Comparison of operative link for gastritis assessment, operative link on gastric intestinal metaplasia assessment, and TAIM stagings among men with atrophic gastritis

BACKGROUND Gastric cancer is the world’s third most lethal malignancy. Most gastric cancers develop through precancerous states of atrophic gastritis and intestinal metaplasia. Two staging systems, operative link for gastritis assessment(OLGA)and operative link on gastric intestinal metaplasia assessment(OLGIM), have been developed to detect high gastric cancer risk. European guidelines recommend surveillance for high-risk OLGA/OLGIM patients(stages Ⅲ–Ⅳ),and for those with advanced stage of atrophic gastritis in the whole stomach mucosa. We hypothesize, that by combining atrophy and intestinal metaplasia into one staging named TAIM, more patients with increased gastric cancer risk could be detected.AIM To evaluate the clinical value of the OLGA, OLGIM, and novel TAIM stagings as prognostic indicators for gastric cancer.METHODS In the Helsinki Gastritis Study, 22346 elderly male smokers from southwestern Finland were screened for serum pepsinogen I(PGI). Between the years 1989 and1993, men with low PGI values(PGI < 25 μg/L), were invited to undergo an oesophagogastroduodenoscopy. In this retrospective cohort study, 1147 men that underwent gastroscopy were followed for gastric cancer for a median of 13.7 years, and a maximum of 27.3 years. We developed a new staging system, TAIM,by combining the topography with the severity of atrophy or intestinal metaplasia in gastric biopsies. In TAIM staging, the gastric cancer risk is classified as low or high.RESULTS Twenty-eight gastric cancers were diagnosed during the follow-up, and the incidence rate was 1.72 per 1000 patient-years. The cancer risk associated positively with TAIM [Hazard ratio(HR) 2.70, 95%CI: 1.09–6.69, P = 0.03]. The risk increased through OLGIM stages 0-Ⅳ(0 vs Ⅳ: HR 5.72, 95%CI: 1.03–31.77, P for trend = 0.004), but not through OLGA stages 0–Ⅳ(0 vs Ⅳ: HR 5.77, 95%CI:0.67–49.77, P for trend = 0.10). The sensitivities of OLGA and OLGIM stages Ⅲ–Ⅳ were low, 21% and 32%, respectively, whereas that of TAIM high-risk was good, 79%. On the contrary, OLGA and OLGIM had high specificity, 85% and81%, respectively, but TAIM showed low specificity, 42%. In all three staging systems, the high-risk men had three-to four-times higher gastric cancer risk compared to the general male population of the same age.CONCLUSION OLGIM and TAIM stagings show prognostic value in assessing gastric cancer risk in elderly male smokers with atrophic gastritis.

Evaluation of the Gastric Microbiome in Patients with Chronic Superficial Gastritis and Intestinal Metaplasia

Objective To evaluate the gastric microbiome in patients with chronic superficial gastritis(CSG)and intestinal metaplasia(IM)and investigate the influence of Helicobacter pylori(H.pylori)on the gastric microbiome.Methods Gastric mucosa tissue samples were collected from 54 patients with CSG and IM,and the patients were classified into the following four groups based on the state of H.pylori infection and histology:H.pylori-negative CSG(n=24),H.pylori-positive CSG(n=14),H.pylori-negative IM(n=11),and H.pylori-positive IM(n=5).The gastric microbiome was analyzed by 16S rRNA gene sequencing.Results H.pylori strongly influenced the bacterial abundance and diversity regardless of CSG and IM.In H.pylori-positive subjects,the bacterial abundance and diversity were significantly lower than in H.pylori-negative subjects.The H.pylori-negative groups had similar bacterial composition and bacterial abundance.The H.pylori-positive groups also had similar bacterial composition but different bacterial relative abundance.The relative abundance of Neisseria,Streptococcus,Rothia,and Veillonella were richer in the I-HP group than in G-HP group,especially Neisseria(t=175.1,P<0.001).Conclusions The gastric microbial abundance and diversity are lower in H.pylori-infected patients regardless of CSG and IM.Compared to H.pylori-positive CSG group and H.pylori-positive IM,the relative abundance of Neisseria,Streptococcus,Rothia,and Veillonella is higher in H.pylori-positive patients with IM than in H.pylori-positive patients with CSG,especially Neisseria.

