact on the mortality rate of stomach cancer. Favorable trends in period and birth cohort effects were observed in these five nations over the past decades.

BRICS countries have made varying progress in reducing stomach cancer mortality. Given the diverse environments, it is recommended to progressively develop customized stomach cancer prevention strategies, utilizing available resources. Healthcare services should be extended to all age groups, with a particular emphasis on vulnerable populations.

Chronic atrophic gastritis (CAG) is considered to be closely related to Helicobacter pylori (H. pylori) infection and characterized by the atrophy and/or intestinal metaplasia (IM) of the gastric mucosa in pathology. CAG is often regarded as the precancerous lesion of gastric cancer and H. pylori infection stimulates the development of atrophy and IM and the progression of gastric cancer through the persistent effect acting on the gastric mucosa, including releasing inflammatory factors such as Interleukin-8(IL-8). From the molecular biology perspective, growing evidence shows that H. pylori probably induce the expression of NF-κB, miR-204, miR-27a, hnRNPA2B1, and JARID1B, which play crucial roles in the progression of CAG into gastric cancer. In addition, H. pylori can increase Epstein-Barr virus (EBV) infection, and the co-infection will jointly increase gastric cancer risk. Furthermore, H. pylori induces cellular senescence and promotes atrophy progression and finally increases the gastric cancer risk. This review aims to explore the carcinogenic mechanisms of H. pylori related CAG in order to provide theoretical foundations for the pathogenesis mechanism and early detection and prevention of gastric cancer.

This study aims to elucidate the relationship between gastric mucosal atrophy, cystic dilatation, and their associated histopathological characteristics.

A comprehensive analysis was conducted on endoscopic biopsy specimens from 527 cases exhibiting gastric mucosal cystic dilatation. Detailed histological observations and immunohistochemical analysis were performed.

This study included 527 endoscopic biopsy and ESD samples, with a male predominance of 313 cases (59.4%) and 214 female cases (40.6%). The age distribution was as follows: 207 cases (39.3%) were ≤ 60 years, while 320 cases (60.7%) were > 60 years. Regarding cystic dilatation types, 287 cases (54.5%) were identified as simple cystic dilatation, and 240 cases (45.5%) were classified as compound cystic dilatation. Gastric mucosal atrophy was observed in all cases of cystic dilatation, with the atrophic process initially disrupting the structural integrity of the gastric glands. This led to increased interstitial tissue and widening of glandular septa, followed by compensatory hyperplasia and cystic cavity formation. Simple cystic dilatation (54.5%) and compound cystic dilatation (45.5%) were distinguished based on the extent of cellular and structural changes. Simple cystic dilatation could progress to early gastric cancer, presenting as gastric papillary cystadenocarcinoma, while compound cystic dilatation could lead to tubular papillary adenocarcinoma. The progression from simple to complex lesions involved low- and high-grade intraepithelial neoplasia, ultimately resulting in mixed cystadenocarcinoma-glandular tube papillary carcinoma, indicative of early-stage gastric cancer.

The classification, grading, and histopathological characteristics of cystic dilatation in the gastric mucosa are crucial for guiding clinicians in precise treatment and vigilant monitoring of malignant transformation. This approach is significant for the prevention and control of gastric cancer progression.

Clinical practice guidelines (CPGs) are intended to offer appropriate recommendations for clinical practice based on the available evidence while acknowledging existing gaps and uncertainties. The quality of CPGs for gastric precancerous lesions (GPL), distribution of evidence quality, and strength of recommendations are unknown.

Systematically evaluate the quality of CPGs for GPL and identify areas for improvement in the development process.

PubMed, Embase, Cochrane Library, Cumulative Index to Nursing and Allied Health Literature, and six online CPG repositories were systematically searched for CPGs related to GPL. Three researchers independently assessed the methodological quality of the included CPGs by using the AGREE II tool. The reporting and recommendation quality of the CPGs were evaluated using the RIGHT and AGREE-REX tools through consensus. Evidence-based CPGs were analyzed using the Grading of Recommendation Assessment, Development, and Evaluation system to determine the distribution of quality of evidence and strength of recommendations.

A total of 4046 records were identified; nine CPGs met the eligibility criteria for this study. The mean overall score for the methodological quality of the CPGs was 46.22%. Among the six domains, the mean score for clarity of presentation was the highest (71.67%), while the mean score for applicability was the lowest (24.56%). Among the nine CPGs, only one was considered high quality. Regarding reporting quality, domains 1, 3, and 4 had mean reporting rates equal to or higher than 60%. The mean overall score for the recommendation quality was 19.11%. In total, 235 recommendations were identified through the screening process, of which 64.4% were classified as strong. However, only 17.5% of the strong recommendations were supported by high-quality evidence.

The overall quality of CPGs for GPL was poor, with uneven quality across domains. In addition, the consistency between the strength of recommendations and the quality of evidence was poor.

Endoscopic resection (ER) has proven effective and safe for T1 esophageal adenocarcinoma (EAC). However, uncertainty remains concerning risk-benefit return of esophagectomy for submucosal lesions (T1b). Surgical series in past decades have reported significant risk of lymph node metastasis (LNM) in T1b EAC, but these rates may be overestimated due to limitations in histological assessment of surgical specimens. We aimed to test this hypothesis by reassessing histological risk features in surgical specimens from T1b EAC cases with documented LNM.

