Gastric Atrophy Research Articles

Autoimmune Gastritis Accompanied by a Schwannoma Presenting as a Subepithelial Tumor

Autoimmune gastritis (AIG), a chronic inflammatory disease occurs as a result of a complex interaction between host-related and environmental factors. AIG may progress to severe atrophic gastritis secondary autoimmune-mediated parietal cell destruction in the stomach. AIG can be diagnosed based on anti-parietal cell antibody tests and endoscopy, which reveals widespread gastric corpus atrophy in patients with low serum pepsinogen I levels, a low pepsinogen I/II ratio, and elevated serum gastrin levels on serological testing. Tissue biopsy findings, which include mucosal atrophy and lymphocytic infiltration of the lamina propria may be useful for diagnostic confirmation. Decreased gastric acid secretion causes hypergastrinemia and enterochromaffin-like (ECL) cell proliferation, which can lead to neuroendocrine tumor development. Additionally, an autoimmune response results in parietal and chief cell injury, and proliferating ECL cells are detected in the deep mucosal layers in patients with AIG. Therefore, this condition may easily be misdiagnosed as a subepithelial tumor, and establishing a differential diagnosis for other types of subepithelial tumor accompanied by AIG is challenging. We present the case of a 54-year-old woman who was diagnosed with AIG with a concomitant subepithelial tumor based on serologic tests and biopsy findings and underwent wedge resection, which confirmed diagnosis of a schwannoma.

Type A, Type B, and Non-atrophic Gastritis

The gastric cancer risk varies based on the etiology and severity of gastritis, which depends on a history of Helicobacter pylori infection and the secretory capacity of the stomach. Type A gastritis is associated with reverse atrophy of the corpus and type B with progressive atrophy extending from the antrum to the corpus. Diffuse or spotty redness in the corpus together with high serum pepsinogen (PG) II levels and a low PG I/II ratio are observed in patients with H. pylori infection when secretory capacity of the stomach is intact. Diffuse-type gastric cancer may develop near the gastric folds, which is a rare site of atrophy. Low serum PG I levels are associated with progressive gastric corpus atrophy and intestinal metaplasia in patients with chronic and previous H. pylori infections. This clinical scenario predisposes patients to intestinal-type gastric cancer, which originates in the atrophic and metaplastic gastric mucosa. Conversely, a high PG I/II ratio is observed in patients without H. pylori infection. Serum PG I levels and the PG I/II ratio are high in patients with acute H. pylori-negative gastritis, including drug-induced gastritis but are significantly low in autoimmune gastritis. Gastric neuroendocrine tumors may develop in patients with autoimmune gastritis or in those with long-term acid suppressant use. Fasting serum gastrin levels and the risk of neuroendocrine tumors are high in both cases. In this review, types of gastritis are summarized along with evaluation performed to determine the secretory capacity of the background gastric mucosa.

Twenty-four-hour pH metry alone is inferior to additional impedance monitoring in the diagnosis of gastroesophageal reflux disease, particularly in presence of reduced gastric acid secretion.

Current gold standard for the diagnosis of gastroesophageal reflux disease (GERD) is 24-hour pH metry though it fails to detect non-acidic reflux. The sensitivity of 24-hour pH metry alone (both catheter-based and Bravo capsule) is questionable, especially if gastric acid secretion is low due to reduced parietal cell mass, Helicobacter pylori-induced gastric atrophy and antisecretory therapy. Accordingly, we analyzed the diagnostic ability of 24-hour pH metry as compared to impedance monitoring in relation to the gastric pH without antisecretory therapy. A retrospective analysis of prospectively collected data from 150 patients with suspected GERD undergoing a 24-hour pH impedance study was done. Among 150 patients with symptoms suggestive of GERD, 106 (70.6%) had confirmed GERD diagnosed either by 24-hour pH metry alone (10 [9.4%]), impedance monitoring alone (49 [46.2%]) or both (47 [44.3%]). Abnormal reflux of acidic and non-acidic gastric contents was detected by 24-hour pH metry and 24-hour impedance monitoring in 57/106 (53.7%) and 96/106 (90.5%) of patients, respectively (p < .00001). Patients with GERD diagnosed by 24-hour impedance monitoring had a higher mean gastric pH (2.9 [median 1.3, IQR 5.3]) than those diagnosed by 24-hour pH metry (2.1 [median 1.4, IQR 2.6]) or both (1.6 [median 1.2, IQR 2.1]) (p = 0.001). Twenty-four-hour impedance monitoring detects GERD more often than 24-hour pH metry. Patients with higher mean gastric pH leading to non-acidic reflux were more often diagnosed by 24-hour impedance monitoring than 24-hour pH metry. Thus, 24-hour pH metry alone is inferior to additional impedance monitoring in the diagnosis of GERD, particularly in presence of reduced gastric acid secretion.

