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OBJECTIVE To determine late results of AS-DD procedure in long-segment (LSBE) and extralong-segment BE (ELSBE) using subjective and objective measurements to ascertain the histological impact over intestinal metaplasia (IM) and progression to EAC. SUMMARY OF BACKGROUND DATA Barrett esophagus (BE) is a known precursor of esophageal adenocarcinoma (EAC), and Nissen fundoplication has proven to be unable to stop mixed reflux among them. Our group proposed a surgical procedure that handles pathophysiological changes responsible for BE. METHODS This prospective study included 127 LSBE and ELSBE subjects submitted to clinical and functional analyses. They were presented to selective vagotomy, fundoplication, partial gastrectomy with Roux-en-Y reconstruction. The changes in IM were determined in both groups. RESULTS Follow-up was completed at a mean of 18 years in 81% of the cases. Visick I-II scores were seen in 88% of LSBE and 65% in ELSBE (P < 0.01). There was significant healing of erosive esophagitis and esophageal peptic ulcers, and strictures were resolved in 71%. There was 38% of IM regression in LSBE. Two cases in each group progressed to EAC at a mean of 15 years. Pathologic acid reflux was abolished in 91% and duodenal in 100%. There was a regression of low-grade dysplasia to IM in 80%. CONCLUSIONS AS-DD permanently eliminates pathologic refluxate to the esophagus. The progression to HGD/EAC is lower compared to medical treatment, with an 8-fold reduction in LSBE and 2.2-fold in ELSBE. AS-DD seems to influence IM behaviors, and it is a tool that could reduce and delay progression to EAC.

Background Barrett's oesophagus (BO) is known precursor of oesophageal adenocarcinoma (EAC). Early EAC includes T1a (invasion into mucosa) and T1b (invasion into submucosa but not muscularis propria). Endoscopic mucosal resection (EMR) provides accurate histological staging and definitive treatment for early EAC. Post EMR, the remaining Barrett's is eradicated with radiofrequency ablation (RFA). However, there is a paucity of long-term Australian data. Aims To investigate the efficacy and long-term outcomes of EMR and RFA in management of early EAC. Methods Retrospective analysis of patients early EAC treated endoscopically at three Western Australian tertiary centres, with at least 12-months follow-up, over last 10-years. Results Sixty-seven patients with early EAC (61 T1a and 6 T1b) were treated with EMR. Complete Barrett's eradication was done by EMR in 31/67 patients whereas 36/67 patients underwent RFA for residual Barrett's. EMR changed pinch biopsy histology from HGD (n=33), HGD suspicious for IMC (n=5) and LGD (n=1) to early EAC in 58.2% (n=39) patients. During a mean follow-up of 37.2 months (IQR 20, 56), complete remission of dysplasia (CRD) and intestinal metaplasia (CRIM) was seen in 97% (n=65) and 89.5% (n=60) patients. One patient with T1b EAC underwent oesophagectomy. No cases developed metachronous EAC, progression to invasive adenocarcinoma or development of nodal/distant metastasis. Complications were endoscopically treated haematemesis (n=1) and strictures (n=16) requiring dilatations. 3 patients died due to causes unrelated to IMC. Conclusion EMR in conjunction with RFA is an effective and safe management for early EAC. EMR provides accurate staging and has low complication rates. This article is protected by copyright. All rights reserved.

This review seeks to summarise the steps in the path from reflux oesophagitis to Barrett oesophagus to oesophageal adenocarcinoma. The epidemiology, clinical presentation, definitions, pathological features, diagnostic pitfalls, and emerging concepts are reviewed for each entity. The histological features of reflux oesophagitis can be variable and are not specific. Cases of reflux oesophagitis with numerous eosinophils are difficult to distinguish from eosinophilic oesophagitis and other oesophagitides with eosinophils (Crohn's disease, medication effect, and connective tissue disorders). In reflux oesophagitis, the findings are often most pronounced in the distal oesophagus, the eosinophils are randomly distributed throughout the epithelium, and eosinophilic abscesses and degranulated eosinophils are rare. For reflux oesophagitis with prominent lymphocytes, clinical history and ancillary clinical studies are paramount to distinguish reflux oesophagitis from other causes of lymphocytic oesophagitis pattern. For Barrett oesophagus, the definition remains a hotly debated topic for which the requirement for intestinal metaplasia to make the diagnosis is not applied unanimously across the globe. Assessing for dysplasia is a challenging aspect of the histological interpretation that guides clinical management. We describe the histological features that we find useful in making this evaluation. Oesophageal adenocarcinoma has been steadily increasing in incidence and has a poor prognosis. The extent of invasion can be overdiagnosed due to a duplicated muscularis mucosae. We also describe the technical factors that can lead to challenges in distinguishing the mucosal and deep margins of endoscopic resections. Lastly, we give an overview of targeted therapies with emerging importance and the ancillary tests that can identify the cases best suited for each therapy.

