Gastric intestinal metaplasia (GIM) is a precancerous condition. Limited data exist on real-world clinical practice relative to guidelines.

The aim of this study was to evaluate adherence to GIM risk stratification and identify factors associated with follow-up endoscopy.

We conducted manual chart review of patients with histologically confirmed GIM at an urban, tertiary medical center were identified retrospectively and details of their demographics, Helicobacter pylori , biopsy protocol, endoscopic/histologic findings, and postendoscopy follow-up were recorded. Multivariable logistic regression was used to identify factors independently associated with follow-up endoscopy.

Among 253 patients, 59% were female, 37% non-Hispanic White (NHW), 26% Hispanic, 16% non-Hispanic Black (NHB). The median age at index endoscopy was 63.4 years (IQR: 55.9 to 70.0), with median follow-up of 65.1 months (IQR: 44.0 to 72.3). H. pylori was detected in 21.6% patients at index EGD. GIM extent and subtype data were frequently missing (22.9% and 32.8%, respectively). Based on available data, 26% had corpus-extended GIM and 28% had incomplete/mixed-type GIM. Compared with NHW, Hispanic patients had higher odds of follow-up EGD (OR=2.48, 95% CI: 1.23-5.01), while NHB patients had 59% lower odds of follow-up EGD (OR=0.41, 95% CI: 0.18-0.96). Corpus-extended GIM versus limited GIM (OR=2.27, 95% CI: 1.13-4.59) was associated with follow-up EGD, but GIM subtype and family history of gastric cancer were not.

We observed suboptimal risk stratification among patients with GIM and notable race and ethnic disparities with respect to endoscopic surveillance. Targeted interventions are needed to improve practice patterns and mitigate observed disparities.

At a population level, the European Society of Gastrointestinal Endoscopy (ESGE), the European Helicobacter and Microbiota Study Group (EHMSG), and the European Society of Pathology (ESP) suggest endoscopic screening for gastric cancer (and precancerous conditions) in high-risk regions (age-standardized rate [ASR] > 20 per 100 000 person-years) every 2 to 3 years or, if cost-effectiveness has been proven, in intermediate risk regions (ASR 10-20 per 100 000 person-years) every 5 years, but not in low-risk regions (ASR < 10).ESGE/EHMSG/ESP recommend that irrespective of country of origin, individual gastric risk assessment and stratification of precancerous conditions is recommended for first-time gastroscopy. ESGE/EHMSG/ESP suggest that gastric cancer screening or surveillance in asymptomatic individuals over 80 should be discontinued or not started, and that patients' comorbidities should be considered when treatment of superficial lesions is planned.ESGE/EHMSG/ESP recommend that a high quality endoscopy including the use of virtual chromoendoscopy (VCE), after proper training, is performed for screening, diagnosis, and staging of precancerous conditions (atrophy and intestinal metaplasia) and lesions (dysplasia or cancer), as well as after endoscopic therapy. VCE should be used to guide the sampling site for biopsies in the case of suspected neoplastic lesions as well as to guide biopsies for diagnosis and staging of gastric precancerous conditions, with random biopsies to be taken in the absence of endoscopically suspected changes. When there is a suspected early gastric neoplastic lesion, it should be properly described (location, size, Paris classification, vascular and mucosal pattern), photodocumented, and two targeted biopsies taken.ESGE/EHMSG/ESP do not recommend routine performance of endoscopic ultrasonography (EUS), computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET)-CT prior to endoscopic resection unless there are signs of deep submucosal invasion or if the lesion is not considered suitable for endoscopic resection.ESGE/EHMSG/ESP recommend endoscopic submucosal dissection (ESD) for differentiated gastric lesions clinically staged as dysplastic (low grade and high grade) or as intramucosal carcinoma (of any size if not ulcerated or ≤ 30 mm if ulcerated), with EMR being an alternative for Paris 0-IIa lesions of size ≤ 10 mm with low likelihood of malignancy.ESGE/EHMSG/ESP suggest that a decision about ESD can be considered for malignant lesions clinically staged as having minimal submucosal invasion if differentiated and ≤ 30 mm; or for malignant lesions clinically staged as intramucosal, undifferentiated and ≤ 20 mm; and in both cases with no ulcerative findings.ESGE/EHMSG/ESP recommends patient management based on the following histological risk after endoscopic resection: Curative/very low-risk resection (lymph node metastasis [LNM] risk < 0.5 %-1 %): en bloc R0 resection; dysplastic/pT1a, differentiated lesion, no lymphovascular invasion, independent of size if no ulceration and ≤ 30 mm if ulcerated. No further staging procedure or treatment is recommended.Curative/low-risk resection (LNM risk < 3 %): en bloc R0 resection; lesion with no lymphovascular invasion and: a) pT1b, invasion ≤ 500 µm, differentiated, size ≤ 30 mm; or b) pT1a, undifferentiated, size ≤ 20 mm and no ulceration. Staging should be completed, and further treatment is generally not necessary, but a multidisciplinary discussion is required. Local-risk resection (very low risk of LNM but increased risk of local persistence/recurrence): Piecemeal resection or tumor-positive horizontal margin of a lesion otherwise meeting curative/very low-risk criteria (or meeting low-risk criteria provided that there is no submucosal invasive tumor at the resection margin in the case of piecemeal resection or tumor-positive horizontal margin for pT1b lesions [invasion ≤ 500 µm; well-differentiated; size ≤ 30 mm, and VM0]). Endoscopic surveillance/re-treatment is recommended rather than other additional treatment. High-risk resection (noncurative): Any lesion with any of the following: (a) a positive vertical margin (if carcinoma) or lymphovascular invasion or deep submucosal invasion (> 500 µm from the muscularis mucosae); (b) poorly differentiated lesions if ulceration or size > 20 mm; (c) pT1b differentiated lesions with submucosal invasion ≤ 500 µm with size > 30 mm; or (d) intramucosal ulcerative lesion with size > 30 mm. Complete staging and strong consideration for additional treatments (surgery) in multidisciplinary discussion.ESGE/EHMSG/ESP suggest the use of validated endoscopic classifications of atrophy (e. g. Kimura-Takemoto) or intestinal metaplasia (e. g. endoscopic grading of gastric intestinal metaplasia [EGGIM]) to endoscopically stage precancerous conditions and stratify the risk for gastric cancer.ESGE/EHMSG/ESP recommend that biopsies should be taken from at least two topographic sites (2 biopsies from the antrum/incisura and 2 from the corpus, guided by VCE) in two separate, clearly labeled vials. Additional biopsy from the incisura is optional.ESGE/EHMSG/ESP recommend that patients with extensive endoscopic changes (Kimura C3 + or EGGIM 5 +) or advanced histological stages of atrophic gastritis (severe atrophic changes or intestinal metaplasia, or changes in both antrum and corpus, operative link on gastritis assessment/operative link on gastric intestinal metaplasia [OLGA/OLGIM] III/IV) should be followed up with high quality endoscopy every 3 years, irrespective of the individual's country of origin.ESGE/EHMSG/ESP recommend that no surveillance is proposed for patients with mild to moderate atrophy or intestinal metaplasia restricted to the antrum, in the absence of endoscopic signs of extensive lesions or other risk factors (family history, incomplete intestinal metaplasia, persistent H. pylori infection). This group constitutes most individuals found in clinical practice.ESGE/EHMSG/ESP recommend H. pylori eradication for patients with precancerous conditions and after endoscopic or surgical therapy.ESGE/EHMSG/ESP recommend that patients should be advised to stop smoking and low-dose daily aspirin use may be considered for the prevention of gastric cancer in selected individuals with high risk for cardiovascular events.