Chronic active and atrophic gastritis as significant contributing factor to the development of gastric cystica profunda

Gastric cystica profunda(GCP)is an uncommon but underestimated gastric lesion.Its precancerous potential determines its significance.In addition to previous mucosa injury due to operations,biopsy or polypectomy,chronic active and atrophic gastritis may also lead to the development of GCPs.By carefully examining the stomach and taking biopsy samples from the susceptible regions,the stage of atrophy can be determined.Chronic atrophic gastritis is a risk factor for cancer evolvement and it can also contribute to GCPs formation.GCPs frequently occur close to early gastric cancers(EGCs)or EGC can arise from the cystic glands.Endoscopic resection is an effective and minimally invasive treat-ment in GCP.

Risk for gastric neoplasias in patients with chronic atrophic gastritis:A critical reappraisal

Chronic atrophic gastritis （CAG） is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue （non-metaplastic atrophy） or by glandular structures inappropriate for location （metaplastic atrophy）. Epidemiological data suggest that CAG is associated with two different types of tumors： Intestinal-type gastric cancer （GC） and type I gastric carcinoid （T I GC）. The pathophysiological mechanisms which lead to the development of these gastric tumors are different, It is accepted that a multistep process initiating from Helico- bacterpylori-related chronic inflammation of the gastric mucosa progresses to CAG, intestinal metaplasia, dysplasia and, finally, leads to the development of GC. The T I GC is a gastrin-dependent tumor and the chronic elevation of gastrin, which is associated with CAG, stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of T I GC. Thus, several events occur in the gastric mucosa before the development of intestinatype GC and/ or T I GC and these take several years. Knowledge ofCAG incidence from superficial gastritis, its prevalence in different clinical settings and possible risk factors as- sociated with the progression of this condition to gastric neoplasias are important issues. This editorial intends to provide a brief review of the main studies regarding incidence and prevalence of CAG and risk factors for the development of gastric neoplasias.

Alteration of sister chromatid exchange frequencies in gastric cancer and chronic atrophic gastritis patients with and without H pylori infection

AIM: To determine, by counting sister chromatid exchange (SCE) frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer (GC). METHODS: Analysis of SCE is a cytogenetic technique used to show DNA damage as a result of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis (CAG), and 15 normal controls. The presence of H pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain. RESULTS: SCE was significantly increased in H pylori- negative GC patients, and in H pylori-negative CAG patients compared with controls (7.41 ± 1.36 and 6.92 ± 1.20, respectively, vs 5.54 ± 0.8, P < 0.001). There was no difference in the SCE frequency between H pylori- negative GC patients and H pylori-negative CAG patients (P > 0.05). On other hand, the SCE frequencies in H pylori-positive GC patients were higher than those in H pylori-positive CAG patients (9.20 ± 0.94 vs 7.93 ± 0.81, P < 0.01). Furthermore, H pylori-positive GC patients had a higher SCE frequency than H pylori- negative GC patients (9.20 ± 0.94 vs 7.41 ± 1.36, P < 0.001). Similarly, a significant difference was detected between H pylori-positive CAG patients and H pylori-negative CAG patients (7.93 ± 0.81 vs 6.92 ± 1.20, P < 0.05). CONCLUSION: We suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis.

Gastric Intestinal Metaplasia Is the Most Common Histopathological Phenotype among Endoscopically Diagnosed Atrophic Gastritis Patients in North-East China

Background: Gastric cancer and gastric precancerous lesions are highly prevalent in China. However, prevalence of the different precancerous lesions has not been reported from the north-east region of China. Detection of precancerous gastric lesions at an early stage complemented with a follow-up strategy for high risk groups would probably aid in declining the mortality rate in patients with gastric cancer. Helicobacter pylori infection, salt intake, smoking, alcohol, family history of gastric cancer, atrophic gastritis and intestinal metaplasia are established risk factors of gastric cancer. The aim of this study was to evaluate the frequency of various histopathological phenotypes among atrophic gastritis patients in this region and to report if gender and increasing age carry risk in the development of these lesions. Methods: This retrospective study was conducted on 518 patients with endoscopic diagnosis of atrophic gastritis. Using the patient number in database, histopathological diagnosis of the biopsy specimen of all patients was recorded. All biopsy specimens were assessed for the presence of inflammation, atrophic gastritis, metaplasia and/or dysplasia. Results: Intestinal metaplasia was observed in 67.38% of patients. Dysplasia and atrophy were present in 9.46% and 3.67% patients, respectively. Gender and increasing age were not found to be risk factors for intestinal metaplasia, dysplasia and atrophic gastritis (p-values 0.08, 0.43, 0.297 and 0.98, 0.20, 0.54;respectively). 19.49% subjects showed inflammatory activity which was significantly associated with female gender (P = 0.0008). Conclusion: Intestinal metaplasia was the most histopathological phenotype among endoscopically diagnosed atrophic gastritis patients. Large-population based on prospective studies should be designed to determine prevalence of precancerous lesions and the risk factors involved in the progression of these lesions in our region.