The mucosa of the body of the stomach (ie, the gastric corpus) uses 2 overlapping, depth-dependent mechanisms to respond to injury. Superficial injury heals via surface cells with histopathologic changes like foveolar hyperplasia. Deeper, usually chronic, injury/inflammation, most frequently induced by the carcinogenic bacteria Helicobacter pylori, elicits glandular histopathologic alterations, initially manifesting as pyloric (also known as pseudopyloric) metaplasia. In this pyloric metaplasia, corpus glands become antrum (pylorus)-like with loss of acid-secreting parietal cells (atrophic gastritis), expansion of foveolar cells, and reprogramming of digestive enzyme-secreting chief cells into deep antral gland-like mucous cells. After acute parietal cell loss, chief cells can reprogram through an orderly stepwise progression (paligenosis) initiated by interleukin-13-secreting innate lymphoid cells (ILC2s). First, massive lysosomal activation helps mitigate reactive oxygen species and remove damaged organelles. Second, mucus and wound-healing proteins (eg, TFF2) and other transcriptional alterations are induced, at which point the reprogrammed chief cells are recognized as mucus-secreting spasmolytic polypeptide-expressing metaplasia cells. In chronic severe injury, glands with pyloric metaplasia can harbor both actively proliferating spasmolytic polypeptide-expressing metaplasia cells and eventually intestine-like cells. Gastric glands with such lineage confusion (mixed incomplete intestinal metaplasia and proliferative spasmolytic polypeptide-expressing metaplasia) may be at particular risk for progression to dysplasia and cancer. A pyloric-like pattern of metaplasia after injury also occurs in other gastrointestinal organs including esophagus, pancreas, and intestines, and the paligenosis program itself seems broadly conserved across tissues and species. Here we discuss aspects of metaplasia in stomach, incorporating data derived from animal models and work on human cells and tissues in correlation with diagnostic and clinical implications.

BACKGROUND & AIMS: A non-endoscopic approach to Barrett’s esophagus (BE) surveillance after radiofrequency ablation (RFA) would offer a less invasive method for monitoring. We assessed the test characteristics and cost-effectiveness of the Cytosponge® in post-RFA patients. METHODS: We performed a multicenter study of dysplastic BE patients after at least one round of RFA. A positive Cytosponge® before endoscopy was defined as intestinal metaplasia (IM) on cytological assessment and/or TFF3 immunohistochemistry. Sensitivity, specificity, and receiver operator characteristic (ROC) curves were calculated. Multivariable regression was used to estimate the odds of a positive Cytosponge® in BE. A microsimulation cost-effectiveness model was performed to assess outcomes of various surveillance strategies: endoscopy-only, Cytosponge®-only, and alternating endoscopy/Cytosponge®. RESULTS: Of 234 patients, Cytosponge® adequately sampled the distal esophagus in 175 (75%). Of the 142 with both endoscopic and histologic data, 19 (13%) had residual/recurrent BE. For detecting any residual Barrett’s, Cytosponge® had a sensitivity of 74%, specificity of 85%, accuracy of 84%, and ROC curve showed an area under the curve of 0.74. The adjusted odds of a positive Cytosponge® in BE were 17.1 (95% CI: 5.2–55.9). Cytosponge®-only surveillance dominated all the surveillance strategies, being both less costly and more effective. Cytosponge®-only surveillance required