Although Helicobacter pylori (H. pylori) is implicated in the development of most cases of gastric cancer with autoimmune gastritis, cases of gastric cancer have been reported in patients testing negative for H. pylori. Here, we aimed to outline the current research status of the factors involved in the development of gastric cancer in H. pylori-negative autoimmune gastritis. Predictive pathological conditions for the development of gastric cancer in H. pylori-negative autoimmune gastritis are postulated to be: (1) Severe atrophy; (2) Hypergastrinemia; (3) Bile reflux; and (4) Low acidity, which are directly related to the pathophysiology of autoimmune gastritis, as well as smoking and family history, which are not related to autoimmune gastritis. In autoimmune gastritis, where there is a possibility of spontaneous disappearance of H. pylori in advanced atrophy, it is difficult to assess H. pylori. Since H. pylori infection begins in the antrum and subsequently progresses to the proximal stomach, it is interpreted as H. pylori-negative autoimmune gastritis if histologically consistent with autoimmune gastritis in the body with spared antrum, and negative for other H. pylori tests. However, it is essential to examine whether the currently prevailing histological interpretation used to evaluate H. pylori infection status is appropriate.

This study aimed to construct and validate diagnostic models for the Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) staging systems using three different methodologies based on magnifying endoscopy with narrow-band imaging (ME-NBI) features, to evaluate model performance, and to analyse risk factors for high-risk OLGA/OLGIM stages.

We enrolled 356 patients who underwent white-light endoscopy and ME-NBI at the Department of Gastroenterology, Dongzhimen Hospital, Beijing University of Chinese Medicine, between January 2022 and September 2023. Clinical data were recorded. Chi-square or Fisher's exact tests were used to analyse differences in endoscopic features between OLGA/OLGIM stages. Variables showing statistical significance underwent collinearity diagnosis before model inclusion. We constructed predictive models using Bayesian stepwise discrimination, random forest, and XGBoost algorithms. Receiver operating characteristic (ROC) curves were plotted using Python 3.12.4. Model accuracy, area under the ROC curve (AUC), sensitivity, and specificity were calculated for comprehensive validation.

All three models demonstrated excellent diagnostic performance, with random forest and XGBoost models showing marginally superior accuracy, AUC values, and sensitivity compared with the Bayesian stepwise discrimination model. For OLGA staging, the AUC values were 0.928, 0.958, and 0.966, with accuracies of 0.854, 0.902, and 0.918 for Bayesian, random forest, and XGBoost models, respectively. For OLGIM staging, the corresponding AUC values were 0.924, 0.975, and 0.979, with accuracies of 0.910, 0.938, and 0.927. Risk factors for high-risk OLGA included lesion location (subcardial and lower body greater curvature), intestinal metaplasia patches, lesion size, demarcation line (DL), and margin regularity of micro-capillary demarcation line (MCDL). Risk factors for high-risk OLGIM included Helicobacter pylori infection status, mucosal condition, lesion location (lesser curvature and lower body greater curvature), erosion, lesion size, DL, vessel and epithelial classification (VEC), white globe appearance (WGA), and MCDL margin regularity.

All three models demonstrated robust accuracy and predictive capability, confirming that conventional white-light endoscopy combined with ME-NBI features provides valuable diagnostic reference for clinical risk assessment of precancerous gastric lesions.

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.

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.

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.

Helicobacter pylori (H. pylori) is the major cause of gastric mucosal precancerous lesions in adulthood, but its impact on pediatric patients remains unclear. We aimed to investigate H. pylori-induced gastric precancerous lesions in children and adolescents globally and analyze their influencing factors for related disease management and prevention.

We conducted a comprehensive literature search in major databases to identify studies including pediatric patients with gastric precancerous lesions and H. pylori infection status. Prevalence rates were computed using random-effects or fixed-effect models. A stratified analysis was conducted based on location, age, universal health coverage (UHC), and publication time.

