Effect of acacetin on inhibition of apoptosis in Helicobacter pyloriinfected gastric epithelial cell line

BACKGROUND Helicobacter pylori(H.pylori)infection can cause extensive apoptosis of gastric epithelial cells,serving as a critical catalyst in the progression from chronic gastritis,gastrointestinal metaplasia,and atypical gastric hyperplasia to gastric carcinoma.Prompt eradication of H.pylori is paramount for ameliorating the pathophysiological conditions associated with chronic inflammation of the gastric mucosa and the primary prevention of gastric cancer.Acacetin,which has multifaceted pharmacological activities such as anti-cancer,anti-inflammatory,and antioxidative properties,has been extensively investigated across various domains.Nevertheless,the impact and underlying mechanisms of action of acacetin on H.pylori-infected gastric mucosal epithelial cells remain unclear.AIM To explore the defensive effects of acacetin on apoptosis in H.pylori-infected GES-1 cells and to investigate the underlying mechanisms.METHODS GES-1 cells were treated with H.pylori and acacetin in vitro.Cell viability was assessed using the CCK-8 assay,cell mortality rate via lactate dehydrogenase assay,alterations in cell migration and healing capacities through the wound healing assay,rates of apoptosis via flow cytometry and TUNEL staining,and expression levels of apoptosis-associated proteins through western blot analysis.RESULTS H.pylori infection led to decreased GES-1 cell viability,increased cell mortality,suppressed cell migration,increased rate of apoptosis,increased expressions of Bax and cle-caspase3,and decreased Bcl-2 expression.Conversely,acacetin treatment enhanced cell viability,mitigated apoptosis induced by H.pylori infection,and modulated the expression of apoptosis-regulatory proteins by upregulating Bcl-2 and downregulating Bax and cleaved caspase-3.CONCLUSION Acacetin significantly improved GES-1 cell viability and inhibited apoptosis in H.pylori-infected GES-1 cells,thereby exerting a protective effect on gastric mucosal epithelial cells.

Effect of Helicobacter pylori infection on gastric epithelial proliferation in progression from normal mucosa to gastric carcinoma

AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.

Loss of FHIT expression in gastric mucosa of patients with family histories of gastric cancer and Helicobacter pylori infection

AIM: To answer the question whether FHIT gene expression is affected by the family history of gastric carcinoma and the presence of Helicobacter pylori (Hpylori) in the gastric mucosa of patients with dyspepsia.METHODS: FHIT gene expression in two different topographic sites of the gastric mucosa of twenty-one patients with dyspepsia and with or without familial gastric carcinoma, infected or not infected with H pylori, was evaluated by reverse transcription-PCR (RT-PCR) and IMAGE QUANT methods. A rapid urease test and histopathological examination were used to determine H pylori colonization.RESULTS: In the gastric mucosa of patients with family histories of gastric carcinoma, the amount of FHIT protein mRNA was reduced down to 32%, and for patients with H pylori colonization, to 24% in comparison to controls with dyspepsia and without cancer in the family. FHIT expression was independent of the topography of specimens (corpus vsantrum), and for the control patients it was less sensitive to infection with H pylori. A considerable statistical difference in FHIT levels was observed in the gastric mucosa from the corpus of patients with family histories of gastric carcinoma in respect to H pylori colonization (P = 0.06). Macroscopic evaluation of the gastric mucosa demonstrated that pathologic changes classified according to the Sydney system had no significant influence on FHIT expression within each tested group of patients.CONCLUSION: Loss of FHIT expression was observed in patients with dyspepsia and family histories of gastric carcinoma, especially those infected with H pylori. Such results may constitute an early indication of the development of gastric carcinoma, which is associated with family factors including heredity and H pylori infection. The loss of the FHIT gene may serve as a marker for early diagnosis and prevention of gastric carcinoma, especially in context of early monitoring of H pylori infection in individuals with a record of familial stomach cancer.