Polymorphism in autophagy-related genes LRP1 and CAPZA1 may promote gastric mucosal atrophy

BackgroundHelicobacter pylori secretes cytotoxin-associated gene A (CagA) into the gastric epithelium, causing gastric mucosal atrophy (GMA) and gastric cancer. In contrast, host cells degrade CagA via autophagy. However, the association between polymorphisms in autophagy-related genes and GMA must be fully elucidated.ResultsWe evaluated the association between single nucleotide polymorphisms (SNPs) in autophagy-related genes (low-density lipoprotein receptor-related protein 1, LRP1; capping actin protein of muscle Z-line alpha subunit 1, CAPAZ1; and lysosomal-associated membrane protein 1, LAMP1) and GMA in 200 H. pylori-positive individuals. The frequency of the T/T genotype at rs1800137 in LRP1 was significantly lower in the GMA group than in the non-GMA group (p = 0.018, odds ratio [OR] = 0.188). The frequencies of the G/A or A/A genotype at rs4423118 and T/A or A/A genotype at rs58618380 of CAPAZ1 in the GMA group were significantly higher than those in the non-GMA group (p = 0.029 and p = 0.027, respectively). Multivariate analysis revealed that C/C or C/T genotype at rs1800137, T/A or A/A genotype at rs58618380, and age were independent risk factors for GMA (p = 0.038, p = 0.023, and p = 0.006, respectively). Furthermore, individuals with the rs1800137 C/C or C/T genotype of LRP1 had a 5.3-fold higher susceptibility to GMA. These genetic tests may provide future directions for precision medicine for individuals more likely to develop GMA.ConclusionLRP1 and CAPZA1 polymorphisms may be associated with the development of GMA.

Degree of Gastric Mucosal Atrophy Correlated Well with Gastric Cancer Occurrence in Patients with Helicobacter pylori-eradicated Status.

Objective This study was performed to clarify the association of the degree of gastric mucosal atrophy (GMA) with the occurrence of gastric cancer in patients with Helicobacter pylori-eradicated status. Subjects and Methods The subjects were 3,058 patients (2,035 men, 1,023 women; mean age 57.9 ± 9.5 years old) with H. pylori eradication who underwent esophago-gastroduodenal endoscopy examinations as part of medical checkups conducted between April 2013 and March 2022. The gender, age at eradication, time since eradication, usage of anti-secretory drugs, degree of endoscopic GMA, and FGP prevalence were compared between subjects with and without gastric cancer occurrence. Results Gastric cancer was newly detected in 26 subjects (0.85%) during the study period, with an older age at H. pylori eradication and severe grade of endoscopic GMA being significant risk factors for its occurrence. The gender, smoking history, and usage of anti-secretory drugs were not significantly different between subjects with and without gastric cancer occurrence. A Cox regression analysis showed that an older age at eradication and the degree of GMA were risk factors significantly related to occurrence. Furthermore, the degree of GMA was inversely correlated with FGP development, and gastric cancer was not detected in 467 subjects with FGP prevalence. Conclusion An older age at the time of H. pylori eradication and the degree of GMA are significant risk factors for gastric cancer occurrence in H. pylori-eradicated patients. The FGP prevalence in subjects with H. pylori eradication was inversely associated with GMA, suggesting it was negatively related with gastric cancer occurrence.