A retrospective cross-sectional study (1994-2005) was conducted. Patients who underwent direct esophagectomy without prior neoadjuvant therapy for suspected T1b EAC with LNM were included. Additional tissue sections were prepared from archival tumor blocks. A consensus diagnosis on tumor depth, differentiation grade, and lymphovascular invasion (LVI) was established by a panel of experienced pathologists.

Specific depth of submucosal invasion (sm1 to sm3) was not specified in 10 of 11 archival case sign-out reports. LVI status was not reported in seven of 11 cases. Following reassessment, one patient was found to have deep tumor invasion into the muscularis propria (T2). The remaining 10 of 11 patients exhibited deep submucosal invasion (sm2-3), with five showing one or more additional risk features (poor differentiation and/or LVI).

Our findings highlight the potential for underestimating tumor depth of invasion and other high-risk features in surgical specimens. Despite the limited cohort size, our study confirmed a consistent high-risk histological profile across all cases. Caution is warranted when extrapolating LNM risk data from historic heterogeneous cross-sectional surgical cohorts to the modern ER era.

Recent advancements in deep learning have significantly improved the intelligent classification of gastrointestinal (GI) diseases, particularly in aiding clinical diagnosis. This paper seeks to review a computer-aided diagnosis (CAD) system for GI diseases, aligning with the actual clinical diagnostic process. It offers a comprehensive survey of deep learning (DL) techniques tailored for classifying GI diseases, addressing challenges inherent in complex scenes, clinical constraints, and technical obstacles encountered in GI imaging. Firstly, the esophagus, stomach, small intestine, and large intestine were located to determine the organs where the lesions were located. Secondly, location detection and classification of a single disease are performed on the premise that the organ's location corresponding to the image is known. Finally, comprehensive classification for multiple diseases is carried out. The results of single and multi-classification are compared to achieve more accurate classification outcomes, and a more effective computer-aided diagnosis system for gastrointestinal diseases was further constructed.

Gastric cancer (GC) is a leading cause of preventable cancer and mortality in certain US populations. The most impactful way to reduce GC mortality is via primary prevention, namely Helicobacter pylori eradication, and secondary prevention, namely endoscopic screening and surveillance of precancerous conditions, such as gastric intestinal metaplasia (GIM). An emerging body of evidence supports the possible impact of these strategies on GC incidence and mortality in identifiable high-risk populations in the United States. Accordingly, the primary objective of this American Gastroenterological Association (AGA) Clinical Practice Update (CPU) Expert Review is to provide best practice advice for primary and secondary prevention of GC in the context of current clinical practice and evidence in the United States.