Enhanced production of leptin in gastric fundic mucosa with Helicobacter pyloriinfection

AIM: To determine the concentrations of leptin in plasma and gastric fundic mucosa in humans, with reference to Helicobacterpylori (Hpylori) infection, and their association with gastric mucosal levels of interleukin (IL)-1β, IL-6 and IL-8, METHODS: Plasma leptin concentrations were determined in 135 outpatients with non-ulcer dyspepsia, consisting of 95 H pylori- infected and 40 uninfected subjects, and 13 patients before and after cure of the infection with anti-H pylori regimen. Using biopsy samples that were endoscopically obtained from the middle corpus along the greater curvature, gastric leptin contents were measured by radioimmunoassay and the mucosal concentrations of IL-Iβ, IL-6 and IL-8 were measured by enzyme linked immunosorbent assay. We also analysed the expression of leptin in the fundic mucosa by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: The mucosal levels of leptin in the fundic mucosa of H pylori-infected patients were significantly higher than those of uninfected patients. The amount of gastric leptin correlated positively with the mucosal levels of IL-1β and IL-6, but not IL-8. Circulating leptin correlated with body mass index, but not with H pylori status, and there was no change in plasma leptin levels following cure of the infection. Leptin immunoreactive cells were noted in the lower half of the fundic glands, and its expression of messenger ribonucleic acid in the oxyntic mucosa was detected by RT-PCR. CONCLUSION: Leptin production is enhanced in H pylori-infected gastric mucosa. Gastric leptin may be involved in immune and inflammatory response during H pylori infection, through interaction with proinflammatory cytokines.

Clinical usefulness of linked color imaging in identifying Helicobacter pylori infection:A systematic review and meta-analysis

BACKGROUND Accurate diagnosis of Helicobacter pylori(H.pylori)infection status is a crucial premise for eradication therapy,as well as evaluation of risk for gastric cancer.Recent progress on imaging enhancement endoscopy(IEE)made it possible to not only detect precancerous lesions and early gastrointestinal cancers but also to predict H.pylori infection in real time.As a novel IEE modality,linked color imaging(LCI)has exhibited its value on diagnosis of lesions of gastric mucosa through emphasizing minor differences of color tone.AIM To compare the efficacy of LCI for H.pylori active infection vs conventional white light imaging(WLI).METHODS PubMed,Embase,Embase and Cochrane Library were searched up to the end of April 11,2022.The random-effects model was adopted to calculate the diagnostic efficacy of LCI and WLI.The calculation of sensitivity,specificity,and likelihood ratios were performed;symmetric receiver operator characteristic(SROC)curves and the areas under the SROC curves were computed.Quality of the included studies was chosen to assess using the quality assessment of diagnostic accuracy studies-2 tool.RESULTS Seven original studies were included in this study.The pooled sensitivity,specificity,positive likelihood rate,and negative likelihood rate of LCI for the diagnosis of H.pylori infection of gastric mucosa were 0.85[95%confidence interval(CI):0.76-0.92],0.82(95%CI:0.78-0.85),4.71(95%CI:3.7-5.9),and 0.18(95%CI:0.10-0.31)respectively,with diagnostic odds ratio=26(95%CI:13-52),SROC=0.87(95%CI:0.84-0.90),which showed superiority of diagnostic efficacy compared to WLI.CONCLUSION Our results showed LCI can improve efficacy of diagnosis on H.pylori infection,which represents a useful endoscopic evaluation modality for clinical practice.

Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection,histological types and staging