PDCD4 and CDX-2 as immunohistochemical markers of gastric mucosa atrophy in chronic gastritis

Introduction Diagnosis of the gastric mucosa atrophy represents an important problem, the solution of which depends on the possibility of secondary prevention of gastric cancer. A possible way of solution is the use of immunohistochemical markers - proteins associated with cellular remodeling of gastric mucosa, PDCD4 and CDX2.The aim of the work is to evaluate the possibility of using immunohistochemical markers PDCD4 and CDX-2 to diagnose atrophy of the gastric mucosa in chronic gastritis and increase the informative value of biopsy examination.Materials and method The object of the study was 155 cases of biopsy examination of the gastric mucosa of patients with chronic gastritis (5 fragments per case − 775 biopsy specimens). A comparative semi-quantitative assessment of immunohistochemical expression of CDX2, PDCD4 at different stages of chronic gastritis was performed. Spearman correlation coefficient was used to assess correlation relationship.Results There were no statistically significant differences in the level of PDCD4 in studied samples depending on the stage of chronic gastritis, p=0.06. Statistically significant increase of CDX2sum index in progressing stage of chronic atrophic gastritis (p=0.005), demonstrated a pronounced positive correlation r=0.70 (p&lt;0.01).Discussion According to the results obtained, it is shown that the decline in PDCD4 protein does not occur with the progression of atrophy severity. Complementary use of immunohistochemical marker CDX2 is able to give an idea of the presence and severity of both metaplastic and absolute atrophic changes in the gastric mucosa.Conclusion Equally high level of PDCD4 protein index in the gastric mucosa at different stages of chronic gastritis excludes the possibility of its use as an immunohistochemical marker of atrophy. Semi-quantitative immunohistochemical index of CDX2 protein can be used as an additional marker in decision support system for assessment of atrophic changes in gastric mucosa.

H. pylori predictors and outcomes among adults undergoing upper endoscopy at a Jamaican teaching hospital: A cross-sectional study.

Recent data on the prevalence of H. pylori infection in Jamaica are lacking. It is postulated that there has been a decline in the prevalence of H. pylori infection and its associated complications. We determined sociodemographic characteristics, prevalence of H. pylori infection and clinical outcomes among adults undergoing esophagogastroduodenoscopy (EGD) and histology at the University Hospital of the West Indies (UHWI) between May 2018 and December 2020. A cross-sectional study of patients (≥18 years old), who underwent EGD and histological evaluation for H. pylori infection, was conducted. Associations of H. pylori positivity and gastric cancer with sociodemographic/clinical variables and endoscopic findings were determined by stepwise logistic regression using backward selection. Unadjusted and adjusted odds ratios with related 95% confidence intervals (Cis) were calculated for H. pylori positivity and gastric cancer status. There were 323 participants (mean age 58.6± 17.8 years, 54.2% females). H. pylori prevalence was 22.2% (n= 70 of 315), 5.6% had gastric neoplasia (GN), 15.5% gastric atrophy, 11.4% intestinal metaplasia and 3.7% dysplasia on histology. Mucositis (64.5%), gastric ulcer (14.9%), and duodenal ulcer (13.9%) were the most common endoscopic findings. Participants with peptic ulcer disease (PUD) (unOR=4.0; p= .017), gastric cancer (unOR=9.5; p= .003), gastric atrophy (unOR=12.8; p< .001), and intestinal metaplasia (unOR=5.0; p< .001) had a significantly higher odds of being H. pylori positive, but after multivariable analyses only gastric atrophy remained significant (aOR=27.3; p< .001). Participants with mucositis had a significantly lower odds of gastric cancer (unOR 0.1; p= .035) while participants with dysplasia had significantly higher odds (unOR 8.0; p= .042), but these were no longer significant after multivariable analyses (aOR=0.2; p= .156 and aOR=18.9; p= .070, respectively). Histology based prevalence of H. pylori infection is lower than previously reported in Jamaica. Gastric atrophy is a significant predictor of H. pylori positivity.

Endoscopic grading of gastric atrophy and histological gastritis staging on risk assessment for early gastric cancer: a case-control study.