Background and aim The severity of atrophic gastritis is significantly associated with the risk of gastric cancer. Although the current gold standard for assessing the gastric cancer risk is esophagogastroduodenoscopy with a pathological examination, the development of less-invasive biomarkers is warranted for efficient risk stratification of gastric cancer. Serum pepsinogens (PGs) are biomarkers used to predict the extent of gastric mucosal atrophy; however, they are not an accurate reflection of gastric mucosal atrophy after Helicobacter pylori eradication. The present study was conducted to investigate the usefulness of plasma ghrelin levels as a marker for gastric mucosal atrophy, and as a risk stratification marker for gastric cancer, even after H. pylori eradication. Methods Patients who received H. pylori eradication treatment were enrolled in the study. The severity of gastric mucosal atrophy was evaluated both endoscopically and histologically. Serum pepsinogen and plasma ghrelin levels were measured before and at 1, 12, 24, and 48 weeks after treatment. The study was approved by the Research Ethics Committee of the Keio University School of Medicine (no. 20140102; 8 July 2014). Results Eighteen patients completed the study protocol. Total and acyl plasma ghrelin levels demonstrated no significant change from before treatment to 48 weeks after eradication; however, there was a significant difference between open-type and closed-type atrophic gastritis. The PG I/II ratio increased significantly from 48 weeks after H. pylori eradication. The severity of the histological intestinal metaplasia scores correlated inversely with plasma total ghrelin levels from before to 48 weeks after H. pylori eradication. Conclusion Plasma levels of ghrelin correlate well with the level of gastric mucosal atrophy, even after H. pylori eradication.KEY MESSAGES Ghrelin plasma levels are associated with the progression of endoscopic atrophic gastritis, even at 48 weeks after H. pylori eradication. Ghrelin plasma levels are also associated with increased severity of histological intestinal metaplasia 48 weeks after H. pylori eradication. Pepsinogen I/II ratios increased immediately after H. pylori eradication and are inappropriate for assessing atrophic gastritis after H. pylori eradication.

BACKGROUND AND AIMS Endoscopic ablation can eradicate neoplastic Barrett's esophagus (BE) without visible lesions. Cryoballoon ablation (CBA) is an established but relatively newer ablative technique that can eliminate BE but data on the durability of its treatment effects are lacking. We assessed the durability of CBA treatment for neoplastic BE. METHODS We performed a single-center cohort study of consecutive BE patients with confirmed low-grade dysplasia (LGD), high-grade dysplasia (HGD) or intramucosal cancer (ImCA) treated with CBA to eradicate all BE. We excluded patients with prior ablative therapy. Visible lesions were removed with endoscopic mucosal resection (EMR) prior to CBA. Outcomes included complete eradication of dysplasia (CE-D) and complete eradication of intestinal metaplasia (CE-IM) at 1 year, durability at 2 and 3 years after initial ablation, cumulative recurrence rate of dysplasia and IM, and rate of neoplastic progression. RESULTS 59 patients (55.9% with HGD; 20.3% with prior EMR) were tracked for a median of 54.3 months. CE-D and CE-IM at 1 year were 94.6% (53/56) and 75% (42/56), respectively. Allowing for retreatment, rates of maintained CE-D and CE-IM for those who have achieved CE-D or CE-IM were 100% (53/53) and 98% (47/48) at 2 years; 100% (45/45) and 98% (40/41), at 3 years, respectively. Cumulative recurrence rate was 1.9% (1/53) for dysplasia and 14.6% (7/48) for IM (not allowing for retreatment). There was no neoplastic progression. CONCLUSION In treatment-naive patients with dysplastic BE, CBA is a durable endoscopic eradication therapy but endoscopic surveillance after eradication is still warranted.