AIM To investigate the expression of multiplegenes and the behavior of cellular biology ingastric cancer（GC）and other gastric mucosallesions and their relations to Helicobacter pylori（H.pylori）infection,tumor staging andhistological subtypes.METHODS Three hundred and twenty-sevenspecimens of gastric mucosa obtained viaendoscopy or surgical resection,and ABCimmunohistochemical staining were used todetect the expression of p53,p16,Bcl-2 andCOX-2 proteins.H.pylori was determined byrapid urea test combined with pathologicalstaining or14C urea breath test.Cellular image analysis was performed in 66 patients withintestinal metaplasia（IM）and/or dysplasia（Dys）.In 30 of them,both cancer and theparacancerous tissues were obtained at the timeof surgery.Histological pattern,tumor staging,lymph node metastasis,grading ofdifferentiation and other clinical data werestudied in the medical records.RESULTS p16 expression of IM or Dys wassignificantly lower in positive H.pylori chronicatrophic gastritis（CAG）than those withnegative H.pylori（CAG:54.8% vs 88.0%,IM:34.4% vs 69.6%,Dys:23.8% vs 53.6%,allP【0.05）,Bcl-2 or COX-2 expression of IM orDys in positive H.pylori cases was significantlyhigher than that without H.pylori（Bcl-2:68.8%vs23.9%,90.5% vs 60.7%;COX-2:50.0% vs10.8%,61.8% vs 17.8%;all P【0.05）.Themean number of most parameters of cellularimage analysis in positive H.pylori group wassignificantly higher than that in negative H.pylori group（Ellipser:53±14,40±12μm,Area1:748±572,302±202 μm2,Area2:3050±1661,1681±1990 μm2,all P【0.05;Ellipseb:79±23,58±15 μm,Ratio1:22%±5%,13%±4%,Ratio2:79%±17%,53%±20%,all P【0.01）.There was significant correlation between Bcl-2and histologic pattern of gastric carcinoma,andbetween COX-2 and tumor staging or lymph nodemetastasis（Bcl-2:75.0% vs 16.7%;COX-2:76.0% vs 20.0%,79.2% vs 16.7%;allP【0.05）.CONCLUSION p1l6, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/ progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infection. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis.

Study of T-lymphocyte subsets,nitric oxide,hexosamine and Helicobacter pylori infection in patients with chronic gastric diseases

Chronic gastritis ( CG ) and peptic ulcer ( PU ) are frequently-occurring diseases. It is now well recognized that Helicobacter pylori (Hp) is a major factor that leads to CG and PU[1-8] In order to study the relationship among T lymphocyte subsets, NO, Hexosamine and Hp infection in patients with chronic gastric diseases, the levelsof blood T lymphocyte subsets, plasma NO and hexosamine in gastric mucosa were measured respectively in 30 patients with CG and 32 patients of PU + CG.

Histological changes of gastric mucosa after Helicobacter pylori eradication:a systematic review and meta-analysis

AIM: To systematically review pathological changes of gastric mucosa in gastric atrophy (GA) and intestinal metaplasia (IM) after Helicobacter pylori (H. pylori) eradication.

Helicobacter pylori and oral pathology:Relationship with the gastric infection

Helicobacter pylori(H.pylori)has been found in the oral cavity and stomach,and its infection is one of the most frequent worldwide.We reviewed the literature and conducted a Topic Highlight,which identified studies reporting an association between H.pylori-infection in the oral cavity and H.pylori-positive stomach bacterium.This work was designed to determine whether H.pylori is the etiologic agent in periodontal disease,recurrent aphthous stomatitis(RAS),squamous cell carcinoma,burning and halitosis.Record selection focused on the highest quality studies and meta-analyses.We selected 48 articles reporting on the association between saliva and plaque and H.pylori-infection.In order to assess periodontal disease data,we included 12 clinical trials and 1 meta-analysis.We evaluated 13 published articles that addressed the potential association with RAS,and 6 with squamous cell carcinoma.Fourteen publications focused on our questions on burning and halitosis.There is a close relation between H.pylori infection in the oral cavity and the stomach.The mouth is the first extra-gastric reservoir.Regarding the role of H.pylori in the etiology of squamous cell carcinoma,no evidence is still available.

Role of polymorphisms in genes that encode cytokines and Helicobacter pylori virulence factors in gastric carcinogenesis

The Helicobacter pylori(H. pylori) infection is a determinant factor in gastric cancer(GC) development. However, the infection outcomes are variable and depend on both host and bacterial characteristics. Some host cytokines such as interleukin(IL)-1β, IL-1 Ra, IL-8, IL-10 and tumor necrosis factor-α play important roles in the host immune system response to the pathogen, in the development of gastric mucosal lesions and in cell malignant transformation. Therefore, these host factors are crucial in neoplastic processes. Certain polymorphisms in genes that encode these cytokines have been associated with an increased risk of GC. On the other hand, various virulence factors found in distinct H. pylori bacterial strains, including cytotoxinassociated antigen A, vacuolating cytotoxin, duodenal ulcer promoting gene A protein, outer inflammatory protein and blood group antigen binding adhesin, have been associated with the pathogenesis of different gastric diseases. The virulent factors mentioned above allow the successful infection by the bacterium and play crucial roles in gastric mucosa lesions, including malignant transformation. Moreover, the role of host polymorphisms and bacterial virulence factors in gastric carcinogenesis seems to vary among different countries and populations. The identification of host and bacterium factors that are associated with an increased risk of GC development may be useful in determining the prognosis of infection in patients, what could help in clinical decision-making and in providing of an optimized clinical approach.