This CPU Expert Review was commissioned and approved by the AGA Institute CPU Committee and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership, and underwent internal peer review by the CPU Committee and external peer review through standard procedures of Gastroenterology. These best practice advice statements were drawn from a review of the published literature and expert opinion. Because systematic reviews were not performed, these best practice advice statements do not carry formal ratings regarding the quality of evidence or strength of the presented considerations. Best Practice Advice Statements BEST PRACTICE ADVICE 1: There are identifiable high-risk groups in the United States who should be considered for GC screening. These include first-generation immigrants from high-incidence GC regions and possibly other non-White racial and ethnic groups, those with a family history of GC in a first-degree relative, and individuals with certain hereditary gastrointestinal polyposis or hereditary cancer syndromes. BEST PRACTICE ADVICE 2: Endoscopy is the best test for screening or surveillance in individuals at increased risk for GC. Endoscopy enables direct visualization to endoscopically stage the mucosa and identify areas concerning for neoplasia, as well as enables biopsies for further histologic examination and mucosal staging. Both endoscopic and histologic staging are key for risk stratification and determining whether ongoing surveillance is indicated and at what interval. BEST PRACTICE ADVICE 3: High-quality upper endoscopy for the detection of premalignant and malignant gastric lesions should include the use of a high-definition white-light endoscopy system with image enhancement, gastric mucosal cleansing, and insufflation to achieve optimal mucosal visualization, in addition to adequate visual inspection time, photodocumentation, and use of a systematic biopsy protocol for mucosal staging when appropriate. BEST PRACTICE ADVICE 4: H pylori eradication is essential and serves as an adjunct to endoscopic screening and surveillance for primary and secondary prevention of GC. Opportunistic screening for H pylori infection should be considered in individuals deemed to be at increased risk for GC (refer to Best Practice Advice 1). Screening for H pylori infection in adult household members of individuals who test positive for H pylori (so-called "familial-based testing") should also be considered. BEST PRACTICE ADVICE 5: In individuals with suspected gastric atrophy with or without intestinal metaplasia, gastric biopsies should be obtained according to a systematic protocol (eg, updated Sydney System) to enable histologic confirmation and staging. A minimum of 5 total biopsies should be obtained, with samples from the antrum/incisura and corpus placed in separately labeled jars (eg, jar 1, "antrum/incisura" and jar 2, "corpus"). Any suspicious areas should be described and biopsied separately. BEST PRACTICE ADVICE 6: GIM and dysplasia are endoscopically detectable. However, these findings often go undiagnosed when endoscopists are unfamiliar with the characteristic visual features; accordingly, there is an unmet need for improved training, especially in the United States. Artificial intelligence tools appear promising for the detection of early gastric neoplasia in the adequately visualized stomach, but data are too preliminary to recommend routine use. BEST PRACTICE ADVICE 7: Endoscopists should work with their local pathologists to achieve consensus for consistent documentation of histologic risk-stratification parameters when atrophic gastritis with or without metaplasia is diagnosed. At a minimum, the presence or absence of H pylori infection, severity of atrophy and/or metaplasia, and histologic subtyping of GIM, if applicable, should be documented to inform clinical decision making. BEST PRACTICE ADVICE 8: If the index screening endoscopy performed in an individual at increased risk for GC (refer to Best Practice Advice 1) does not identify atrophy, GIM, or neoplasia, then the decision to continue screening should be based on that individual's risk factors and preferences. If the individual has a family history of GC or multiple risk factors for GC, then ongoing screening should be considered. The optimal screening intervals in such scenarios are not well defined. BEST PRACTICE ADVICE 9: Endoscopists should ensure that all individuals with confirmed gastric atrophy with or without GIM undergo risk stratification. Individuals with severe atrophic gastritis and/or multifocal or incomplete GIM are likely to benefit from endoscopic surveillance, particularly if they have other risk factors for GC (eg, family history). Endoscopic surveillance should be considered every 3 years; however, intervals are not well defined and shorter intervals may be advisable in those with multiple risk factors, such as severe GIM that is anatomically extensive. BEST PRACTICE ADVICE 10: Indefinite and low-grade dysplasia can be difficult to reproducibly identify by endoscopy and accurately diagnose on histopathology. Accordingly, all dysplasia should be confirmed by an experienced gastrointestinal pathologist, and clinicians should refer patients with visible or nonvisible dysplasia to an endoscopist or center with expertise in the diagnosis and management of gastric neoplasia. Individuals with indefinite or low-grade dysplasia who are infected with H pylori should be treated and have eradication confirmed, followed by repeat endoscopy and biopsies by an experienced endoscopist, as visual and histologic discernment may improve once inflammation subsides. BEST PRACTICE ADVICE 11: Individuals with suspected high-grade dysplasia or early GC should undergo endoscopic submucosal dissection with the goal of en bloc, R0 resection to enable accurate pathologic staging with curative intent. Eradication of active H pylori infection is essential, but should not delay endoscopic intervention. Endoscopic submucosal dissection should be performed at a center with endoscopic and pathologic expertise. BEST PRACTICE ADVICE 12: Individuals with a history of successfully resected gastric dysplasia or cancer require ongoing endoscopic surveillance. Suggested surveillance intervals exist, but additional data are required to refine surveillance recommendations, particularly in the United States. BEST PRACTICE ADVICE 13: Type I gastric carcinoids in individuals with atrophic gastritis are typically indolent, especially if <1 cm. Endoscopists may consider resecting gastric carcinoids <1 cm and should endoscopically resect lesions measuring 1-2 cm. Individuals with type I gastric carcinoids >2 cm should undergo cross-sectional imaging and be referred for surgical resection, given the risk of metastasis. Individuals with type I gastric carcinoids should undergo surveillance, but the intervals are not well defined. BEST PRACTICE ADVICE 14: In general, only individuals who are fit for endoscopic or potentially surgical treatment should be screened for GC and continued surveillance of premalignant gastric conditions. If a person is no longer fit for endoscopic or surgical treatment, then screening and surveillance should be stopped. BEST PRACTICE ADVICE 15: To achieve health equity, a personalized approach should be taken to assess an individual's risk for GC to determine whether screening and surveillance should be pursued. In conjunction, modifiable risk factors for GC should be distinctly addressed, as most of these risk factors disproportionately impact people at high risk for GC and represent health care disparities.

Genotypic methods for detecting antibiotic resistance in Helicobacter pylori infection offer a rapid, convenient, and accurate approach for tailored therapy. However, existing studies predominantly examine single sample types and lack comparative analyses across different samples. This study comprehensively detects and compares genotypic resistance to clarithromycin and levofloxacin in gastric mucosa, gastric fluid, and fecal samples from the same patients. The study enrolled 183 participants, comprising 124 H. pylori-positive and 59 H. pylori-negative patients. All participants provided fecal samples and underwent gastroscopy for the collection of gastric mucosa and gastric fluid. Real-time PCR was employed to detect genotypic resistance to clarithromycin and levofloxacin in conjunction with bacterial culture and antibiotic susceptibility testing. Genotypic resistance detection rates for clarithromycin were 100% in gastric mucosa, 99.2% in gastric fluid, and 79.8% in fecal samples. For levofloxacin, detection rates were 97.6%, 96.8%, and 72.6%, respectively. The results showed that PCR detection for clarithromycin exhibited high sensitivity (0.94-0.95) and specificity (0.88-0.89) across all sample types. However, PCR detection for levofloxacin demonstrated slightly lower sensitivity (0.79-0.89) and specificity (0.79-0.83). The comparison of genotypic resistance results by PCR among the three sample types showed that gastric mucosa and gastric juice exhibited higher consistency, while the consistency between feces and both gastric mucosa and gastric juice was lower. This study confirmed good consistency between genotypic and phenotypic resistance in clarithromycin and levofloxacin. While both gastric mucosa and gastric fluid samples demonstrated high detection performance, the efficiency of detecting fecal samples was constrained by challenges in DNA extraction.