Prevalence and Factors Associated with Intestinal Metaplasia in Chronic Helicobacter pylori Gastritis in a Country with High Endemicity: Ivory Coast Case

Context/Objective: Few studies have been carried out in a country with high endemicity for Helicobacter pylori (H. pylori) infection in Sub-Saharan Africa looking for the association of intestinal metaplasia (IM) with chronic gastritis. We hypothesize that IM is correlated with the intensity of H. pylori infection in a country with high endemicity, Ivory Coast. The objective of this study was to determine the prevalence of intestinal metaplasia in chronic H. pylori gastritis in Ivory Coast. Methods: This was a prospective, cross-sectional, multicenter study, carried out over a period of 5 months, in the reference hospital centers of Abidjan, specialized in Gastroenterology. All patients who had undergone Gastroscopy with biopsies according to the criteria of the Sydney System for the anatomopathological study, those with chronic gastritis and/or H. pylori intestinal metaplasia on histology and in whom all the parameters of the Sydney system classification had been well informed. The quantitative variables were expressed by their means accompanied by their standard deviations and the qualitative variables by their numbers and percentages. Chi-square and Fischer tests were used to look for associations between variables. The significance level was set at 5%. Results: 152 patients were retained. The mean age was 44.9 ± 12.9 years. The prevalence of intestinal metaplasia was 11.8%. In univariate analysis, no significant association was found between clinical and pathological sociodemographic factors (age, sex, ethnicity, educational level, profession) and intestinal metaplasia in chronic Helicobacter pylori gastric cases. In multivariate analysis we found that prolonged use of Proton Pump Inhibitors (PPIs) and a history of Gastroesophageal Reflux Disease (GERD) were significantly associated with the absence of IM. Conclusion: Chronic H. pylori gastritis is the main risk factor for intestinal metaplasia. Prolonged use of PPIs and a history of GERD were significantly identified as factors that would protect against intestinal metaplasia.

Yangyin Huowei mixture alleviates chronic atrophic gastritis by inhibiting the IL-10/JAK1/STAT3 pathway

BACKGROUND The Chinese medicine Yangyin Huowei mixture(YYHWM)exhibits good clinical efficacy in the treatment of chronic atrophic gastritis(CAG),but the mechanisms underlying its activity remain unclear.AIM To investigate the therapeutic effects of YYHWM and its underlying mechanisms in a CAG rat model.METHODS Sprague-Dawley rats were allocated into control,model,vitacoenzyme,and low,medium,and high-dose YYHWM groups.CAG was induced in rats using Nmethyl-N′-nitro-N-nitrosoguanidine,ranitidine hydrochloride,hunger and satiety perturbation,and ethanol gavage.Following an 8-wk intervention period,stomach samples were taken,stained,and examined for histopathological changes.ELISA was utilized to quantify serum levels of PG-I,PG-II,G-17,IL-1β,IL-6,and TNF-α.Western blot analysis was performed to evaluate protein expression of IL-10,JAK1,and STAT3.RESULTS The model group showed gastric mucosal layer disruption and inflammatory cell infiltration.Compared with the blank control group,serum levels of PGI,PGII,and G-17 in the model group were significantly reduced(82.41±3.53 vs 38.52±1.71,23.06±0.96 vs 11.06±0.70,and 493.09±12.17 vs 225.52±17.44,P<0.01 for all),whereas those of IL-1β,IL-6,and TNF-αwere significantly increased(30.15±3.07 vs 80.98±4.47,69.05±12.72 vs 110.85±6.68,and 209.24±11.62 vs 313.37±36.77,P<0.01 for all),and the protein levels of IL-10,JAK1,and STAT3 were higher in gastric mucosal tissues(0.47±0.10 vs 1.11±0.09,0.49±0.05 vs 0.99±0.07,and 0.24±0.05 vs 1.04±0.14,P<0.01 for all).Compared with the model group,high-dose YYHWM treatment significantly improved the gastric mucosal tissue damage,increased the levels of PGI,PGII,and G-17(38.52±1.71 vs 50.41±3.53,11.06±0.70 vs 15.33±1.24,and 225.52±17.44 vs 329.22±29.11,P<0.01 for all),decreased the levels of IL-1β,IL-6,and TNF-α(80.98±4.47 vs 61.56±4.02,110.85±6.68 vs 89.20±8.48,and 313.37±36.77 vs 267.30±9.31,P<0.01 for all),and evidently decreased the protein levels of IL-10 and STAT3 in gastric mucosal tissues(1.11±0.09 vs 0.19±0.07 and 1.04±0.14 vs 0.55±0.09,P<0.01 for both).CONCLUSION YYHWM reduces the release of inflammatory factors by inhibiting the IL-10/JAK1/STAT3 pathway,alleviating gastric mucosal damage,and enhancing gastric secretory function,thereby ameliorating CAG development and cancer transformation.