Among the 3359 relevant articles screened, 24 studies (7036 participants) met the inclusion criteria. The overall prevalence of precancerous lesions in H. pylori-infected patients was 17.2%, in which atrophic gastritis (AG) and intestinal metaplasia (IM) were 13.5% and 3.6%, respectively. Precancerous lesion rates in infected individuals across different regions were as follows: Africa at 33.8% (AG: 32.6%), Latin America at 22.1% (AG: 17.9%, IM: 4.0%), Asia at 18.1% (AG: 12.4%, IM: 4.4%, Dysplasia: 1.2%), and Europe at 6.3% (AG: 4.3%, IM: 1.7%). Infected adolescents (> 10 years) exhibited a higher prevalence of precancerous lesions than younger children (≤ 10 years) at 14.2% (AG: 9.7%, IM: 2.9%) versus 3.4% (AG: 2.3%, IM: 1.1%), respectively. The prevalence of precancerous lesions in infected patients was higher in areas with low-medium UHC compared with high UHC (24.0% vs. 12.5%).

H. pylori infection causes significant gastric mucosal precancerous lesions in pediatric patients, representing a major concern for this population and a previously neglected area. Future in-depth investigations and proper management for related disease prevention are warranted.

 PROSPERO number: CRD42023424683.

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.

Autoimmune atrophic gastritis (AAG) is a frequently underdiagnosed disease due to its broad-spectrum clinical presentation. The diagnosis is based on histological confirmation of corpus-restricted metaplastic chronic atrophic gastritis.

To thoroughly describe the histological features of a European cohort of AAG patients.

Clinical and pathological data of 57 out of 676 patients diagnosed with AAG were reviewed.

Thirty-nine patients were female and eighteen were male. The mean age was 62 years. Antibodies were identified in 32/42 patients (76 %). Vitamin B12 levels were low (< 200 pg/mL) in 37/54 patients (69 %). Serum gastrin levels was elevated (> 115 pg/mL) in all cases tested. Associated autoimmune/inflammatory conditions were identified in 20/57 patients (35 %). Histologically, deep chronic inflammation was present in 46/57 (81 %) patients. Complete destruction of oxyntic glands was observed in 45/57 (79 %) patients. Pyloric metaplasia was present in 54/57 (95 %) patients, intestinal metaplasia in 51/57 (89 %) patients, and pancreatic metaplasia in 20/57 (35 %) patients. Among ECL cell proliferation, linear hyperplasia was present in all 57/57 patients, micronodular hyperplasia in 55/57 patients, and adenomatoid hyperplasia in 10/57 patients. ECL cell dysplasia was identified in 5/57 patients, and neuroendocrine microtumor in 4/57 patients.

The diagnosing of AAG remains challenging due to the greater variability in symptoms than previously recognized. It is important to consider chronic AAG, especially with other concurrent autoimmune conditions. The importance of accurate diagnosis and surveillance is based on the potential development of type 1 gastric neuroendocrine tumor and increased risk of gastric adenocarcinoma.

Gastric atrophy (GA), or atrophic gastritis, is a pre-neoplastic lesion of gastric cancer (GC). It is part of the Correa cascade, which culminates in intestinal-type gastric adenocarcinoma. The cascade posits that intestinal-type gastric adenocarcinoma develops along a defined pathway of pre-neoplastic stages. The cascade begins with chronic gastritis, most commonly caused by Helicobacter pylori (H. pylori) infection, and proceeds through GA, gastric intestinal metaplasia (GIM), both complete and incomplete, dysplasia, both low and high-grade, and culminating in intestinal-type gastric adenocarcinoma. Attempts in Europe have been made to identify patients at risk of developing GC and target them with surveillance oesophagogastroduodenoscopy (OGD). However, there remains uncertainty about GA's risk of developing into GC. This poses issues in terms of guiding the need for and determining intervals for surveillance OGDs, which are a costly form of surveillance. As such, we attempted to gather all available studies assessing the risk of GC developing from GA, which is the first step in the Correa cascade. This study was a comprehensive systematic review of published papers, reported per the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. This systematic review, which included a substantial 25,455 patients across 18 studies, found that the relative risk (RR) of GC in those with GA, using standardised incidence ratios as a measure of RR, was 15.1, with a 95% confidence interval ranging from 13.5 to 16.9. We conclude that GA does increase the risk of developing GC, and this risk may be higher than previously appreciated. Further large-scale studies are needed in Western cohorts of patients to precisely define this risk and guide the need for surveillance programs. These future studies must be standardised to account for H. pylori status, the topographical distribution of the GA, and the methods for assessing the degree of GA.

Intestinal metaplasia (IM) of the gastric mucosa is strongly associated with the risk of gastric cancer (GC). This study was performed to investigate the usefulness of endoscopic and histological risk stratification for GC using IM.

This was a post-hoc analysis of a multicenter prospective study involving 10 Japanese facilities (UMINCTR000027023). The ridge/tubulovillous pattern, light blue crest (LBC), white opaque substance (WOS), endoscopic grading of gastric IM (EGGIM) score using non-magnifying image-enhanced endoscopy, and operative link on gastric IM assessment (OLGIM) were evaluated for their associations with GC risk in all patients.

In total, 380 patients (115 with GC and 265 without GC) were analyzed. The presence of an LBC (limited to antrum: odds ratio [OR] 2.4 [95% confidence interval 1.1-5.0], extended to corpus: OR 3.6 [2.1-6.3]), the presence of WOS (limited to antrum: OR 3.0 [1.7-5.3], extended to corpus: OR 4.2 [2.1-8.2]), and histological IM (limited to antrum: OR 3.2 [1.4-7.4], extended to corpus: OR 8.5 [4.5-16.0]) were significantly associated with GC risk. Additionally, the EGGIM score (5-8 points: OR 8.8 [4.4-16.0]) and OLGIM (stage III/IV: OR 12.5 [6.1-25.8]) were useful for stratification of GC risk. The area under the receiver operating characteristic curve value for GC risk was 0.740 for OLGIM and 0.706 for EGGIM.

The LBC, WOS, EGGIM, and OLGIM were strongly associated with GC risk in Japanese patients. This finding can be useful for GC risk assessment in daily clinical practice.

We aimed to identify predictive markers for metachronous gastric cancer (MGC) in early gastric cancer (EGC) patients curatively treated with endoscopic submucosal dissection (ESD).