Molecular cross-talk between Helicobacter pylori and human gastric mucosa

Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host,but confers a risk for serious diseases including gastric cancer.During its long coexistence with humans,H.pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and in? ammation,as well as immune effector activity.The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H.pylori/human gastric mucosa interaction (and its pathological sequelae),which is the result of millennia of co-evolution of,and thus of reciprocal knowledge between,the pathogen and its human host.

Effects of Helicobacterpyloriinfection on gastric emptying rate in patients with non-ulcer dyspepsia

AIM:The pathogenesis of delayed gastric emptying in patients with non-ulcer dyspepsia(NUD)remains unclear. We aimed to examine whether gastric emptying rate in NUD patients was associated with Helicobacter pylori(Hpylori) infection and whether it was affected by eradication of the infection. METHODS:Gastric emptying rate of a mixed solid-liquid meal was assessed by the paracetamol absorption method in NUD patients and asymptomatic controls(n=17).Hpylori status was assessed by serology and biopsy urease test. H pylori-positive NUD patients(n=23)received 10-day triple eradication therapy.Hpyloristatus was re-assessed by biopsy urease test four weeks later,and if eradication was confirmed,gastric emptying rate was re-evaluated. RESULTS:Thirty-three NUD patients and 17 controls were evaluated.NUD patients had significantly delayed gastric emptying compared with controls.The mean maximum plasma paracetamol concentration divided by body mass (Cmax/BM)was 0.173 and 0.224 mg/L.kg respectively (P=0.02),the mean area under plasma paracetamol concentration-time curve divided by body mass(AUC/BM) was 18.42 and 24.39 mg.min/L.kg respectively(P=0.01). Gastric emptying rate did not differ significantly between H pylori-positive and H pylori-negative NUD patients.The mean Cmax/BM was 0.172 and 0.177 mg/L·kg respectively (P=0.58),the mean AUC/BM was 18.43 and 18.38 mg·min/ L·kg respectively(P=0.91).Among 14 NUD patients who were initially H pylori-positive,confirmed eradication of the infection did not significantly alter gastric emptying rate. The mean Cmax/BM was 0.171 and 0.160 mg/L.kg before and after Hp eradication,respectively(P=0.64),the mean AUC/BM was 17.41 and 18.02 mg.min/L.kg before and after eradication,respectively(P=0.93). CONCLUSION:Although gastric emptying is delayed in NUD patients compared with controls,gastric emptying rate is not associated with H pylori status nor it is affected by eradication of the infection.

Helicobacter pylori eradication:Exploring its impacts on the gastric mucosa

Helicobacter pylori(H.pylori)infects approximately 50%of all humans globally.Persistent H.pylori infection causes multiple gastric and extragastric diseases,indicating the importance of early diagnosis and timely treatment.H.pylori eradication produces dramatic changes in the gastric mucosa,resulting in restored function.Consequently,to better understand the importance of H.pylori eradication and clarify the subsequent recovery of gastric mucosal functions after eradication,we summarize histological,endoscopic,and gastric microbiota changes to assess the therapeutic effects on the gastric mucosa.

Helicobacter pylori and its reservoirs:A correlation with the gastric infection

Helicobacter pylori(H. pylori) has long been found to cause gastric diseases such as gastritis, gastric ulcers and gastric cancer. The transmission medium of this bacterium has yet to be determined, though several studies have speculated that the oral cavity is a reservoir for H. pylori. Others have also reported that the oral cavity may be a source of both transmission and gastric reinfection; however, such results are controversial. We reviewed the literature and selected studies that report an association among H. pylori detections in the oral cavity(dental plaque, saliva, tongue, tonsil tissue, root canals, oral mucosa) in humans and in animals, as well as in the human stomach. The oral cavity may be considered the main reservoir for H. pylori. There are a correlations between H. pylori infection in the oral cavity and periodontal disease, oral tissue inflammation, H. pylori transmission, and gastric reinfection. We believe that the mouth is a reservoir and that it plays a crucial role in both H. pylori transmission and gastric infection.