Inflammatory cytokine gene polymorphisms increase the risk of atrophic gastritis and intestinal metaplasia

AIM: To investigate the effects of interleukin-8 (IL-8 ), macrophage migration inhibitory factor (MIF ) gene polymorphisms, Helicobacter pylori (H. pylori ) infection, on the risk of developing severe chronic atrophic gastritis (SCAG) and intestinal metaplasia (IM). METHODS: A total of 372 cases were selected from a cohort study in Linqu County, a high risk area for gastric cancer (GC) in northern China. To obtain a sufficient group size, patients with normal or superficial gastritis were included. Based on an average follow-up period of 56 mo, the 372 cases were divided into no progres-sion group (no histological progression from normal or superficial gastritis, n = 137), group Ⅰ (progressed from normal or superficial gastritis to SCAG, n = 134) and group Ⅱ (progressed from normal or superficial gastritis to IM, n = 101). IL-8 , MIF gene polymorphisms were detected by polymerase chain reaction-based denaturing high-performance liquid chromatography analysis and DNA sequencing. RESULTS: An increased risk of SCAG was found in subjects with IL-8-251 AA genotype [odds ratio (OR) = 2.62, 95% CI: 1.23-5.72] or IL-8-251 A allele carriers (AA + AT) (OR = 1.81, 95% CI: 1.06-3.09). An elevated risk of IM was found in subjects with IL-8-251 AT genotype (OR = 2.27, 95% CI: 1.25-4.14) or IL-8-251 A allele carriers (OR = 2.07, 95% CI: 1.16-3.69). An increased risk of SCAG was found in subjects with MIF-173 GC genotype (OR = 2.36, 95% CI: 1.38-4.02) or MIF-173 C allele carriers (GC + CC) (OR = 2.07, 95% CI: 1.21-3.55). An elevated risk of IM was found in subjects with MIF-173 CC genotype (OR = 2.27, 95% CI: 1.16-4.46) or MIF-173 C allele carriers (OR = 3.84, 95% CI: 1.58-9.34). The risk of SCAG and IM was more evident in subjects carrying IL-8-251 A allele (OR = 6.70, 95% CI: 1.29-9.78) or MIF-173 C allele (OR = 6.54, 95% CI: 2.97-14.20) and positive for H. pylori infection. CONCLUSION: IL-8-251 and MIF-173 gene polymorphisms are significantly associated with the risk of SCAG and IM in a population with a high risk of GC in Linqu County, Shandong Province, China.

Chronic atrophic gastritis detection with a convolutional neural network considering stomach regions

BACKGROUND The risk of gastric cancer increases in patients with Helicobacter pylori-associated chronic atrophic gastritis(CAG).X-ray examination can evaluate the condition of the stomach,and it can be used for gastric cancer mass screening.However,skilled doctors for interpretation of X-ray examination are decreasing due to the diverse of inspections.AIM To evaluate the effectiveness of stomach regions that are automatically estimated by a deep learning-based model for CAG detection.METHODS We used 815 gastric X-ray images(GXIs)obtained from 815 subjects.The ground truth of this study was the diagnostic results in X-ray and endoscopic examinations.For a part of GXIs for training,the stomach regions are manually annotated.A model for automatic estimation of the stomach regions is trained with the GXIs.For the rest of them,the stomach regions are automatically estimated.Finally,a model for automatic CAG detection is trained with all GXIs for training.RESULTS In the case that the stomach regions were manually annotated for only 10 GXIs and 30 GXIs,the harmonic mean of sensitivity and specificity of CAG detection were 0.955±0.002 and 0.963±0.004,respectively.CONCLUSION By estimating stomach regions automatically,our method contributes to the reduction of the workload of manual annotation and the accurate detection of the CAG.