From EGC patients who underwent ESD, bulk RNA sequencing was performed on non-cancerous gastric mucosa samples at the time of initial EGC diagnosis. This included 23 patients who developed MGC, and 23 control patients without additional gastric neoplasms for over 3 years (1:1 matched by age, sex, and Helicobacter pylori infection state). Candidate differentially-expressed genes were identified, from which biomarkers were selected using real-time quantitative polymerase chain reaction and cell viability assays using gastric cell lines. An independent validation cohort of 55 MGC patients and 125 controls was used for marker validation. We also examined the severity of gastric intestinal metaplasia, a known premalignant condition, at initial diagnosis.

From the discovery cohort, 86 candidate genes were identified of which KDF1 and CDK1 were selected as markers for MGC, which were confirmed in the validation cohort. CERB5 and AKT2 isoform were identified as markers related to intestinal metaplasia and were also highly expressed in MGC patients compared to controls (p < 0.01). Combining these markers with clinical data (age, sex, H. pylori and severity of intestinal metaplasia) yielded an area under the curve (AUC) of 0.91 (95% CI, 0.85-0.97) for MGC prediction.

Assessing biomarkers in non-cancerous gastric mucosa may be a useful method for predicting MGC in EGC patients and identifying patients with a higher risk of developing MGC, who can benefit from rigorous surveillance.

Gastric cancer remains a disease with an ominous prognosis, while early gastric cancer has a good-to-excellent prognosis, with 5-year survival rates of up to 92.6% after successful endoscopic resection. In this context, the accurate identification of patients with established gastric precancerous lesions, namely chronic atrophic gastritis and intestinal metaplasia, is the first step in a stepwise approach to minimize cancer risk. Although current guidelines advocate for the execution of random biopsies to stage the extent and severity of gastritis/intestinal metaplasia, modern biopsy protocols are still imperfect as they have limited reproducibility and are susceptible to sampling error. The advent of novel imaging-enhancing modalities, i.e., high-definition with virtual chromoendoscopy (CE), has revolutionized the inspection of gastric mucosa, leading to an endoscopy-based staging strategy for the management of these premalignant changes in the stomach. Nowadays, the incorporation of CE-targeted biopsies in everyday clinical practice offers not only the robust detection of premalignant lesions but also an improvement in quality, by reducing missed diagnoses along with mean biopsies and, thus, the procedural costs and the environmental footprint. In this review, we summarize the recent evidence regarding the endoscopic grading and sampling of gastric precancerous lesions.

Helicobacter pylori eradication therapy reduces the risk of gastric cancer. However, it is unclear whether the severity of risk factors for gastric cancer such as atrophy and intestinal metaplasia are reduced after eradication in the long term. We aimed to study long-term changes in endoscopic risk factors for gastric cancer up to 20 years post-eradication. The endoscopic severity of gastritis according to the Kyoto Classification of Gastritis in 167 patients was retrospectively evaluated over an average follow-up 15.7 years. A significant improvement in mean total gastric cancer risk score (4.36 ± 1.66 to 2.69 ± 1.07, p < 0.001), atrophy (1.73 ± 0.44 to 1.61 ± 0.49, p = 0.004), and diffuse redness (1.22 ± 0.79 to 0.02 ± 0.13, p < 0.001) was observed compared to baseline in the Eradication group. However, there was no change in the never infection and current infection groups. The frequency of map-like redness increased over time until 15 years (3.6% to 18.7%, p = 0.03). The Cancer group had significantly higher risk scores at all time points. Endoscopic atrophy significantly improved in eradicated patients over long-term, suggested that eradication is one of the key elements in gastric cancer prevention. Individualized surveillance strategies based on endoscopic gastritis severity before eradication may be important for those at risk of gastric cancer.

Gastric intestinal metaplasia (GIM) is a high-risk factor for the development of gastric cancer. Narrow-band imaging (NBI) enables endoscopic grading of GIM (EGGIM). In the era of climate change, gastrointestinal endoscopists are expected to reduce greenhouse gas emissions and medical waste. Based on the diagnostic performance of NBI endoscopy, this study measured the environmental impact and reduced cost of implementing EGGIM during gastroscopy.

Using NBI endoscopy in 242 patients, EGGIM classification and operative link on GIM (OLGIM) staging were prospectively performed in five different areas (lesser and greater curvatures of the corpus and antrum, and the incisura angularis). We estimated the environmental impact and cost reduction of the biopsy procedures and pathological processing if EGGIM were used instead of OLGIM.

The diagnostic accuracy of NBI endoscopy for GIM was 93.0-97.1% depending on the gastric area. When a high EGGIM score ≥ 5 was the cut-off value for predicting OLGIM stages III-IV, the area under the curve was 0.862, sensitivity was 81.9%, and specificity was 90.4%. The reduction in the carbon footprint by EGGIM was -0.4059 kg carbon dioxide equivalents per patient, equivalent to 1 mile driven by a gasoline-powered car. The cost savings were calculated to be $47.36 per patient.

EGGIM is a reliable method for identifying high-risk gastric cancer patients, thereby reducing the carbon footprint and medical costs in endoscopy practice.

At the end of the last century, a far-sighted 'working party' held in Sydney, Australia addressed the clinicopathological issues related to gastric inflammatory diseases. A few years later, an international conference held in Houston, Texas, USA critically updated the seminal Sydney classification. In line with these initiatives, Kyoto Global Consensus Report, flanked by the Maastricht-Florence conferences, added new clinical evidence to the gastritis clinicopathological puzzle.The most relevant topics related to the gastric inflammatory diseases have been addressed by the Real-world Gastritis Initiative (RE.GA.IN.), from disease definitions to the clinical diagnosis and prognosis. This paper reports the conclusions of the RE.GA.IN. consensus process, which culminated in Venice in November 2022 after more than 8 months of intense global scientific deliberations. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus. After lively debates on the most controversial aspects of the gastritis spectrum, the RE.GA.IN. Faculty amalgamated complementary knowledge to distil patient-centred, evidence-based statements to assist health professionals in their real-world clinical practice. The sections of this report focus on: the epidemiology of gastritis; Helicobacter pylori as dominant aetiology of environmental gastritis and as the most important determinant of the gastric oncogenetic field; the evolving knowledge on gastric autoimmunity; the clinicopathological relevance of gastric microbiota; the new diagnostic horizons of endoscopy; and the clinical priority of histologically reporting gastritis in terms of staging. The ultimate goal of RE.GA.IN. was and remains the promotion of further improvement in the clinical management of patients with gastritis.