This study, with a large sample size, comprehensively tested both Helicobacter pylori-negative and -positive patients, including rapid urease test, histopathological evaluation and staining, bacterial culture, susceptibility testing, and resistance gene mutation analysis. By simultaneously examining gastric mucosa, gastric juice, and fecal samples from the same individuals, we minimized confounding factors arising from different sample sources, ensuring the reliability of our results. This approach effectively delineated the differences and characteristics in detection performance among different sample types, offering crucial reference data for selecting appropriate detection samples and identifying areas for improvement. The findings revealed robust concordance between genotypic and phenotypic resistance, with both gastric mucosa and gastric juice samples demonstrating excellent detection performance. However, the efficiency of detecting resistance in fecal samples was hampered by challenges in DNA extraction.

To investigate the diagnostic utility of aldehyde dehydrogenase 1 (ALDH1) and gastrin 17 (G-17) levels in the gastric juice of patients with gastric cancer and to track changes in the levels of these markers in the gastric juice of these patients.

126 individuals were diagnosed via gastroscopy. This trial includes gastric mucosal histology and gastroscopy performed at Hefei Second People's Hospital between March 2023 and March 2024. On the basis of the results of gastroscopy and gastric mucosal histology, all the participants were categorized into three groups: 30 patients with gastric cancer (GC), 34 patients with gastric ulcer (GU) and 62 patients with gastritis. Thirty patients with chronic nonatrophic gastritis were chosen from the physical examination center, and thirty-two patients with chronic atrophic gastritis (CAG) composed the gastritis group. As the control group, they were chosen at the physical testing center. An enzyme-related immunosorbent assay (ELISA) was used to quantify the levels of G-17 and ALDH1 in each group. A correlation study was performed on the levels of ALDH1 and G-17 in the gastric juice. By using binomial logistic regression analysis, the impact of G-17 and ALDH1 in gastric juice on the incidence of gastric cancer was examined. To illustrate the predictive usefulness of G-17 and ALDH1 in gastric juice for GC diagnosis, a receiver operating characteristic (ROC) curve was generated.

The gastric juice of the gastric cancer group had higher levels of ALDH1 and G-17 than did the gastric juice of the gastritis group and GU group (P < 0.05). The levels of ALDH1 and G-17 in gastric juice of gastric ulcer group were higher than those of atrophic gastritis group and control group (P < 0.05). The levels of ALDH1 and G-17 in gastric juice of atrophic gastritis group were statistically significant compared with those of control group (P < 0.05). The development of gastric cancer was significantly influenced by elevated levels of ALDH1 and G-17 in gastric juice (OR= 1.095, 1.018; both P <0.05); the AUCs for the combined diagnosis of gastric cancer and elevated levels of G-17 and ALDH1 in gastric juice were 0.792, 0.757, and 0.695, respectively.

The development of gastric cancer is influenced by increased levels of ALDH1 and G-17 in gastric juice. The diagnosis of gastric cancer may be made more accurately by combining the two gastric fluid markers, which can be found in gastric juice.

Chronic atrophic gastritis (CAG), precancerous lesions of gastric cancer (PLGC), and gastric cancer (GC), seriously threaten human health. Traditional Chinese medicine (TCM) has been employed in the treatment of chronic diseases for a long time and has shown remarkable efficacy.

Recently, there has been an increasing use of TCM in treating CAG, PLGC, and GC. The objective of this study is to compile a comprehensive overview of the existing research on the effects and molecular mechanisms of TCM, including formulas, single herbs, and active components.

To obtain a comprehensive understanding of traditional use of TCM in treating these diseases, we reviewed ancient books and Chinese literature. In addition, keywords such as "TCM", "CAG", "PLGC", "GC", and "active ingredients" were used to collect modern research on TCM published in databases such as CNKI, Web of Science, and Pubmed up to April 2024. All collected information was then summarized and analyzed.

This study analyzed 174 articles, which covered the research progress of 20 TCM formulas, 14 single herbs, and 50 active ingredients in treating CAG, PLGC, and GC. Sources, effects, and molecular mechanisms of the TCM were summarized.

This article reviews the progress of TCM in the management of CAG, PLGC, and GC, which will provide a foundation for the clinical application and further development of TCM.

Operative link on gastritis assessment (OLGA) and operative link on gastric intestinal metaplasia assessment (OLGIM) systems are histological staging systems of gastritis for gastric cancer (GC) risk estimation. Intermediate OLGA/OLGIM stages are of concern in a region with high incidence of GC. This study aimed to validate OLGA and OLGIM staging systems for early GC (EGC) in Chinese population.

This single-centre, case-control study included 196 patients with EGC and 196 age-matched and sex-matched health screening control subjects. OLGA and OLGIM systems, and other clinical parameters were evaluated using logistic regression analysis.

OLGA and OLGIM stages II/III/IV were more prevalent in patients with EGC than in the control subjects. Multivariable analysis revealed family history of GC, previous Helicobacter pylori (H. pylori) infection, OLGA stages II and III-IV, OLGIM stages II and III-IV as independent risk factors for EGC (ORs, 4.04, 1.87, 2.52, 6.79, 4.11 and 10.78, respectively). Area under the receiver operating characteristic curve on EGC risk estimation was improved for OLGIM compared with OLGA (0.78 vs 0.71, p<0.001). Autoantibody seropositivity of gastric mucosa was not associated with EGC risk stratified by H. pylori status.