Gastric intestinal metaplasia is associated with gastric dysplasia but is inversely correlated with esophageal dysplasia

AIMTo determine which clinical factors might be associated with gastric intestinal metaplasia (IM) in a North American population. METHODSPathology and endoscopy databases at an academic medical center were reviewed to identify patients with and without gastric IM on biopsies for a retrospective cohort study. Patient demographics, insurance status, and other clinical factors were reviewed. RESULTSFour hundred and sixty-eight patients with gastric IM (mean age: 61.0 years ± 14.4 years, 55.5% female) and 171 without gastric IM (mean age: 48.8 years ± 20.8 years, 55.0% female) were compared. The endoscopic appearance of atrophic gastritis correlated with finding gastric IM on histopathology (OR = 2.05, P = 0.051). Gastric IM was associated with histologic findings of chronic gastritis (OR = 2.56, P P = 0.015), gastric dysplasia (OR = 6.11, P = 0.038), and gastric cancer (OR = 6.53, P = 0.027). Histologic findings of Barrett’s esophagus (OR = 0.28, P = 0.003) and esophageal dysplasia (OR = 0.11, P = 0.014) were inversely associated with gastric IM. Tobacco use (OR = 1.73, P = 0.005) was associated with gastric IM. CONCLUSIONPatients who smoke or have the endoscopic finding of atrophic gastritis are more likely to have gastric IM and should have screening gastric biopsies during esophagogastroduodenoscopy (EGD). Patients with gastric IM are at increased risk for having gastric dysplasia and cancer, and surveillance EGD with gastric biopsies in these patients might be reasonable.

Gastric Atrophy, Intestinal Metaplasia in Helicobacter pylori Gastritis: Prevalence and Predictors Factors

Gastric atrophy and intestinal metaplasia represent the most important premalignant lesions in gastric carcinogenesis. The severity of gastric mucosal inflammation depends on the bacterium Helicobacter pylori (HP), on the host and on environmental factors. The aim of our study is to determine the prevalence and factors associated with Gastric atrophy and intestinal metaplasia in patients infected with Helicobacter pylori. Methods: This is a prospective study over a period of 4 years (May 2009 - January 2015) conducted in the service of Hepatology and Gastroenterology in hospital university Hassan II of Fez in collaboration with microbiology and molecular biology laboratory and epidemiology service of Faculty of Medicine and Pharmacy Fes. We included in our study all patients aged over 15 years, having ulcerative dyspepsia, peptic ulcer disease, gastritis or esophagitis. Results: During the study period, 1190 patients were included of which 70% had HP infection (N = 833). The average age was 48.21 years [16 - 99 years], sex ratio M/F was 1, 11. 60% of patients were older than 45 years. Chronic smoking was found in 12% of patients. Gastric atrophy was observed in 84% (N = 699) of patients infected with HP. Gastric atrophy was localized in 70% in the antrum and 30% in the fundus and 24% in both. The activity of gastritis (p = 0.0001) and the density of the HP (p = 0.005) were factors associated with atrophy. Intestinal metaplasia was observed in 13.5% of patients (N = 112). The density of HP (p = 0.037) and severe atrophy (p = 0.001) were factors associated with metaplasia. Other factors studied: age, sex, smoking, CagA+ genotype were not associated with either gastric atrophy or intestinal metaplasia. Conclusion: In our study, the prevalence of atrophic gastritis and intestinal metaplasia in patients infected with Helicobacter pylori was 84% and 13.5% respectively, which was a high prevalence. The activity of gastritis, and density of HP were factors associated with atrophy. The density of HP and severe atrophy were factors associated with metaplasia.