Global warming caused by increased greenhouse gas (GHG) emissions has a direct impact on human health. Gastrointestinal (GI) endoscopy contributes significantly to GHG emissions due to energy consumption, reprocessing of endoscopes and accessories, production of equipment, safe disposal of biohazardous waste, and travel by patients. Moreover, GHGs are also generated in histopathology through tissue processing and the production of biopsy specimen bottles. The reduction in unnecessary surveillance endoscopies and biopsies is a practical approach to decrease GHG emissions without affecting disease outcomes. This narrative review explores the role of precision medicine in GI endoscopy, such as image-enhanced endoscopy and artificial intelligence, with a focus on decreasing unnecessary endoscopic procedures and biopsies in the surveillance and diagnosis of premalignant lesions in the esophagus, stomach, and colon. This review offers strategies to minimize unnecessary endoscopic procedures and biopsies, decrease GHG emissions, and maintain high-quality patient care, thereby contributing to sustainable healthcare practices.

Introduction. The OLGA system has been proved to be useful in Asia and Europe as a risk marker of gastric cancer. However, its usefulness in high-risk populations in Colombia is still unknown. Objective. To assess potential associations between the OLGA staging system and an increased risk of gastric cancer and dysplasia in a high-risk Colombian population and to establish diagnostic capacity of the scale to assess the risk. Materials and methods. We carried out a multicenter study including patients with cancer and dysplasia (cases) and patients with atrophy and intestinal metaplasia (controls). A total of 506 patients were recruited from three centers in an area with a high risk population in Colombia. The endoscopic and histopathologic studies were evaluated according to the Sydney system and the OLGA staging system proposed by Rugge. The effect of each variable on the disease (gastric cancer and dysplasia) was evaluated using bivariate and multivariate models. Statistical significance was set considering a p value inferior to 0.05. Results. Advanced stages of the OLGA system (III-IV) were associated with a higher risk of dysplasia and gastric cancer (adjusted OR = 8.71; CI95% = 5.09-14.9; p=0.001), sensitivity=54.9%, specificity=89.3% and positive likelihood ratio=5.17. Conclusions. The OLGA staging system is a risk marker for gastric cancer and dysplasia in the studied population. We recommend its implementation to improve the timely diagnosis and follow-up of patients with the highest cancer risk.

Gastric intestinal metaplasia (GIM), which denotes conversion of gastric mucosa into an intestinal phenotype, can occur in all regions of the stomach, including cardiac, fundic, and pyloric mucosa. Since the earliest description of GIM, its association with gastric cancer of the differentiated (intestinal) type has been a well-recognized concern. Many epidemiologic studies have confirmed GIM to be significantly associated with subsequent gastric cancer development. Helicobacter pylori, the principal etiologic factor for gastric cancer, plays the most important role in predisposing to GIM. Although the role of GIM in the stepwise progression model of gastric carcinogenesis (the so-called "Correa cascade") has come into question recently, we review the scientific evidence that strongly supports this long-standing model and propose a new progression model that builds on the Correa cascade. Eradication of H pylori is the most important method for preventing gastric cancer globally, but the effect of eradication on established GIM, is limited, if any. Endoscopic surveillance for GIM may, therefore, be necessary, especially when there is extensive corpus GIM. Recent advances in image-enhanced endoscopy with integrated artificial intelligence have facilitated the identification of GIM and neoplastic lesions, which will impact preventive strategies in the near future.

Gastric cancer (GC) is associated with chronic gastritis. To evaluate the risk, the Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) system was constructed and showed a higher GC risk in stage III or IV patients, determined by the degree of intestinal metaplasia (IM). Although the OLGIM system is useful, evaluating the degree of IM requires substantial experience to produce precise scoring. Whole-slide imaging is becoming routine, but most artificial intelligence (AI) systems in pathology are focused on neoplastic lesions.

Hematoxylin and eosin-stained slides were scanned. Images were divided into each gastric biopsy tissue sample and labeled with an IM score. IM was scored as follows: 0 (no IM), 1 (mild IM), 2 (moderate IM), and 3 (severe IM). Overall, 5753 images were prepared. A deep convolutional neural network (DCNN) model, ResNet50, was used for classification.

ResNet50 classified images with and without IM with a sensitivity of 97.7% and specificity of 94.6%. IM scores 2 and 3, involved as criteria of stage III or IV in the OLGIM system, were classified by ResNet50 in 18%. The respective sensitivity and specificity values of classifying IM between scores 0 and 1 and 2 and 3 were 98.5% and 94.9%, respectively. The IM scores classified by pathologists and the AI system were different in only 438 images (7.6%), and we found that ResNet50 tended to miss small foci of IM but successfully identified minimal IM areas that pathologists missed during the review.

Our findings suggested that this AI system would contribute to evaluating the risk of GC accuracy, reliability, and repeatability with worldwide standardization.

Gastric cancer in the United States has a low survival rate mainly because of the late stage of diagnosis. Furthermore, there are no well-established guidelines concerning screening and surveillance even for higher risk patients such as those with nondysplastic noncardia gastrointestinal metaplasia (GIM), and thus they are not routinely performed. This study was designed to provide new evidence-based data that can be used to support the implementation of biennial surveillance guidelines in individuals with nondysplastic noncardia GIM. This practice can help detect early malignant lesions, thereby decreasing morbidity and mortality. We evaluated the cost-effectiveness of surveillance endoscopies for noncardia gastric cancer in populations with two different pathological diagnoses: mixed GIM and incomplete GIM (iGIM).