Surveillance of intermediate-risk patients (OLGA/OLGIM II) should be emphasised in our region. The OLGIM may be preferred over the OLGA for EGC risk estimation.

The relationship between autoimmune gastritis (AIG) and gastric polyps (GPs) is not well understood.

To explore the clinical characteristics and risk factors of AIG with GPs in patients.

This double center retrospective study included 530 patients diagnosed with AIG from July 2019 to July 2023. We collected clinical, biochemical, serological, and demographic data were of each patient. Logistic regression analyses, both multivariate and univariate, were conducted to pinpoint independent risk factors for GPs in patients with AIG patients. Receiver operating characteristic curves were utilized to establish the optimal cutoff values, sensitivity, and specificity of these risk factors for predicting GPs in patients with AIG.

Patients with GPs had a higher median age than those without GPs [61 (52.25-69) years vs 58 (47-66) years, P = 0.006]. The gastrin-17 levels were significantly elevated in patients with GPs compared with those without GPs [91.9 (34.2-138.9) pmol/mL vs 60.9 (12.6-98.4) pmol/mL, P < 0.001]. Additionally, the positive rate of parietal cell antibody (PCA) antibody was higher in these patients than in those without GPs (88.6% vs 73.6%, P < 0.001). Multivariate and univariate analyses revealed that PCA positivity [odds ratio (OR) = 2.003, P = 0.017], pepsinogen II (OR = 1.053, P = 0.015), and enterochromaffin like cells hyperplasia (OR = 3.116, P < 0.001) were significant risk factors for GPs, while pepsinogen I was identified as a protective factor.

PCA positivity and enterochromaffin like cells hyperplasia are significant risk factor for the development of GPs in patients with AIG. Elevated gastrin-17 levels may also play a role in this process. These findings suggest potential targets for further research and therapeutic intervention in managing GPs in patients with AIG.

Zuojin formula (ZJF) is a well-known herbal medicine in Pharmacopoeia of China, which is widely used for gastritis. Modified Zuojin formula (MZJF) was adapted based on traditional Chinese medicine (TCM) theories concerning gastric atrophy and dysplasia, along with extensive clinical experience, has been clinically employed to treat chronic atrophic gastritis (CAG). However, the underlying mechanisms by which MZJF intervenes in CAG remain to be fully elucidated.

The aim of this study was to evaluate the effects of MZJF intervention in CAG and explore its potential mechanisms.

Four induction factors were used to establish a CAG rat model. HE and AB-PAS staining was utilized to assess the effects of MZJF in the intervention of CAG. The stomach weight index and gastric acid pH was used to assess the overall state of stomach. ELISA was used to assess the gastric mucosal inflammatory response. Using transmission electron microscopy to observe chief cells and parietal cells, we evaluated the improvement of ultrastructure by MZJF. Through network pharmacology analysis, the possible regulatory mechanism of MZJF in CAG was preliminarily explored. Binding interactions between MZJF components and predicted targets were explored using molecular docking. Subsequently, quantitative real-time PCR (qRT-PCR), Western blot, biochemical analysis and TUNEL staining were applied to validate the effect of MZJF on predicted pathway.

MZJF treatment ameliorated gastric mucosal pathology, inflammation, cellular ultrastructural damage and PG levels, halted the exacerbation of CAG in rats, along with a reduction in stomach weight index and gastric acid pH. A total of 79 compounds in MZJF targeting 203 CAG-related molecules were identified through network pharmacology. Enrichment analysis of the core targets was focused on the hypoxia inducible factor-1α (HIF-1α) signaling pathway. Molecular docking results identified HIF-1α as stable binding targets for MZJF primary components. Subsequently, PCR, WB, and biochemical results showed that MZJF suppressed the gene and protein expression levels of HIF-1α and its downstream molecules including glycolytic enzymes and transporters, modulated glucose, pyruvic acid and lactate levels in gastric mucosal tissue. Moreover, MZJF induced apoptosis of gastric epithelial cells, as evidenced by the upregulation of cleaved caspase-3, Bax, Bax/Bcl-2 and TUNEL positive cells ratio.

MZJF suppressed the HIF-1α-mediated glycolytic pathway, and promoted cell apoptosis, thereby halting the malignant transformation of CAG. The study provides a valuable reference point for applying TCM in preventing and treating CAG.

As digestive endoscopy becomes more prevalent, an increasing number of autoimmune gastritis (AIG) cases have been diagnosed, which has contributed to a growing body of research on AIG. We report the case of a patient with AIG who was diagnosed due to receiving endoscopic surgery after discovering a gastric neuroendocrine tumor (GNET) during gastroscopy twice within 3 years. The patient was admitted to our hospital for endoscopic submucosal dissection (ESD) due to GNET recurrence discovered during gastroscopy. The patient had previously undergone ESD due to a GNET discovered during gastroscopy 3 years ago. Recent repeat gastroscopy revealed severe mucosal atrophy in the gastric body and fundus, an ulcer in the gastric antral, and two mucosal bulges in the gastric body. Pathology indicated Grade 2 (G2)-GNET, and ESD was performed again. The patient also had iron deficiency anemia and thyroid dysfunction, elevated gastrin, and decreased pepsinogen I (PG I) and PG I/II. Hence, AIG was diagnosed. Recurrent GNET cases, especially those with concurrent anemia and abnormal thyroid function, may experience AIG. In addition to symptomatic treatment, the clinician must evaluate the patient's overall condition.