Gastric-and-Intestinal Mixed Intestinal Metaplasia Is Irreversible Point with Eradication of Helicobacter pylori

Helicobacter pylori (H. pylori) represents an important factor in the development of atrophic gastritis, intestinal metaplasia (IM), and gastric cancer. Eradication of H. pylori has been reported to prevent gastric cancer only in cases without atrophy or IM. However, histological changes with eradication have yet to be fully clarified. We evaluated 38 H. pylori-positive cases before and after eradication at the gland level;pyloric glands were classified as showing gastric proper (G) and IM gland types, with the latter including gastric-and-intestinal mixed IM (GI-IM) and solely intestinal IM (I-IM), depending on the remaining gastric phenotypes. On eradication, acute and chronic inflammation attenuated rapidly and gradually, respectively, whereas levels of MUC5AC and MUC6 expression were not markedly altered. Gland width, size of nuclei and cytoplasm and their ratio in surface foveolar epithelium, the number of Ki-67-positive cells and the length of the proliferating zone in each gland were significantly decreased in G glands after eradication compared with those in GI-IM and I-IM. The number of mitotic phase cells, positive for phosphorylated histone H3 at serine 28, was increased in both types of IM compared to that in G glands in the H. pylori-infected state, but unexpectedly remained unchanged with eradication. These results suggest that GI-IM, as the beginning of IM, could represent a histological irreversible point with eradication and be considered as a “histological point of no return”.

History of chronic gastritis:How our perceptions have changed

Currently,the diagnostic strategy for chronic gastritis(CG)is aimed not just at fixing the presence of gastric mucosal inflammation,but also at gastric cancer(GC)risk stratification in a particular patient.Modern classification approach with the definition of the stage of gastritis determines the need,activities and frequency of dynamic monitoring of a patient.However,this attitude to the patient suffering from CG was far from always.The present publication is a literature review describing the key milestones in the history of CG research,from the description of the first observations of inflammation of the gastric mucosa,assessment of gastritis as a predominantly functional disease,to the advent of endoscopy of the upper digestive tract and diagnostic gastric biopsy,assessment of the role of Helicobacter pylori infection in progression of inflammatory changes to atrophy,intestinal metaplasia,dysplasia and GC.

Operative link for gastritis assessment vs operative link on intestinal metaplasia assessment

AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in which intestinal-type gastric cancer(GC)most frequently develops.The operative link for gas-tritis assessment(OLGA)staging system ranks the GC risk according to both the topography and the severity of gastric atrophy(as assessed histologically on the ba-sis of the Sydney protocol for gastric mucosal biopsy).Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages Ⅲ-Ⅳ with a higher risk of GC.A recently-proposed modification of the OLGA staging system(OLGIM)basically incorporates the OLGA frame,but replaces the atrophy score with an assessment of intestinal metaplasia(IM)alone.A series of 4552 consecutive biopsy sets(2007-2009)was re-trieved and reassessed according to both the OLGA and the OLGIM staging systems.A set of at least 5 biopsy samples was available for all the cases considered.RESULTS:In 4460 of 4552 cases(98.0%),both the high-risk stages(Ⅲ + Ⅳ)and the low-risk stages(0 +Ⅰ + Ⅱ)were assessed applying the OLGA and OL-GIM criteria.Among the 243 OLGA high-risk stages,14(5.8%)were down-staged to a low risk using OLGIM.The 67(1.5%)incidentally-found neoplastic lesions(intraepithelial or invasive)were consistently associated with high-risk stages,as assessed by both OLGA and OLGIM(P < 0.001 for both).Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage(stage Ⅲ)were associated with a low-risk OLGIM stage(stage Ⅱ).CONCLUSION:Gastritis staging systems(both OLGA and OLGIM)convey prognostically important informa-tion on the gastritis-associated cancer risk.Because of its clinical impact,the stage of gastritis should be included as a conclusive message in the gastritis histol-ogy report.Since it focuses on IM alone,OLGIM staging is less sensitive than OLGA staging in the identif ication of patients at high risk of gastric cancer.