Markov state transition models were developed using a cohort simulation of 1000 hypothetical patients. Analysis was conducted for both mixed and iGIM. Quality-adjusted life-years and transition probabilities were derived from the published medical literature. Costs associated with endoscopy, cancer care, and surgery were based on Medicare reimbursement. A willingness-to-pay threshold of $100,000 per quality-adjusted life-year was used to determine cost-effectiveness.

Our study determined that it is significantly cost-effective to perform biennial endoscopy surveillance in patients who have been incidentally found to have noncardia mixed GIM, with a cost savings of $5783.84 per person, and in those with iGIM, with a cost savings of $8093.08 per person.

Biennial endoscopy surveillance should be considered in all individuals found to have mixed or incomplete noncardia GIM on endoscopy. Furthermore, screening specifically for iGIM after differentiating between the two groups can lead to further cost savings. As such, we recommend that pathologists routinely differentiate between the two and recommend robust routine surveillance of iGIM.

The operative link for the gastritis assessment (OLGA) system can objectively reflect the stratification of gastric cancer risk in patients with chronic atrophic gastritis (CAG).

We developed a real-time video monitoring model for the endoscopic diagnosis of CAG and OLGA staging based on U-Net deep learning (DL). To further validate and improve its performance, we designed a study to evaluate the diagnostic evaluation indices.

A prospective nested case-control study.

Our cohort consisted of 1306 patients from 31 July 2021 to 31 January 2022. According to the pathological results, patients in the cohort were divided into the CAG group and the chronic non-atrophic gastritis group to evaluate the diagnostic evaluation indices. Each atrophy lesion was automatically labeled and the atrophy severity was assessed by the model. Propensity score matching was used to minimize selection bias.

The diagnostic evaluation indices and the consistency between OLGA staging and pathological diagnosis of the model were superior to those of endoscopists [sensitivity (89.31% versus 67.56%), specificity (90.46% versus 70.23%), positive predictive value (90.35% versus 69.41%), negative predictive value (89.43% versus 68.40%), accuracy rate (89.89% versus 68.89%), Youden index (79.77% versus 37.79%), odd product (79.23 versus 4.91), positive likelihood ratio (9.36 versus 2.27), negative likelihood ratio (0.12 versus 0.46)], areas under the curves (AUC) (95% CI) (0.919 (0.893-0.945) versus 0.749 (0.707-0.792), p < 0.001) and kappa (0.816 versus 0.291)].

Our study demonstrated that the DL model can assist endoscopists in real-time diagnosis of CAG during gastroscopy and synchronous identification of high-risk OLGA stage (OLGA stages III and IV) patients.

ChiCTR2100044458.

Intestinal metaplasia plays a crucial role in the risk stratification of gastric cancer development. The objective of the study was to develop a prediction model for Operative Link on Gastric Intestinal Metaplasia (OLGIM) Stage III-IV.

We analyzed 7945 high-risk gastric cancer individuals from 115 hospitals who underwent questionnaires and gastroscope. The participants were assigned to either the development or validation cohort randomly. Demographics and clinical characteristics were obtained. The outcome measurement was OLGIM III-IV. Univariate logistic regression was used for feature selection and multivariate logistic analysis was performed to develop the nomogram. Area under the curves, calibration plots, decision curve and clinical impact analysis were used to assess the performance of the nomogram.

4600 individuals and 3345 individuals were included in the development and validation cohort, of which 124 and 86 individuals were diagnosed with OLGIM III-IV, respectively. Parameters in the training validation cohort matched well and there was no significant difference between two cohorts. A nomogram model for predicting OLGIM Stage III-IV consisted of 4 significantly associated variables, including age, gender, PG I and G-17 (AUC 0.723 and 0.700 for the 2 cohorts). The nomogram demonstrated excellent performance in the calibration curve. Decision curve and clinical impact analysis suggested clinical benefit of the prediction model.

This reliable individualized nomogram might contribute to more accurate management for patients with OLGIM III-IV. Therefore, we suggest that this study be used as an incentive to promote the application.

The association between circulating copper and the risk of liver cancer has been investigated by previous studies, while the findings were inconsistent. Thus, we aimed to evaluate the association between circulating copper and liver cancer by using meta-analysis and Mendelian randomization (MR). For meta-analysis, PubMed and Web of Science were searched to identify eligible studies published before April 4, 2022. Standardized mean difference (SMD) with 95% confidence interval (CI) in circulating copper level between liver cancer patients and controls were pooled. Furthermore, we selected genetic instruments for circulating copper from a genome-wide association study (GWAS) to conduct MR analysis. The summary statistics related to liver cancer were obtained from two large independent cohorts, UKBB and FinnGen, respectively. MR analysis was performed mainly by inverse-variance weighted (IVW) approach, followed by maximum-likelihood method as sensitivity analysis. In meta-analysis of eight studies, circulating copper was found to be higher in liver cancer patients (SMD: 1.65; 95% CI: 0.65 to 2.65) with high heterogeneity (I2 = 96.40%, P = 0.001). However, inconsistent findings were observed among subgroups with high evidence. In MR analysis, genetically predicted circulating copper was not significantly associated with the risk of liver cancer by IVW in UKBB (OR: 1.38; 95% CI: 0.72 to 2.65) and FinnGen (OR: 1.10; 95% CI: 0.69 to 1.73) separately, and the pooled results produced similar results (OR: 1.18, 95% CI: 0.81 to 1.72). Moreover, non-significant finding was confirmed by using maximum-likelihood method. There is no sufficient evidence to demonstrate that high levels of circulating copper increase the risks of liver cancer.

Gastric atrophy (GA) and intestinal metaplasia (IM) are early stages in the development of gastric cancer. Evaluations are based on the Updated Sydney System, which includes a biopsy of the incisura angularis (IA), and the Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastritis Assessment using Intestinal Metaplasia (OLGIM) gastric cancer risk staging systems.