Chronic atrophic gastritis (CAG) is a prevalent form of chronic gastritis that presents with chronic inflammation of the gastric mucosa, localised gastric mucosal glandular atrophy and intestinal metaplasia. Despite the existence of diagnostic criteria, effective therapeutic strategies for this condition remain to be developed. The objective of this study was to examine the potential therapeutic benefits of epiberberine in mitigating MNNG-induced CAG and to elucidate the underlying mechanisms. MNNG was employed to establish a CAG mouse model and a GES-1 cell model, and EPI was observed to be efficacious in ameliorating the gastric mucosal injury and inflammatory infiltration induced by MNNG in the CAG model mice, a finding that was subsequently validated in the GES-1 model cells. Bioinformatics analysis indicated that EPI may exert a direct effect on EGFR, thereby regulating the expression of IL-33 and thereby achieving the therapeutic effect of CAG. This hypothesis was also validated by molecular docking prediction, CETSA, and overexpression of EGFR in GES-1 model cells, using EGFR agonists and inhibitors to further demonstrate that EPI may act as an antagonist supplement to EGFR for the treatment of CAG.

Inflammation is an important physiological response of the organism to restore homeostasis upon pathogenic or damaging stimuli. However, the persistence of the harmful trigger or a deficient resolution of the process can evolve into a state of low-grade, chronic inflammation. This condition is strongly associated with the development of several increasingly prevalent and serious chronic conditions, such as obesity, cancer, and cardiovascular diseases, elevating overall morbidity and mortality worldwide. The current pandemic of chronic diseases underscores the need to address chronic inflammation, its pathogenic mechanisms, and potential preventive measures to limit its current widespread impact. The present review discusses the current knowledge and research gaps regarding the association between low-grade chronic inflammation and chronic diseases, focusing on obesity, cardiovascular diseases, digestive diseases, and cancer. We examine the state of the art in selected aspects of the topic and propose future directions and approaches for the field.

Autoimmune gastritis (AIG) leads to increased gastrin (G) levels due to hypo-achlorhydria, providing proliferative stimuli on the gastric mucosa.

To evaluate the incidence and characteristics of gastric polyps in AIG patients across six tertiary centers in Italy.

A multicentric, cross-sectional study enrolled patients with AIG diagnosed from January 2000 to June 2023, who underwent at least one endoscopy. Data on demographics, clinical history, biochemical profiles, and endoscopic and histopathological findings were systematically collected.

Among 612 AIG patients followed for a median of 4 years, 222 (36.3 %) developed at least one gastric polyp. Of these, 214 were non-endocrine lesions detected in 162 patients, including 151 inflammatory (70.5 %), 29 adenomatous (13.6 %), 18 fundic gland polyps (8.4 %), 13 adenocarcinomas (6.1 %), and one MALT lymphoma. Additionally, 108 patients had gastric neuroendocrine neoplasms (gNENs), with 48 also having non-endocrine polyps. Older age and higher gastrin and chromogranin A levels were associated with polyp occurrence. No differences in OLGA/OLGIM stages or Helicobacter pylori status were noted among patients with and without lesions.

This large multicentric study underscores the substantial occurrence of gastric polyps in AIG patients, including notable rates of gNENs and adenocarcinomas, emphasizing the importance of proactive endoscopic surveillance and histopathological examination for effective management.

Atrophic gastritis (AG) is characterized by atrophy of gastric glands-in particular, oxyntic glands-in the setting of chronic inflammation; it is often autoimmune. The diagnosis is confirmed by immunohistochemistry (IHC) for gastrin (to confirm biopsy site), and pathologists often use IHC for neuroendocrine markers to evaluate for enterochromaffin-like cell hyperplasia (ECL-H). The utility of neuroendocrine staining is unclear, and we undertook this study to determine whether ECL pattern provided any additional information in cases of Helicobacter-negative AG.

We reviewed clinicopathologic findings in 184 cases from 184 patients with histologic AG and no evidence of Helicobacter infection. Using neuroendocrine IHC markers, cases were divided into 3 groups: Group 1 showed complete ECL-H (both qualitative and quantitative criteria met), group 2 showed focal ECL-H (qualitative but not quantitative criteria met), and group 3 showed no ECL-H (neither criteria met).

Group 1 patients were more likely to have positive autoantibody serologies (73%, P = .0007 vs group 2) and higher mean gastrin levels (700 pg/mL, P = .017 vs group 3), and only these patients developed gastric neuroendocrine tumors. Group 2 patients were more likely to take proton pump inhibitors (64%, P = .0002 vs group 1). Group 3 patients were more likely to be male (70%, P = .008 vs group 1) and to have microcytic anemia (44%, P = .022 vs group 2) and less likely to have intestinal metaplasia (50%, P = .044 vs group 1).

Stratification based on degree of ECL-H is not necessary for diagnosis of AG but does lead to statistically significant clinical and pathologic differences among groups.

Chronic atrophic gastritis (CAG) is a chronic disease of the gastric mucosa characterized by a reduction or an absolute disappearance of the original gastric glands, possibly replaced by pseudopyloric fibrosis, intestinal metaplasia, or fibrosis. CAG develops progressively into intestinal epithelial metaplasia, dysplasia, and ultimately, gastric cancer. Epidemiological statistics have revealed a positive correlation between the incidence of CAG and age. Mesenchymal stem cells (MSCs) are a type of adult stem cells derived from mesoderm, with strong tissue repair capabilities. Therefore, the restoration of the gastric mucosa may serve as an efficacious strategy to ameliorate CAG and avert gastric cancer. However, the mechanisms by which MSCs inhibit the relentless progression of aging atrophic gastritis remain to be elucidated. This study endeavored to assess a novel approach utilizing MSCs to treat CAG and forestall carcinogenics.