Histopathological classification and follow-up analysis of chronic atrophic gastritis

BACKGROUND The pathological diagnosis and follow-up analysis of gastric mucosal biopsy have been paid much attention,and some scholars have proposed the pathological diagnosis of 12 kinds of lesions and accompanying pathological diagnosis,which is of great significance for the treatment of precision gastric diseases,the improvement of the early diagnosis rate of gastric cancer,and the reduction of missed diagnosis rate and misdiagnosis rate.AIM To perform a histopathological classification and follow-up analysis of chronic atrophic gastritis(CAG).METHODS A total of 2248 CAG tissue samples were collected,and data of their clinical characteristics were also gathered.Based on these samples,the expression levels of Mucin 1(MUC1),MUC2,MUC5AC,and MUC6 in CAG tissue were tested by immunohistochemical assay.Moreover,we followed these patients for up to four years.The difference between different stages of gastroscopic biopsy was observed.RESULTS Through observation,it is believed that CAG should be divided into four types,simple type,hyperplasia type,intestinal metaplasia(IM)type,and intraepithelial neoplasia(IEN)type.Simple CAG accounted for 9.1%(205/2248),which was more common in elderly people over 60 years old.The main change was that the lamina propria glands were reduced in size and number.Hyperplastic CAG accounted for 29.1%(654/2248),mostly occurring between 40 and 60 years old.The main change was that the lamina propria glands were atrophy accompanied by glandular hyperplasia and slight expansion of the glands.IM CAG accounted for 50.4%(1132/2248),most of which increased with age,and were more common in those over 50 years.The atrophy of the lamina propria glands was accompanied by significant IM,and the mucus containing sialic acid or sulfate was distinguished according to the nature of the mucus.The IEN type CAG accounted for 11.4%(257/2248),which developed from the previous types,with severe gland atrophy and reduced mucus secretion,and is an important precancerous lesion.CONCLUSION The histological typing of CAG is convenient to understand the property of lesion,determine the follow-up time,and guide the clinical treatment.

Helicobacter pylori infection with intestinal metaplasia: An independent risk factor for colorectal adenomas

AIM To explore the association between Helicobacter pylori (H. pylori) infection status, intestinal metaplasia (IM), and colorectal adenomas. METHODS We retrospectively reviewed 1641 individuals aged >= 40 years who underwent physical examination, laboratory testing, C-13-urea breath testing, gastroscopy, colonoscopy, and an interview to ascertain baseline characteristics and general state of health. Histopathological results were obtained by gastric and colorectal biopsies. RESULTS The prevalence of H. pylori infection and adenomas was 51.5% (845/1641) and 18.1% (297/1641), respectively. H. pylori infection was significantly correlated with an increased risk of colorectal adenomas (crude OR = 1.535, 95% CI: 1.044-1.753, P = 0.022; adjusted OR = 1.359, 95% CI: 1.035-1.785, P = 0.028). Individuals with IM had an elevated risk of colorectal adenomas (crude OR = 1.664, 95% CI: 1.216-2.277, P = 0.001; adjusted OR = 1.381, 95% CI: 0.998-1.929, P = 0.059). Stratification based on H. pylori infection stage and IM revealed that IM accompanied by H. pylori infection was significantly associated with an increased risk of adenomas (crude OR = 2.109, 95% CI: 1.383-3.216, P = 0.001; adjusted OR = 1.765, 95% CI: 1.130-2.757, P = 0.012). CONCLUSION H. pylori-related IM is associated with a high risk of colorectal adenomas in Chinese individuals.

Clinical applicability of gastroscopy with narrow-band imaging for the diagnosis of Helicobacter pylori gastritis, precancerous gastric lesion, and neoplasia

Premalignant gastric lesions such as atrophic gastritis and intestinal metaplasia frequently occur in subjects with long-term Helicobacter pylori(H.pylori)infection.The regular arrangement of collecting venules(RAC)is seen in the normal gastric corpus,whereas mucosal swelling and redness without RAC are observed in H.pylori-infected mucosa.Despite successful H.pylori eradication,the presence of atrophic gastritis and/or gastric intestinal metaplasia(GIM)is a risk factor for gastric cancer.With the development of advanced imaging technologies,recent studies have reported the usefulness of narrow-band imaging(NBI)for endoscopic diagnosis of atrophic gastritis and GIM.Using NBI endoscopy with magnification(M-NBI),atrophic gastritis is presented as irregular coiled microvessels and loss of gastric pits.Typical M-NBI endoscopic findings of GIM are a light blue crest and a white opaque substance.Based on the microvascular patterns,fine network,core vascular,and unclear patterns are useful for predicting gastric dysplasia in polypoid lesions.For diagnosis of early gastric cancer(EGC),a systematic classification using M-NBI endoscopy has been proposed on the basis of the presence of a demarcation line and an irregular microvascular/microsurface pattern.Furthermore,M-NBI endoscopy has been found to be more accurate for determining the horizontal margin of EGC compared to conventional endoscopy.In this review,we present up-to-date results on the clinical usefulness of gastroscopy with NBI for the diagnosis of H.pylori gastritis,precancerous gastric lesion,and neoplasia.