Role of Helicobacter pylori virulence factor cytotoxin-associated gene A in gastric mucosa-associated lymphoid tissue lymphoma

Helicobacter pylori(H.pylori)infection might initiate and contribute to the progression of lymphoma from gastric mucosa-associated lymphoid tissue(MALT).Increasing evidence shows that eradication of H.pylori with antibiotic therapy can lead to regression of gastric MALT lymphoma and can result in a 10-year sustained remission.The eradication of H.pylori is the standard care for patients with gastric MALT lymphoma.Cytotoxin-associated gene A(CagA)protein,one of the most extensively studied H.pylori virulence factors,is strongly associated with the gastric MALT lymphoma.CagA possesses polymorphisms according to its C-terminal structure and displays different functions among areas and races.After being translocated into B lymphocytes via typeⅣsecretion system,CagA deregulates intracellular signaling pathways in both tyrosine phosphorylation-dependent and-independent manners and/or some other pathways,and thereby promotes lymphomagenesis.A variety of proteins including p53and protein tyrosine phosphatases-2 are involved in the malignant transformation induced by CagA.Mucosal inflammation is the foundational mechanism underlying the occurrence and development of gastric MALT lymphoma.

Helicobacter pylori infection and gastric carcinoma:Not all the strains and patients are alike

Gastric carcinoma(GC) develops in only 1%-3% of Helicobacter pylori(H. pylori) infected people. The role in GC formation of the bacterial genotypes, gene polymorphisms and host's factors may therefore be important. The risk of GC is enhanced when individuals are infected by strains expressing the oncoprotein CagA, in particular if CagA has a high number of repeats containing the EPIYA sequence in its C'-terminal variable region or particular amino acid sequences flank the EPIYA motifs. H. pylori infection triggers an inflammatory response characterised by an increased secretion of some chemokines by immunocytes and colonised gastric epithelial cells; these molecules are especially constituted by proteins composing the interleukin-1beta(IL-1β) group and tumour necrosis factor-alpha(TNF-α). Polymorphisms in the promoter regions of genes encoding these molecules, could account for high concentrations of IL-1β and TNF-α in the gastric mucosa, which may cause hypochlorhydria and eventually GC. Inconsistent results have been attained with other haplotypes of inflammatory and anti-inflammatory cytokines. Genomic mechanisms of GC development are mainly based on chromosomal or microsatellite instability(MSI) and deregulation of signalling transduction pathways. H. pylori infection may induce DNA instability and breaks of double-strand DNA in gastric mucocytes. Different H. pylori strains seem to differently increase the risk of cancer development run by the host. Certain H. pylori genotypes(such as the cagA positive) induce high degrees of chronic inflammation and determine an increase of mutagenesis rate, oxidative-stress, mismatch repair mechanisms, down-regulation of base excision and genetic instability, as well as generation of reactive oxygen species that modulate apoptosis; these phenomena may end to trigger or concur to GC development.

Helicobacter pylori and gastric mucosa-associated lymphoid tissue lymphoma:Recent progress in pathogenesis and management

Recent progress in the research regarding the molecular pathogenesis and management of gastric mucosa-associated lymphoid tissue (MALT) lymphoma is reviewed. In approximately 90% of cases, Helicobacter pylori (H. pylori) infection plays the causative role in the pathogenesis, and H. pylori eradication is nowadays the first-line treatment for this disease, which leads to complete disease remission in 50%-90% of cases. In H. pylori-dependent cases, microbe-generated immune responses, including interaction between B and T cells involving CD40 and CD40L co-stimulatory molecules, are considered to induce the development of MALT lymphoma. In H. pylori-independent cases, activation of the nuclear factor-&#x003ba;B pathway by oncogenic products of specific chromosomal translocations such as t(11;18)/API2-MALT1, or inactivation of tumor necrosis factor alpha-induced protein 3 (A20) are considered to contribute to the lymphomagenesis. Recently, a large-scale Japanese multicenter study confirmed that the long-term clinical outcome of gastric MALT lymphoma after H. pylori eradication is excellent. Treatment modalities for patients not responding to H. pylori eradication include a &#x0201c;watch and wait&#x0201d; strategy, radiotherapy, chemotherapy, rituximab immunotherapy, and a combination of these. Because of the indolent behavior of MALT lymphoma, second-line treatment should be tailored in consideration of the clinical stage and extent of the disease in each patient.