To compare the OLGA and OLGIM classifications with and without IA biopsy. In addition, to determine the prevalence of Helicobacter pylori (HP) and pre-neoplastic changes (GA and IM) in different biopsied regions and to identify the exclusive findings of IA.

Observational, prospective, descriptive, unicentric study with 350 patients without a diagnosis of gastric cancer, who underwent upper digestive endoscopy with biopsies at Gastroclínica Itajaí, from March 2020 to May 2022. The histopathological classification of gastritis followed the Updated Sydney System, and the gastric cancer risk assessment followed the OLGA and OLGIM systems. The methodology applied evaluated the scores of the OLGA and OLGIM systems with and without the assessment of the IA biopsy. Statistical analysis was performed using descriptive measures (frequencies, percentages, mean, standard deviation, 95% confidence interval). Ranks were compared using the Kruskal-Wallis or Wilcoxon tests. To analyze the relationship between the frequencies, the bilateral Fisher’s exact test was used. Wilson’s score with continuity correction was applied to the confidence interval.

The median age was 54.7 years, with 52.57% female and 47.43% male patients. The comparison between the used biopsies protocol (corpus + antrum [CA] vs corpus + antrum + incisura angularis [CAI]) and the OLGA and OLGIM stages showed a significant decrease in both staging systems when the biopsy protocol restricted to the corpus and antrum was applied (OLGA CAI vs CA; P=0.008 / OLGIM CAI vs CA; P=0.002). The prevalence of pre-malignant lesions (GA, IM and dysplasia) of the gastric mucosa was (33.4%, 34% and 1.1%, respectively) in the total sample. The antrum region exhibited significantly higher numbers of alteration (P<0.001), except for HP infection, which was present in 24.8% of the patients.

Incisura angularis biopsy is important because it increased the number of cases diagnosed in more advanced stages of intestinal metaplasia and atrophy. The study had limitations, with the main one being the relatively small sample size, consisting mostly of healthy individuals, although mostly elderly.

Gastric intestinal metaplasia (GIM) is a precancerous lesion that increases gastric cancer (GC) risk. The Operative Link on GIM (OLGIM) is a combined clinical-histopathologic system to risk-stratify patients with GIM. The identification of molecular biomarkers that are indicators for advanced OLGIM lesions may improve cancer prevention efforts.

This study was based on clinical and genomic data from four cohorts: 1) GAPS, a GIM cohort with detailed OLGIM severity scoring (N=303 samples); 2) the Cancer Genome Atlas (N=198); 3) a collation of in-house and publicly available scRNA-seq data (N=40), and 4) a spatial validation cohort (N=5) consisting of annotated histology slides of patients with either GC or advanced GIM. We used a multi-omics pipeline to identify, validate and sequentially parse a highly-refined signature of 26 genes which characterize high-risk GIM.

Using standard RNA-seq, we analyzed two separate, non-overlapping discovery (N=88) and validation (N=215) sets of GIM. In the discovery phase, we identified 105 upregulated genes specific for high-risk GIM (defined as OLGIM III-IV), of which 100 genes were independently confirmed in the validation set. Spatial transcriptomic profiling revealed 36 of these 100 genes to be expressed in metaplastic foci in GIM. Comparison with bulk GC sequencing data revealed 26 of these genes to be expressed in intestinal-type GC. Single-cell profiling resolved the 26-gene signature to both mature intestinal lineages (goblet cells, enterocytes) and immature intestinal lineages (stem-like cells). A subset of these genes was further validated using single-molecule multiplex fluorescence in situ hybridization. We found certain genes (TFF3 and ANPEP) to mark differentiated intestinal lineages, whereas others (OLFM4 and CPS1) localized to immature cells in the isthmic/crypt region of metaplastic glands, consistent with the findings from scRNAseq analysis.

using an integrated multi-omics approach, we identified a novel 26-gene expression signature for high-OLGIM precursors at increased risk for GC. We found this signature localizes to aberrant intestinal stem-like cells within the metaplastic microenvironment. These findings hold important translational significance for future prevention and early detection efforts.

Gastric cancer (GC) incidence based on the endoscopic Kyoto classification of gastritis has not been systematically investigated using time-to-event analysis.

To examine GC incidence in an endoscopic surveillance cohort.

This study was retrospectively conducted at the Toyoshima Endoscopy Clinic. Patients who underwent two or more esophagogastroduodenoscopies were enrolled. GC incidence was based on Kyoto classification scores, such as atrophy, intestinal metaplasia (IM), enlarged folds (EFs), nodularity, diffuse redness (DR), and total Kyoto scores. Hazard ratios (HRs) adjusted for age and sex were calculated using a Cox hazard model.

A total of 6718 patients were enrolled (median age 54.0 years; men 44.2%). During the follow-up period (max 5.02 years; median 2.56 years), GC developed in 34 patients. The average frequency of GCs per year was 0.19%. Kyoto atrophy scores 1 [HR with score 0 as reference: 3.66, 95% confidence interval (CI): 1.06 to 12.61], 2 (11.60, 3.82-35.27), IM score 2 (9.92, 4.37-22.54), EF score 1 (4.03, 1.63-9.96), DR scores 1 (6.22, 2.65-14.56), and 2 (10.01, 3.73-26.86) were associated with GC incidence, whereas nodularity scores were not. The total Kyoto scores of 4 (HR with total Kyoto scores 0-1 as reference: 6.23, 95%CI: 1.93 to 20.13, P = 0.002) and 5-8 (16.45, 6.29-43.03, P < 0.001) were more likely to develop GC, whereas the total Kyoto scores 2-3 were not. The HR of the total Kyoto score for developing GC per 1 rank was 1.75 (95%CI: 1.46 to 2.09, P < 0.001).

A high total Kyoto score (≥ 4) was associated with GC incidence. The endoscopy-based diagnosis of gastritis can stratify GC risk.

The incidence of type I gastric neuroendocrine neoplasms (gNENs) has increased significantly over the past 50 years. Although autoimmune gastritis (AIG) increases the likelihood of developing gNENs, the exact incidence and prevalence of this association remain unclear.