Background & Aims: Dysbiosis is associated with gastric cancer (GC) development. However, no longitudinal study was carried out to identify key bacteria that could predict for GC progression. Here, we aimed to investigate changes in bacterial metagenome prior to GC and develop a microbiome-based predictive model to accurately classify patients at risk of GC. Methods: Bacterial 16S rDNA was sequenced from 89 gastric antral biopsies obtained from 43 participants. This study was nested in a prospective, longitudinal study, whereby study participants underwent screening gastroscopy, with further 1-2 yearly surveillance gastroscopies for at least 5 years. Putative bacterial taxonomic and functional features associated with GC carcinogenesis were identified by comparing between controls, patients with gastric intestinal metaplasia (IM) and patients with early gastric neoplasia (EGN). Results: Patients with EGN had enrichment of Proteobacteria (in particular Proteus genus) and depletion of Bacteroidetes (in particular S24-7 family) in their gastric mucosa. Sequencing identified more patients with Helicobacter pylori compared to histopathological assessment, while H. pylori was also significantly enriched in EGN. Furthermore, a total of 261 functional features, attributing to 97 KEGG pathways were differentially abundant at baseline between patients who subsequent developed EGN (n = 13/39) and those who did not. At the same time, a constellation of six microbial taxonomic features present at baseline, provided the highest classifying power for subsequent EGN (AUC = 0.82). Conclusion: Our study highlights early microbial changes associated with GC carcinogenesis, suggesting a potential role for prospective microbiome surveillance for GC.

Objectives The Kyoto classification of gastritis was established for diagnosing Helicobacter pylori (H. pylori) infection via endoscopic findings. We investigated the role of the Kyoto classification of gastritis in the diagnosis of H. pylori infection and histological gastritis in Japanese individuals. Moreover, the histological findings of gastritis in H. pylori infection were examined based on age and sex differences. Methods We selected 561 patients aged 20-79 years who underwent gastroduodenal endoscopy at our hospital between 2010 and 2018. Endoscopic biopsy specimens from the antrum and corpus were used to investigate H. pylori infection and histology. Endoscopic findings were based on the Kyoto classification of gastritis, and histological findings were based on the updated Sydney System. Results Endoscopic findings based on the Kyoto classification of gastritis (H. pylori positive, 303 patients; H. pylori negative, 258 patients, based on endoscopic findings) had 98.7% sensitivity and 98.4% specificity for histological gastritis. In addition, endoscopic findings in the three age groups (20-39, 40-59, and 60-79 years) had high sensitivity and specificity. Atrophy and intestinal metaplasia were found only in the H. pylori-positive group and progressed with age. Histological inflammation of pyloric mucosa in the younger age group of H. pylori-positive patients was significantly higher than that in the elderly group. Significant inflammation was observed in young women. Conclusions The Kyoto classification of gastritis can not only diagnose H. pylori infection but also detect histological gastritis. Histological gastritis has varying characteristics of inflammation, atrophy, and intestinal metaplasia, depending on age and sex.

Endoscopic mucosal resection (EMR) and radiofrequency ablation (RFA) for Barrett’s esophagus (BE)-related high-grade dysplasia (HGD) and early esophageal adenocarcinoma (EAC) are considered effective treatments for eradication of BE. Little is known about the impact of achieving complete eradication of intestinal metaplasia (CE-IM) following the complete eradication of neoplasia (CE-N), specifically if CE-IM reduces the risk of recurrent dysplasia. Retrospective cohort study of consecutive patients with BE and HGD or intramucosal cancer (IMC)-treated endoscopically at a tertiary referral center between 2001 and 2019. Association between CE-IM and recurrent dysplasia after CE-N was evaluated. A total of 433 patients treated with EMR and/or RFA were included. Of these, 381 (88%) achieved CE-N, of which 345 (80%) had adequate follow-up for inclusion in the analysis. A total of 266 (77%) patients achieved CE-IM; with a median follow-up since initial treatment for HGD/IMC of 45.9 months (IQR 25.9, 93.1); 20 patients (5.8%) had recurrent dysplasia after achieving CE-N. Kaplan Meier survival curves revealed that time free of recurrence in those who achieved CE-IM was significantly higher (p = 0.002). In the multivariable analysis, CE-IM was associated with a significant lower hazard of recurrence (HR 0.2, 95% CI 0.1, 0.6), whereas the number of endoscopic treatments to achieve CE-N was associated with a significant higher hazard of recurrence (HR 1.1, 95% CI 1.0, 1.2). Achieving CE-IM following CE-N reduces the risk of recurrent dysplasia and should be considered a treatment target among patients with BE undergoing endoscopic therapies for HGD or EAC.