In this study, we selected mice with atrophic gastritis from naturally aging mice and administered human umbilical cord-derived mesenchymal stem cells (hUMSCs) via tail vein injection to evaluate the therapeutic effects of hUMSCs on age-related chronic atrophic gastritis. Initially, we employed methods such as ELISA, immunohistochemical analysis, and TUNEL assays to detect changes in the mice post-hUMSC injection. Proteomic and bioinformatics analyses were conducted to identify differentially expressed proteins, focusing on NADH: ubiquinone oxidoreductase core subunit S8 (Ndufs8). Co-culturing hUMSCs with Ndufs8 knockout gastric mucosal epithelial cells (GMECs), we utilized flow cytometry, Western blotting, real-time quantitative PCR, and immunofluorescence to investigate the mechanisms of action of hUMSCs.

We observed that hUMSCs are capable of migrating to and repairing damaged gastric mucosa. Initially, hUMSCs significantly enhanced the secretion of gastric proteins PG-1 and G17, while concurrently reducing inflammatory cytokines. Furthermore, hUMSCs mitigated gastric fibrosis and apoptosis in mucosal cells. Proteomic and bioinformatic analyses revealed alterations in the protein network involved in mitochondrial autophagy, with Ndufs8 playing a pivotal role. Upon knocking out Ndufs8 in GMECs, we noted mitochondrial damage and reduced autophagy, leading to an aged phenotype in GMECs. Co-culturing Ndufs8-knockout GMECs with hUMSCs demonstrated that hUMSCs could ameliorate mitochondrial dysfunction and restore the cell cycle in GMECs.

Chronic atrophic gastritis (CAG) is a prevalent digestive system disease characterized by atrophy of the gastric mucosa and the disappearance of inherent gastric glands. According to the theory of Correa's cascade, CAG is an important pathological stage in the transformation from normal condition to gastric carcinoma. In recent years, the global incidence of CAG has been increasing due to pathogenic factors, including Helicobacter pylori infection, bile reflux, and the consumption of processed meats. In this review, we comprehensively described the etiology and clinical diagnosis of CAG. We focused on elucidating the regulatory mechanisms and promising therapeutic targets in CAG, with the expectation of providing insights and theoretical support for future research on CAG.

The role of endoscopic submucosal dissection (ESD) in the treatment of Barrett esophagus-associated neoplasia (BEN) has been evolving. We examined the efficacy and safety of ESD and endoscopic mucosal resection (EMR) for BEN.

A database search was performed for studies reporting efficacy and safety outcomes of ESD and EMR for BEN. Pooled proportional and comparative meta-analyses were performed.

47 studies (23 ESD, 19 EMR, 5 comparative) were included. The mean lesion sizes for ESD and EMR were 22.5 mm and 15.8 mm, respectively; most lesions were Paris type IIa. For ESD, pooled analysis showed rates of en bloc, R0, and curative resection, and local recurrence of 98%, 78%, 65%, and 2%, respectively. Complete eradication of dysplasia and intestinal metaplasia were achieved in 94% and 59% of cases, respectively. Pooled rates of perforation, intraprocedural bleeding, delayed bleeding, and stricture were 1%, 1%, 2%, and 10%, respectively. For EMR, pooled analysis showed rates of en bloc, R0, and curative resection, and local recurrence of 37%, 67%, 62%, and 6%, respectively. Complete eradication of dysplasia and intestinal metaplasia were achieved in 94% and 75% of cases. Pooled rates of perforation, intraprocedural bleeding, delayed bleeding, and stricture were 0.1%, 1%, 0.4%, and 8%, respectively. The mean procedure times for ESD and EMR were 113 and 22 minutes, respectively. Comparative analysis showed higher en bloc and R0 resection rates with ESD compared with EMR, with comparable adverse events.

ESD and EMR can both be employed to treat BEN depending on lesion type and size, and center expertise.

Introduction: Performing a tandem endoscopy and colonoscopy in selected individuals has advantages, such as the early detection of benign and/or precancerous foregut diseases; it is efficient, and it may allow added therapies. It may also have disadvantages, such as generating anxiety from false-positive screening, possible harm from further testing, and unproven cost-effectiveness. Aims: We aimed to examine the prevalence of foregut endoscopic and histologic abnormalities in subjects referred for screening/surveillance colonoscopy who also underwent a tandem endoscopy. We wanted to (1) assess implications for cancer detection, intervention, and surveillance of precancerous foregut abnormalities, (2) identify benign foregut lesions, and (3) generate data on the utilities of this tandem approach. Patients and Methods: A retrospective cohort study of consecutive subjects referred for screening or surveillance colonoscopy who also underwent an endoscopy. Based on national screening guidelines, responses to prompting questions, personal or family history, or other risk factors, subjects were assigned to tandem endoscopy with biopsies (modified Seattle and Sydney protocols), under one anesthesia. Results: Of the 1004 patients referred for colonoscopy, 317 (32%) underwent tandem endoscopy. There were 214 women and 103 men. There were 237 Whites, 16 Asians, 40 Blacks, and 24 Hispanics. Median age was 59 (range 19-85). At endoscopy, we identified actionable benign (45%) peptic, inflammatory, and H. pylori-related abnormalities, and premalignant findings (i.e., intestinal metaplasia, 27%, dysplasia, 2%, and cancer 0.9%), comparable to the premalignant (40.3%) and malignant (0.6%) colonoscopy yield. Conclusions: When implemented based on national screening guidelines, tandem EGD and colonoscopy combines Barrett's esophagus and gastric cancer screening in one examination, and it has a high yield in a diverse US population.