To assess the predictive value of endoscopic grading of gastric atrophy (Kimura-Takemoto classification), histological grading systems of operative link on gastritis assessment (OLGA) and operative link on gastric intestinal metaplasia (OLGIM) on risk stratification for early gastric cancer (EGC) and to investigate other potential risk factors of EGC. A single center, case-control study was conducted including 68 patients with EGC treated with endoscopic submucosal dissection and 68 age and sex-matched control subjects. Kimura-Takemoto classification, OLGA and OLGIM systems, and other potential risk factors were evaluated between the two groups. Of the 68 EGCs, 22 (32.4%) were well differentiated, 38 (55.9%) with moderately differentiated, and 8 (11.8%) with poorly differentiated. Multivariate analysis revealed O-type Kimura-Takemoto classification (AOR 3.282, 95%CI 1.106-9.744, P=0.032) and OLGIM stage III/IV (AOR 17.939, 95%CI 1.874-171.722, P=0.012) were significantly related to higher risk of EGC. Especially, O-type Kimura-Takemoto classification (AOR 4.78, 95%CI 1.65-13.845, P=0.004) had independently significant association with the EGC risk within 6-12 months. AUCs of the three systems for EGC were similar. This study confirms the role of endoscopic Kimura-Takemoto classification and histological OLGIM stage III/IV as independent risk factors for EGC. It may simplify every day practice by reducing the need for biopsies to stratify EGC risk. Further muti-center prospective study of large size is needed. This article is protected by copyright. All rights reserved.

Association between salt intake and gastric atrophy by Helicobacter pylori infection: first results from the Epidemiological Investigation of Gastric Malignancy (ENIGMA).

Gastric atrophy (GA), usually linked to chronic infection with Helicobacter pylori (H. pylori), may over time evolve into gastric malignancy. Besides H. pylori, high salt intake may play a role in GA development. This study evaluates cross sectionally the association between salt intake and GA in Chilean adults. Population-based samples were recruited from two sites, Antofagasta and Valdivia, partaking in the Epidemiological Investigation of Gastric Malignancies. At recruitment, participants answered questionnaires and provided biospecimens. Salt intake (g/day) was estimated from casual spot urine samples using the Tanaka equation. GA was determined by serum pepsinogen levels. Only participants ≥ 40 to 70years of age were considered in this analysis, n = 565. For the association between salt intake (as sex-specific quartiles) and GA, odds ratios (ORs) and the corresponding 95% confidence intervals (CI) were estimated through multivariable logistic regression. In women, the multivariable-adjusted OR for GA comparing quartile 4 of the estimated salt intake (12.8g/day) to quartile 1 (6.6g/day) was 1.18 (95% CI 0.52-2.68, P-trend = 0.87). The corresponding OR in men was 0.49 (95% CI 0.19-1.27, P-trend = 0.17) with salt intakes of 12.8g/day and 7.1g/day for quartiles 4 and 1, respectively. There was little evidence for an association between salt intake estimated from spot urine and GA risk in our cross-sectional analysis of middle aged and older adults in Chile. Reverse causation bias cannot be ruled out and the sample size was limited to provide more precise estimates.

Relationship between endoscopic gastric atrophy according to Kimura - Takemoto classification and histopathological characteristics in H. Pylori infected patients

Background: Endoscopic gastric atrophy according to Kimura-Takemoto classification has been shown to be closely related to histopathological atrophy. Gastric atrophy and intestinal metaplasia are considered precancerous gastric lesions that need to be assessed and monitored for early detection of dysplasia and cancer, especially in H. pylori infected patients. The aim of this study was to evaluate the associations between these endoscopic atrophy according to Kimura - Takemoto classification and pathologic characteristics. Methods: A cross-sectional study was conducted in 72 dyspepsia patients at Hue University of Medicine and Pharmacy Hospital, assigned endoscopic assessment and testing H. pylori positive. Assessing endoscopic gastric atrophy according to Kimura-Takemoto classification and compared with histopathological precancerous lesions (atrophy, intestinal metaplasia, dysplasia) according to the modified Sydney system. Results: The mean age was 55.6 ± 13.13, male/female ratio was 1.4/1.0. The rate of endoscopic gastric atrophy at stage C1 was 37.5%, C2: 40.3%, C3: 9.7%, O1: 11.1% and O3: 1.4%. On histo-pathology, the rate of gastric atrophy in antrum was 81.9%, in both antrum and body: 16.7%. The rate of intestinal metaplasia in antrum, body, both antrum and body was 36.1%, 2.5% and 11.1%, respectively. The rate of low-grade dysplasia 12.5% (9/72), high-grade dysplasia 6.9% (5/72) and 2 cases of early gastric cancer. Endoscopic gastric atrophy stages C2 and C3 had a higher rate of atrophy on histopathology than stage C1 (91.7% vs 63%) and stages O had a higher rate of intestinal metaplasia than stages C (77.8% vs 30.2%) with p &lt; 0.05. Conclusion: The degree of endoscopic gastric atrophy was related to the degree of histopathologic atrophy and intestinal metaplasia, the more severe the stage of endoscopic gastric atrophy, the higher the frequency of atrophy and metaplasia on histopathology. Evaluation of endoscopic gastric atrophy according to Kimura-Takemoto classification is a relatively simple strategy for monitoring for each patient with H. pylori chronic gastritis to detect dysplasia and early cancer. Key words: Atrophic gastritis, H. pylori, Kimura-Takemoto classification