Background: Based on evidence that Helicobacter pylori eradication reduces the development of gastric cancer and other diseases such as peptic ulcer, eradication therapy has prevailed. However, gastric cancer can develop even after successful eradication. Summary: In this review article, we searched for studies that identified the characteristics of primary and metachronous gastric cancers after H. pylori eradication, the risk factors for the development of these cancers after successful H. pylori eradication, and whether image-enhanced endoscopy is useful for diagnosing gastric cancer after eradication. A gastritis-like appearance is seen as a characteristic endoscopic finding, which corresponds to an epithelium with low-grade atypia – also known as nonneoplastic epithelium – covering the surface of the cancerous glands. This finding may make endoscopic detection of early gastric cancer difficult after H. pylori eradication. Similar risk factors, such as the male sex, endoscopic atrophy, histologic intestinal metaplasia, and late eradication, have been reported as predictors for the development of both primary and metachronous gastric cancers. Image-enhanced endoscopy, such as linked color imaging, may be useful for the detection and risk stratification of gastric cancer after eradication. Key Messages: Based on these findings, we believe that effective surveillance of high-risk patients leads to early detection of gastric cancer in the era of H. pylori eradication.

Background Peroral endoscopic myotomy (POEM) has been increasingly used to treat achalasia. Previous studies have reported high frequency of muscular eosinophilic infiltration in achalasia. Esophageal mucosal changes in achalasia have only been studied in esophagectomy specimens. Cardia mucosal changes in achalasia have not been reported previously. We aimed to further characterize the esophageal, gastric cardia, and muscularis propria changes in achalasia. Methods This was a pilot study. Patients with clinically and radiographically confirmed achalasia who underwent POEM were enrolled in the study. Mucosal biopsies were taken 1 cm proximal and 1 cm distal to the gastroesophageal junction, and muscularis propria biopsies were taken from the mid esophagus. Tissues were submitted for histological evaluation. Results Eighteen patients (10 male and eight female, mean age: 60.7 (standard deviation (SD): 13) years) were enrolled in this pilot study. Nine patients had type II achalasia, two type III, one type I, five esophageal gastric outlet obstruction, and one unspecific type achalasia. The mean duration of symptoms prior to POEM was 79 (range 1 - 480) months. All patients had a dilated esophagus on examination, but no endoscopic evidence of Barrett's esophagus. Esophageal, gastric cardia, and muscular biopsies were performed in 17, 13, and 17 patients, respectively. Basal hyperplasia, spongiosis, ballooning, and parakeratosis were seen in 92.3%, 100%, 100%, and 76.5% of cases, respectively. Intraepithelial lymphocytosis was seen in 70.5% of cases, and active esophagitis was seen in 23.5% of case. Six (35.3%) cases had few intraepithelial eosinophils, but none of them had > 15 eosinophils per high power field. Histologic findings in gastric cardia mucosa included carditis (69.2%), H. pylori gastritis (7.6%), and reactive gastropathy (15.4%). One case (7.6%) showed low-grade dysplasia arising from intestinal metaplasia in the cardia. Absence of ganglion cells in the muscular biopsies was noted in 88.2% of cases, and the remaining two showed rare residual ganglion cells with ganglionitis in one case (5.8%). Muscular atrophy and interstitial fibrosis were observed in 52.9% and 82.3% of the cases, respectively. Two cases (11.7%) had eosinophilic inflammation in the muscularis propria and one of them was accompanied by lymphocytic inflammation. Conclusions Muscular biopsies in our study revealed loss of ganglion cells, supporting the view that achalasia is a primary esophageal disease with ganglion cell depletion. Squamous mucosa in achalasia showed changes mimicking reflux and lymphocytic esophagitis. Cardia mucosa in achalasia patients often were inflamed and uncommonly showed intestinal metaplasia and glandular dysplasia.

The inflammatory spectrum of gastric diseases includes different clinico-pathological entities, the etiology of which was recently established in the international Kyoto classification. A diagnosis of gastritis combines the information resulting form the gross examination (endoscopy) and histology (microscopy). It is important to consider the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative mucosal biopsy samples. Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory diseases, and the latter are epidemiologically, biologically and clinically linked to the onset of gastric cancer (i.e. "inflammation-associated cancer"). Different biological models of inflammation-associated gastric oncogenesis have been proposed. Helicobacter pylori (H. pylori) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis may also be triggered by the immune-mediated destruction of gastric parietal cells, resulting in autoimmune gastritis. In both H. pylori-related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term follow-up studies consistently demonstrate the prognostic impact of the histological staging of gastritis in gastric cancer secondary prevention strategies.