Autoimmune metaplastic atrophic gastritis (AMAG) is a precancerous condition that predisposes to gastric neuroendocrine tumors (gNETs). There exist no methods to stratify patients with AMAG for gNET risk.

We identified a cohort of patients with AMAG within a university health system using histopathologic and serologic criteria. We analyzed features predictive of prevalent gNET.

We identified 181 patients with AMAG and 41 (22.7%) with prevalent gNET. Gastrin levels were elevated in gNET (1,859.8 vs 679.5 pg/mL, P < 0.001), and gastrin titers demonstrated good discrimination (c = 0.799, 95% CI 0.707-0.892) for gNET.

Gastrin levels differ significantly between patients with AMAG with and without gNET.

Autoimmune gastritis is an immune-mediated disease characterized by the destruction of parietal cells and atrophy of the oxyntic mucosa due to anti-parietal cell antibodies. It may lead to serious conditions including iron/vitamin B12 and micronutrient deficiencies, neurological disorders, and gastric malignancies. The exact mechanism of this disease is not exactly understood; however, dysregulated immunological mechanisms appear to be major contributors. Patients with this disease are often asymptomatic but may present with gastrointestinal symptoms and/or iron/vitamin B12 deficiencies. Although important serological markers are available and despite advanced endoscopic techniques, the definitive diagnosis relies on histopathological examination of gastric corporal biopsy specimens. Autoimmune gastritis is closely related with increased risk of gastric neuroendocrine tumors and gastric adenocarcinoma. Patients with autoimmune gastritis do not benefit from specific treatments, thus, management is directed to restore micronutrient deficiencies and to prevent occurrence of neoplastic transformation with appropriate endoscopic surveillance.

Atrophic gastritis and intestinal metaplasia may progress to gastric malignancy. Non-invasive serum biomarkers have been extensively studied and proven to be useful as a screening tool to stratify risk and identify patients for endoscopy to detect early gastric cancer. These non-invasive biomarkers have been endorsed and recommended by many international consensus guidelines. In this letter, we reviewed the literature and evidence supporting the use of serum biomarkers as a dynamic test to monitor the status of atrophic gastritis.

Chronic gastritis caused by Helicobacter pylori (H. pylori) infection can progress to gastric cancer through atrophic gastritis (AG). The risk of gastric cancer increases with the progression of AG. Therefore, investigating the risk factors for the progression of AG is important.

Using the GTEx and GEO databases, we extracted thirty-four candidate genes involved in the progression of AG. Then, with in silico analysis using HaploReg v4.1 and JASPAR (Matrix ID: MA0113.3), we extracted rs1231760 of RGS2 as a key single-nucleotide polymorphism (SNP) that could be involved in the functional change in the candidate gene. A correlation analysis between the selected SNP and AG in 200 H. pylori-positive and 302 H. pylori-negative participants was conducted. For functional analysis of the SNP, a dual-luciferase assay using reporter plasmids with a major or minor allele sequence was carried out.

The frequency of the C/C genotype of rs1231760 was higher in the AG group than in the non-AG group (p = 0.0471). Functional analysis showed that the transcriptional activities were higher at the dexamethasone-stimulating C allele than at the others (p < 0.05).

The C/C genotype of rs1231760 in RGS2 could be a biomarker of high-risk H. pylori-positive AG because of an increase in RGS2 expression.

Introduction. Autoimmune metaplastic atrophic gastritis (AMAG, also termed autoimmune gastritis) is a chronic gastritis of autoimmune pathogenesis. Although its clinical and pathological features are well-documented in many countries, data from Middle Eastern populations remain scarce. This study examined the prevalence of AMAG in gastric specimens from the region, specifically from Saudi Arabia. Methods. We conducted a retrospective review of the pathology database of gastric specimens with a diagnosis of AMAG between 2020 and 2023. Detailed clinical, endoscopic, and pathological features of identified features were described. Result. Of the 978 gastric biopsies received, 17 patients were diagnosed with AMAG. The cohort comprised 11 women (64.7%) and 6 men (35.3%), presenting at a median age of 50 years (range: 32-85). Clinical manifestations varied widely, from abdominal pain (n = 6), dyspepsia (n = 2), symptomatic anemia with significant vitamin B12 deficiency (2 of 17) to asymptomatic/incidentally diagnosed patients (5 of 17). The tissue samples showed varying histological characteristics, with some showing lymphoplasmacytic infiltrate, mucosal atrophy, and hyperplasia of enterochromaffin-like cells. Conclusion. The observed prevalence of AMAG in our study aligns with global averages reported for other populations. The diverse clinical presentations highlight the need for awareness of findings in AMAG in gastric biopsies to ensure appropriate clinical management.