What’s Hidden Under the Gastric Intestinal Metaplasia? Diffuse-Type Adenocarcinoma Discovered by Targeted Biopsies: A Case-Report

Gastric corpus atrophy and intestinal metaplasia are two well established gastric precancerous conditions and scientific evidence shows a confidential relationship between this precancerous condition and intestinal type gastric cancer, according to Lauren classification. Differently, the background histological gastric mucosa characteristics from whom diffuse type gastric cancer may arise, need to be clarified. In this case, report we present a case of an 81-year-old female with corpus atrophic gastritis in whom we arrived at the diagnosis of diffuse type gastric cancer by following specific guidelines related to the characterization and the endoscopic-histological surveillance of gastric precancerous conditions.

Patients with Whipple's disease have a high prevalence of Helicobacter pylori infection

IntroductionWhipple's disease is a rare systemic infection due to an impaired immunological response against T. whipplei in genetically predisposed individuals. Since we previously noted development of H. pylori related complications in some patients with Whipple's disease, our aim was to study the prevalence of H. pylori infection and H. pylori related disorders in Whipple's disease. MethodsWhipple's disease patients diagnosed from Jan-2002 to Dec-2021 and two controls per patient, matched for age, gender, ethnicity and year of H. pylori testing were enrolled. Results34 patients with Whipple's disease and 68 controls were enrolled. H. pylori infection (13/34 vs 8/68, p<0.01), H. pylori-related gastritis (p<0.01) and gastric atrophy (p = 0.01) were significantly more common in patients with Whipple's disease than controls. H. pylori infection and Whipple's disease were diagnosed synchronously in 6/13 patients, and during follow-up in the remaining 7. Interestingly, these last 7 patients were all on trimethoprim-sulfamethoxazole long-term therapy. Two patients developed H. pylori-related gastric malignancies during follow-up. No patients on doxycycline developed H. pylori infection. ConclusionsH. pylori infection and related disorders are common in patients with Whipple's disease and should always be excluded both at time of diagnosis and during follow-up. These findings should be taken into account when selecting antibiotics for Whipple's disease long-term prophylaxis.

Risk of gastric cancer development according to the combination of anti–Helicobacter pylori antibody titer and degree of atrophic gastritis.

297 Background: Helicobacter pylori is known as the main risk factor for gastric cancer. It is also well known that gastric atrophy which is the result of long-term H. pylori infection induces spontaneous regression of H. pylori infection and such atrophic status with negative H. pylori infection is related with high risk of gastric cancer, as in so called “ABC method”. However the implication of anti- H. pylori antibody titer is not well investigated. This study was designed to identify the risk for gastric cancer according to the combination of level of anti- H. pylori antibody titer and gastric atrophy. Methods: Those who had health checkups including upper endoscopy and serum anti- H. pylori antibody test between 2003 and 2018 were enrolled. Among them, those who had positive results for anti- H. pylori antibody were included in this study and those who had followed up for less than 1 year were excluded. Kimura-Takemoto classification C3 or more was defined as gastric atrophy. Individuals were classified into 4 groups: low B (low titer without atrophy), high B (high titer without atrophy), high C (high titer with atrophy), and low C (low titer with atrophy). Their risks for gastric cancer were compared under adjustment with other risk factors. Results: During median 5.7 years of follow-up, among 28,311 subjects, 231 developed new gastric cancer. Among them, 159 were intestinal type, 68 were diffuse type, and 4 were type-unknown. For intestinal type gastric cancer, high C group and low C group showed significantly high risk compared with low B group (high C: aHR 10.516; 95% CI, 6.485-17.054) (low C: aHR 11.191; 95% CI, 7.096-17.649). However, for diffuse type gastric cancer, high B group showed higher risk compared with low B group (aHR, 1.713; 95% CI, 1.021-2.875). When those two factors were taken separately, grade of atrophy was related with the risk for intestinal type gastric cancer (aHR, 2.047; 95% CI, 1.862-2.251), while the level of anti- H. pylori antibody titer was related with the risk for diffuse type gastric cancer (aHR, 1.158; 95% CI, 1.041-1.288). Conclusions: Among those with current H. pylori infection, high anti- H. pylori antibody titer is related with diffuse type gastric cancer. The risk was prominent especially among those without atrophy. Therefore, those with high level of anti- H. pylori antibody titer need to be considered as high risk group even without atrophy and should be considered as good candidates for H. pylori eradication and intensive screening.