Effects of Granule Dendrobii on chronic atrophic gastritis induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats

BACKGROUND Dendrobium officinale is an herb of Traditional Chinese Medicine(TCM)commonly used for treating stomach diseases.One formula of Granule Dendrobii(GD)consists of Dendrobium officinale and American Ginseng(Radix Panacis quinquefolii),and is a potent TCM product in China.Whether treatment with GD can promote gastric acid secretion and alleviate gastric gland atrophy in chronic atrophic gastritis(CAG)requires verification.AIM To determine the effect of GD treatment on CAG and its potential cellular mechanism.METHODS A CAG model was induced by feeding rats N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)for 12 wk.After oral administration of low,moderate,and high doses of GD in CAG rats for 8 wk,its effects on body weight,gastric mucosa histology,mucosal atrophy,intestinal metaplasia,immunohistochemical staining of proliferating cell nuclear antigen(PCNA)and B-cell lymphoma-2,and hemoglobin and red blood cells were examined.RESULTS The body weights of MNNG-induced CAG model rats before treatment(143.5±14.26 g)were significantly lower than that of healthy rats(220.2±31.20 g,P<0.01).At the 8th week of treatment,the body weights of rats in the low-,moderate-,and high-dose groups of GD(220.1±36.62 g)were significantly higher than those in the untreated group(173.3±28.09 g,all P<0.01).The level of inflammation in gastric tissue of the high-dose group(1.68±0.54)was significantly reduced(P<0.01)compared with that of the untreated group(3.00±0.00,P<0.05).The number and thickness of gastric glands in the high-dose group(31.50±6.07/mm,306.4±49.32μm)were significantly higher than those in the untreated group(26.86±6.41/mm,244.3±51.82μm,respectively,P<0.01 and P<0.05),indicating improved atrophy of gastric mucosa.The areas of intestinal metaplasia were significantly lower in the high-dose group(1.74%±1.13%),medium-dose group(1.81%±0.66%)and low-dose group(2.36%±1.08%)than in the untreated group(3.91%±0.96%,all P<0.01).The expression of PCNA in high-dose group was significantly reduced compared with that in untreated group(P<0.01).Hemoglobin level in the high-dose group(145.3±5.90 g/L),medium-dose group(139.3±5.71 g/L)and low-dose group(137.5±7.56 g/L)was markedly increased compared with the untreated group(132.1±7.76 g/L;P<0.01 or P<0.05).CONCLUSION Treatment with GD for 8 wk demonstrate that GD is effective in the treatment of CAG in the MNNG model by improving the histopathology of gastric mucosa,reversing gastric atrophy and intestinal metaplasia,and alleviating gastric inflammation.

Autoimmune gastritis studies and gastric cancer: True renaissance or bibliometric illusion

A bibliometric analysis of studies dedicated to autoimmune gastritis(AIG)recently published demonstrated a noteworthy surge in publications over the last three years.This can be explained by numerous publications from different regions of the world reporting the results of several studies that stimulated reassessment of our view of AIG as a precancerous condition.Follow-up studies and retrospective analyses showed that the risk of gastric cancer(GC)in AIG patients is much lower than expected if the patients ever being infected with Helicobacter pylori(H.pylori)were excluded.The low prevalence of precancerous lesions,such as the incomplete type of intestinal metaplasia,may explain the low risk of GC in AIG patients because the spasmolytic polypeptide-expressing metaplasia commonly observed in AIG does not involve clonal reprogramming of the gastric gland and can be considered as an adaptive change rather than a true precancerous lesion.However,changes in gastric secretion due to the progression of gastric atrophy during the course of AIG cause changes in the gastric microbiome,stimulating the growth of bacterial species such as streptococci,which may promote the development of precancerous lesions and GC.Thus,Streptococcus anginosus exhibited a robust proinflammatory response and induced the gastritis-atrophy-metaplasia-dysplasia sequence in mice,reproducing the wellestablished process for carcinogenesis associated with H.pylori.Prospective studies in H.pylori-naïve patients evaluating gastric microbiome changes during the long-term course of AIG might provide an explanation for the enigmatic increase in GC incidence in the last decades in younger cohorts,which has been reported in economically developed countries.