To evaluate the incidence and prevalence of type I gNENs in a cohort of patients with a histological diagnosis of AIG.

Patients with a histological diagnosis of AIG were enrolled between October 2020 and May 2022. Circulating levels of CgA and gastrin were assessed at enrollment. Included patients underwent regular endoscopic follow-up to detect gastric neoplastic lesions, enterochromaffin-like (ECL) cell hyperplasia, and the development of gNEN.

We included 176 patients [142 women (80.7%), median age 64 years, interquartile range (IQR) 53-71 years] diagnosed with AIG between January 1990 and June 2022. At enrollment. One hundred and sixteen patients (65.9%) had ECL hyperplasia, of whom, 29.5% had simple/linear, 30.7% had micronodular, and 5.7% had macronodular type. The median follow-up time was 5 (3-7.5) years. After 1032 person-years, 33 patients developed a total of 50 type I gNENs, with an incidence rate of 0.057 person-years, corresponding to an annual cumulative incidence of 5.7%. Circulating CgA levels did not significantly differ between AIG patients who developed gNENs and those who did not. Conversely, gastrin levels were significantly higher in AIG patients who developed gNENs [median 992 pg/mL IQR = 449-1500 vs 688 pg/mL IQR = 423-1200, P = 0.03]. Calculated gastrin sensitivity and specificity were 90.9% and 1.4%, respectively, with an overall diagnostic accuracy of 30% and a calculated area under the gastrin receiver operating characteristic curve (AUROC or AUC) of 0.53.

Type I gNENs are a significant complication in AIG. Gastrin's low diagnostic accuracy prevents it from serving as a marker for early diagnosis. Effective strategies for early detection and treatment are needed.

Patients suffering from chronic gastritis and developing gastric mucosa atrophy are at increased risk of the development of gastric cancer. The diagnosis of chronic atrophic gastritis (CAG) is a complex procedure involving a detailed history taking, a thorough physical examination and the use of laboratory and instrumental diagnostic methods among which the endoscopy of the upper digestive tract is the cornerstone because it allows the assessment of the topography of gastritis and identification of erosions and areas of intestinal metaplasia with the use of NBI endoscopy. However, the diagnosis of CAG requires morphological examination of the gastric mucosa. So, in addition to assessing macroscopic changes in the gastric mucosa, it is necessary to take biopsy specimens in accordance with the protocols for their morphological and immunohistochemical examination. In the absence of specific diagnostic stigmas of CAG, close cooperation between a clinician, endoscopist and pathologist is necessary. The article presents systematized data on the histopathological assessment of the gastric mucosa atrophy to predict the risk of gastric cancer.

It has been shown the methylenetetrahydrofolate reductase (MTHFR) 677TT (rs 1801133) genotype predicts histopathological alterations in the incisura of patients with chronic atrophic gastritis (CAG). MTHFR is a crucial enzyme in fatty acid (FA) metabolism. This study aimed to evaluate the influence of FA supplementation in CAG patients without Helicobacter pylori infection and the MTHFR C677T (rs 1801133) genotype as a potential CAG predictor.

A total of 96 CAG patients, aged 21 to 72 years old, were enrolled in this study. After 6 months of treatment, histopathological outcomes were compared among patients treated with weifuchun (WFC) (1.44 g 3 times per os per day), those treated with WFC and FA (5 mg once daily), and those treated with WFC, FA, and vitamin B12 (VB12) (0.5 mg 3 times per day) based on the Operative Link on Gastritis/Intestinal Metaplasia assessment staging systems.

Atrophic lesions in patients treated with WFC and FA improved more than in patients treated only with WFC therapy (78.1% vs 53.3%, P = .04). Atrophic or intestinal metaplasia (IM) lesions in the incisura of patients with the TT genotype were better than those in patients with the CC/CT genotype (P = .02).

The treatment of CAG patients with 5 mg of FA supplements daily for 6 months improved their gastric atrophy status, especially for the Operative Link on Gastritis/Intestinal Metaplasia assessment stages I/II. Moreover, our study is the first to reveal that patients with the MTHFR 677TT genotype require more timely and effective FA treatment than those with the CC/CT genotype.

Kyoto Classification of Gastritis is a newly proposed gastric cancer risk assessment in recent years. It selects important gastroscopic manifestations that have been reported and calculates score values. Although it has been extensively employed in clinical practice, there is no thorough review or systematic summary of its usage.

We looked for works published before May 2022 on the correlation between the Kyoto Classification of Gastritis and gastric cancer (GC) risk in Web of Science, EMBASE, China National Knowledge Infrastructure, PubMed, Wanfang database, and other suitable sources. Statistical analysis was carried out using Stata 14.0 and RevMan 5.40. Two statistical methods were employed.

Eight case-control studies involving 6927 patients (continuous variables group: 1961 patients; dichotomy variables group: 4966 patients) were included, and the meta-analysis results showed a significant association between Kyoto Classification of Gastritis and GC. A Kyoto classification score ≥ 4 might indicate a risk of GC (odds ratios 7.30; 95% confidence intervals [CI] 3.62-14.72; P < .00001. There was a significant difference between gastritis and GC scores (mean difference [MD] 0.86; 95% CI 0.73-0.99; P < .00001). Moreover, we found that intestinal metaplasia and atrophy highly affected the Kyoto Classification score (MD = 0.35, MD = 0.72 95% CI 0.20-0.50,0.56-0.88). However, there was considerable heterogeneity in both statistical analyses. We found the source of heterogeneity in the first analysis method but failed to find it in the second analysis method, which may be due to the small number of studies.

The Kyoto Classification of gastritis score is crucial for detecting early stomach cancer. A score >4 suggests a significant risk for gastric cancer, with atrophy and intestinal metaplasia having the most impact. This score may be promoted at primary hospitals; however, because of the small number and quality of included studies, the results mentioned above need to be verified by randomized control trials with large samples and high-quality methods.