Value of Serological Biomarker Panel in Diagnosis of Atrophic Gastritis and Helicobacter pylori Infection.

Background: Gastric cancer is one of the most common types of cancer worldwide. Helicobacter pylori infection is clearly correlated with gastric carcinogenesis. Therefore, the use of a new non-invasive test, known as the GastroPanel test, can be very helpful to identify patients at a high risk, including those with atrophic gastritis, intestinal metaplasia, and dysplasia. This study aimed to compare the results of GastroPanel test with the pathological findings of patients with gastric atrophy to find a safe and simple alternative for endoscopy and biopsy as invasive methods. Methods: This cross-sectional study was performed on patients with indigestion, who were referred to Motahari Clinic and Shahid Faghihi Hospital of Shiraz, Iran, since April 2017 until August 2017 for endoscopy of the upper gastrointestinal tract. The serum levels of gastrin-17 (G17), pepsinogen I (PGI), and pepsinogen II (PGII), as well as H. pylori antibody IgG, were determined by ELISA assays. Two biopsy specimens from the antrum and gastric body were taken for standard histological analyses and rapid urease test. A pathologist examined the biopsy specimens of patients blindly. Results: A total of 153 patients with indigestion (62.7% female; mean age, 63.7 years; 37.3% male; mean age, 64.9 years) were included in this study. The G17 levels significantly increased in patients with chronic atrophic gastritis (CAG) of the body (9.7 vs. 32.8 pmol/L; P = 0.04) and reduced in patients with antral CAG (1.8 vs. 29.1 pmol/L; P = 0.01). The results were acceptable for all three types of CAG, including the antral, body, and multifocal CAG (AUCs of 97%, 91%, and 88% for body, antral, and multifocal CAG, respectively). The difference in PGII level was not significant. Also, the PGI and PGI/PGII ratio did not show a significant difference (unacceptably low AUCs for all). The H. pylori antibody levels were higher in patients infected with H. pylori (251 EIU vs. 109 EIU, AUC = 70, P = 0.01). There was a significant relationship between antibody tests and histopathology. Conclusion: Contrary to Biohit's claims, the GastroPanel kit is not accurate enough to detect CAG; therefore, it cannot be used for establishing a clinical diagnosis.

Tumor heterogeneity and carcinoma in resected specimens of gastric low-grade dysplasia: A retrospective single center study.

Lesions diagnosed as gastric low-grade dysplasia (LGD) may be pathologically upgraded to early gastric cancer (EGC) or high-grade dysplasia (HGD) after endoscopic resection (ER). In this study, we investigated the risk factors for pathological upgrades after ER and assessed the reason for these upgrades by retrospectively analyzing ER data between January 1999 and December 2019. We enrolled patients with LGD confirmed by forceps biopsy; the patients were classified into pathologically concordant (LGD) and upgraded (HGD and EGC) groups according to the pathology of their resected specimen. To determine the risk factors for upgrade, we compared the endoscopic findings of the concordant and upgraded groups via 1:1 matched case-control design. To find the reasons for discordance, all upgraded cases were pathologically re-evaluated. Among 1,643 cases of LGD, pathological upgrades were observed in 423 (25.7%) resected specimens and EGC was found in 111 (6.7%) lesions. After matching the upgraded and concordant cases, lesion sizes exceeding 1.5 cm (odds ratio (OR): 1.8; 95% CI: 1.1-3.0), mucosal nodularity (OR: 10.8; 95% CI: 5.6-21.0), heterogeneous color (OR: 3.0; 95% CI: 1.7-5.3), presence of erosion (OR: 2.7; 95% CI: 1.8-5.3), and open-type gastric atrophy (OR: 2.9; 95% CI: 1.7-4.9) were noted to be significantly associated with upgraded pathology to EGC. Among the EGC cases, 99 (89.2%) were found to have pre-existing dysplasia. In conclusion, endoscopic evaluations should be performed because of possible pathological upgrades and co-existence of carcinomas in LGDs, especially when they exhibit surface nodularity, erosion, heterogeneous color, and large size.