Association between mucosal surface pattern under near focus technology and Helicobacter pylori infection

BACKGROUND Many studies evaluated magnification endoscopy(ME)to correlate changes on the gastric mucosal surface with Helicobacter pylori(H.pylori)infection.However,few studies validated these concepts with high-definition endoscopy without ME.AIM To access the association between mucosal surface pattern under near focus technology and H.pylori infection status in a western population.METHODS Cross-sectional study including all patients referred to routine upper endoscopy.Endoscopic exams were performed using standard high definition(S-HD)followed by near focus(NF-HD)examination.Presence of erythema,erosion,atrophy,and nodularity were recorded during S-HD,and surface mucosal pattern was classified using NF-HD in the gastric body.Biopsies were taken for rapid urease test and histology.RESULTS One hundred and eighty-seven patients were analyzed from August to November 2019.Of those,47(25.1%)were H.pylori+,and 42(22.5%)had a previous H.pylori treatment.In the examination with S-HD,erythema had the best sensitivity for H.pylori detection(80.9%).Exudate(99.3%),nodularity(97.1%),and atrophy(95.7%)demonstrated better specificity values,but with low sensitivity(6.4%-19.1%).On the other hand,the absence of erythema was strongly associated with H.pylori-(negative predictive value=92%).With NF-HD,56.2%of patients presented type 1 pattern(regular arrangement of collecting venules,RAC),and only 5.7%of RAC+patients were H.pylori+.The loss of RAC presented 87.2%sensitivity for H.pylori detection,70.7%specificity,50%positive predictive value,and 94.3%negative predictive value,indicating that loss of RAC was suboptimal to confirm H.pylori infection,but when RAC was seen,H.pylori infection was unlikely.CONCLUSION The presence of RAC at the NF-HD exam and the absence of erythema at S-HD were highly predictive of H.pylori negative status.On the other hand,the loss of RAC had a suboptimal correlation with the presence of H.pylori.

Mucosal patterns of Helicobacter pylori-related gastritis without atrophy in the gastric corpus using standard endoscopy

AIM:To identify the mucosal patterns of Helicobacter pylori(H.pylori )-related gastritis in the gastric corpus using standard endoscopy and to evaluate their reproducibility.METHODS:A total of 112 consecutive patients underwent upper gastrointestinal endoscopy.The endoscopists classified the endoscopic findings into 4 patterns.In the second part of the study,90 images were shown to 3 endoscopists in order to evaluate the inter-observer and intra-observer variability in image assessment.RESULTS:The mucosal patterns of the gastric bodywere categorized into 4 types.Type 1 pattern was defined as cleft-like appearance,type 2 as regular arrangement of red dots,type 3 pattern as the mosaic mucosal pattern and type 4 pattern as the mosaic pattern with a focal area of hyperemia.Type 1 and type 2 mucosal patterns were statistically significant in predicting H.pylorinegative status as compared with other mucosal types(χ 2 = 12.79 and 61.25 respectively,P < 0.01).Type 3 and type 4 mucosal patterns were statistically significant in predicting a H.pylori-positive status as compared with other mucosal types(χ 2 = 21.22 and 11.02 respectively,P < 0.01).Furthermore,the sensitivity,specificity,positive and negative predictive values of type 3 plus type 4 patterns for predicting H.pylori-positive gastric mucosa were 100%,86%,94%,and 100%,respectively.The mean κ values for inter-and intra-observer agreement in assessing the various endoscopic patterns were 0.808(95% CI,0.678-0.938) and 0.826(95% CI,0.727-0.925) respectively.CONCLUSION:Our study suggests that mucosal patterns in H.pylori-infected gastric mucosa without atrophy can be reliably identified using standard endoscopy in the gastric corpus.