Characteristics of different types of Helicobacter pylori: New evidence from non-amplified white light endoscopy.

Different types of Helicobacter pylori (H. pylori) were analyzed to determine their infection characteristics using serology, pathology, and non-magnification white light endoscopy combined with the Kimura-Takemoto classification, and the regular arrangement of collecting venules (RAC) as well. A retrospective analysis of 685 inpatients who have completed the 14C-urea breath test, the H. pylori antibody typing classification, the serum gastric function tests (PGI/PGII/G-17), the endoscope detection, and the pathological examinations. The levels of PGI, PGII, and G-17 were in descending order from the type I H. pylori infection group to the type II H. pylori infection group than the control group (F = 14.31; 26.23; 9.12, P < 0.01). Using the Kimura-Takemoto classification, there were significant differences among the three groups of different degrees of atrophy ( =29.81; 482.78; 292.5, P< 0.01). Based on the characteristics of RAC, the H. pylori infection rates were in descending order from the type I H. pylori infection group to the type II H. pylori infection group than the control group ( = 200.39; 174.72; 143.51, P < 0.01). The type I H. pylori infection group had higher grades than those of the type II H. pylori infection group in the OLGA and OLGIM staging systems, while the differences are statistically significant only in the OLGA staging system ( =10.63, P < 0.05). With the aid of non-amplified white light endoscopy, we found new evidence of type I H. pylori infection accelerating the progression of gastric mucosal atrophy through the degree of atrophy and the range of infection, whereas type II H. pylori infection has a low ability of migration and atrophy progression. Individual virulence factor-based eradication therapy may be a better choice in future.

Functional gene polymorphisms and expression alteration of selected microRNAs and the risk of various gastric lesions in Helicobacter pylori-related gastric diseases.

Background: Helicobacter pylori (Hp) persistent infection is an important pathogenic factor for a series of chronic gastric diseases from chronic gastritis to gastric cancer. Genetic and epigenetic abnormalities of microRNAs may play a vital role in the pathological evolution of gastric mucosa in Helicobacter pylori-related gastric diseases (HPGD). This study aimed to investigate the relationship between miR-146a, miR-196a2, miR-149, miR-499 and miR-27a gene single nucleotide polymorphisms (SNPs) and their expressions with pathological changes in gastric mucosa, and to further analyze the interactions between SNPs and Hp. Methods: Subjects in this study included patients diagnosed with HPGD and healthy controls. MiR-146a rs2910164, miR-196a2 rs11614913, miR-149 rs2292832, miR-499 rs3746444 and miR-27a rs895819 were genotyped by direct sequencing. Fluorescence quantitative PCR was used to detect microRNA expressions. Gene-gene and gene-environment interactions were evaluated by multifactor dimensionality reduction (MDR) method. Results: we found that frequency distribution of miR-196a2 rs11614913 CT genotype in gastric precancerous lesion (GPL) group and gastric cancer (GC) group was significantly higher than normal control (NOR) group [adjusted OR = 6.16, 95%CI (1.46-26.03); adjusted OR = 11.83, 95%CI (1.65-84.72), respectively]. CT genotype and C allele of miR-27a rs895819 were associated with increased risk of GC [adjusted OR = 10.14, 95%CI (2.25-45.77); adjusted OR = 3.71, 95%CI(1.46-9.44), respectively]. The MDR analysis results showed that the interaction between miR-196a2 rs11614913 and Hp was associated with the risk of GPL (p = 0.004). Meanwhile, the expression level of miR-196a2 in GC group was significantly higher than NOR, chronic inflammation (CI) and early precancerous lesion (EPL) groups among Hp-positive subjects. And expressions of miR-499 and miR-27a in GC group were both higher than EPL group. Also, miR-27a expression in GC group was higher than CI and gastric atrophy (GA) groups. Conclusion: miR-196a2 rs11614913 and miR-27a rs895819 may affect the genetic susceptibility to GPL or GC. MiR-196a2 rs11614913 and Hp have a synergistic effect in the occurrence and development of GPL. The up-regulation of miR-499, miR-196a2 and miR-27a expression caused by Hp infection may be an important mechanism of gastric carcinogenesis.

Non-atrophic gastric mucosa is an independently associated factor for superficial non-ampullary duodenal epithelial tumors: a multicenter, matched, case-control study.

The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studies have reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastric mucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopic gastric mucosal atrophy. This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopic or surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophy and the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies at two of the seven participating institutions. For H. pylori infection, 85 of 177 (48.0%) patients exhibited SNADETs and 112 of 531 (21.1%) control patients were non-infected (p<0.001). Non-atrophic mucosa (C0 to C1) was observed in 96 of 177 (54.2%) patients with SNADETs and 112 of 531 (21.1%) control patients (p<0.001). Conditional logistic regression analysis revealed that non-atrophic gastric mucosa was an independent risk factor for SNADETs (odds ratio, 5.10; 95% confidence interval, 2.44-8.40; p<0.001). Non-atrophic gastric mucosa, regardless of H. pylori infection status, was a factor independently associated with SNADETs.

A digital pathology workflow for the segmentation and classification of gastric glands: Study of gastric atrophy and intestinal metaplasia cases.

Gastric cancer is one of the most frequent causes of cancer-related deaths worldwide. Gastric atrophy (GA) and gastric intestinal metaplasia (IM) of the mucosa of the stomach have been found to increase the risk of gastric cancer and are considered precancerous lesions. Therefore, the early detection of GA and IM may have a valuable role in histopathological risk assessment. However, GA and IM are difficult to confirm endoscopically and, following the Sydney protocol, their diagnosis depends on the analysis of glandular morphology and on the identification of at least one well-defined goblet cell in a set of hematoxylin and eosin (H&E) -stained biopsy samples. To this end, the precise segmentation and classification of glands from the histological images plays an important role in the diagnostic confirmation of GA and IM. In this paper, we propose a digital pathology end-to-end workflow for gastric gland segmentation and classification for the analysis of gastric tissues. The proposed GAGL-VTNet, initially, extracts both global and local features combining multi-scale feature maps for the segmentation of glands and, subsequently, it adopts a vision transformer that exploits the visual dependences of the segmented glands towards their classification. For the analysis of gastric tissues, segmentation of mucosa is performed through an unsupervised model combining energy minimization and a U-Net model. Then, features of the segmented glands and mucosa are extracted and analyzed. To evaluate the efficiency of the proposed methodology we created the GAGL dataset consisting of 85 WSI, collected from 20 patients. The results demonstrate the existence of significant differences of the extracted features between normal, GA and IM cases. The proposed approach for gland and mucosa segmentation achieves an object dice score equal to 0.908 and 0.967 respectively, while for the classification of glands it achieves an F1 score equal to 0.94 showing great potential for the automated quantification and analysis of gastric biopsies.

Cytosponge: A Review on new non-endoscopic cell collection device

Cytosponge is a non-invasive device having a similar size to the tablets of regular taking that is used in place of endoscopy in some areas of detection because it is accurate, safe, and relatively inexpensive when compared to endoscopy. It is also called ‘sponge on a string’ because of pill attached with a string that is taken with water and lidocaine throat spray may be used to reduce the minor discomforts during application of the cytosponge and after 3 to 5 min withdraw by the string. It is made up of polyester sponge material compressed within a capsule 8.5 mm in diameter and 25 mm in length and the outer layer is made up of gelatin attach to 70mm long string. It is given to the patients with a sufficient amount of water and the gelatin part disappears when the cytosponge reaches the stomach. It collects about a million cells from the oral cavity and stomach, including Fusobacterium, Megasphaera, Campylobacter, Capnocytophaga, and Dialister. The cells are isolated and tests are performed to determine whether the cells are malignant or normal for detection and any detection is carried out by different biomarkers like TFF3, Aura-k, TFPI2, TWIST1, ZNF345, and ZNF569. The most used biomarker is TFF3. Cytosponge is used for the detection of Barrett’s oesophagus, Eosinophilic Esophagitis, oesophageal microbiota, Precancerous Mucosal Changes like Gastric intestinal metaplasia (GIM) and gastric atrophy (GA), Esophageal dysplasia, other gastrointestinal pathologies, Esophageal Diseases, and H. pylori. It is also used as a gastrointestinal endoscopy during the COVID-19 pandemic. New research is being taken for AI and cytosponge combine technology.