Aim: To evaluate the prevalence of Helicobacter pylori (H. pylori) and related histopathological lesions in gastric mucosa samples in this single-center study. Methods: Esophagogastroduodenoscopy and endoscopic biopsy reports of 1605 elective cases were retrospectively evaluated. Histopathological examination was evaluated according to the Sydney classification. The data were analyzed according to the prevalence of H. pylori, age, gender, gastric atrophy and intestinal metaplasia rates, and the distribution of the study group in the population below 40 years old and over 40 years old. Results: 584 males (Mean age 51.5 ± 16.5 years) and 1021 females (mean age 49.6 ± 16 years), (p = 0.03), a total of 1605 cases were included in the study. The rate of atrophy, metaplasia and H. pylori positivity in total study population were 0.2%, 16%, 71%, respectively. The rate of atrophy in men and women were 1.2% and 0.8%, respectively (p = 0.006). The rate of metaplasia in men and women were 20.9% and 13.7%, respectively (p

Background: Dyspepsia is a clinical syndrome including manifestations related to the upper gastrointestinal tract. Options for evaluating dyspeptic patients include therapeutic trials, testing for Helicobacter pylori, upper gastrointestinal (UGI) radiography, and endoscopy. Objective: To compare the endoscopic and histopathologic diagnosis of gastritis in patients presented with chronic gastric dyspepsia to evaluate the relative frequency and pattern of different types of gastritis in patients presented with chronic gastric dyspepsia. Patient and method: Prospective cross-sectional study on 120 patients with chronic dyspepsia more than 8 weeks. All patients underwent gastroscopy. The findings of gastric inspection were recorded for all patients. Biopsy specimens were taken. Two from the anterior and posterior antrum, two from the anterior and posterior body, and two from any additional area of abnormality. Diagnostic criteria were applied to histological features and each histopathological parameter (chronic inflammation, activity, atrophy, intestinal metaplasia and H. pylori density) were graded for assessment of their severity as 0= absent, 1= mild, 2=moderate or 3= severe in the corpus and antrum. Results: Endoscope revealed normal gastric mucosa in 33 patients (27.5%), gastritis in 64 patients (53.3%) and other lesions in 23 patients (19.2%). As regard gastritis, there was edema in 61 patients (95.3%), erythema in 45 patients (70.3%), atrophy in 10 patients (15.6%) and mucosal nodularity in 10 patients (15.6%). As regard location of gastritis, it was pan-gastritis in 44 patients (68.8%), Antrum predominant gastritis in 10 patients (15.6%) & corpus predominant gastritis in 10 patients (15.6%).As regard other lesions, there was Duodenal ulcer in 7 patients (30.4%), peptic ulcer in 3 patients (13%), esophagitis in 2 patients (8.7%), erosive gastritis in 4 patients (17.4%), upper GIT suspecting malignancy in 2 patients (8.7%) and hiatal hernia in 5 patients (21.7%). Histopathology results were Normal in 18 (18.6%), Chronic inflammation in 79 (81.4%), Neutrophilic infiltration in 60 (61.7%), Glandular atrophy in 10 (10.3%), Intestinal metaplasia in 3 (3.1%) and H. pylori density in 47 (48.5%). Gastritis was detected by Endoscopy in 64 (53.3%) and in 79 (81.4%) by histopathology. This difference was statistically significant (p-value: 0.014). Conclusion: The prevalence of gastritis among the dyspeptic patients is very high since we observed endoscopically gastritis in 64 patients (53.3%) and other lesions in 23 patients (19.2%). The concordance between endoscopic findings and histopathological diagnosis of gastritis was (81%). High prevalence of H.Pylori among the dyspeptic patients (48.5%). Gastritis was better detected by histopathology.

Barret esophagus is considered as a precursor lesion for esophageal adenocarcinomas. Histopathological examination is required for the barret esophagus, where endoscopic examination takes an important place. Intestinal metaplasia is revealed with hematoxylin & eosin (H&E) and alcian blue (AB) in histopathological examinations. There are 2 different opinions on this issue. One of them is to perform histochemical examination for AB or PAS-AB when intestinal metaplasia is suspected in routine H&E staining, while the other is to perform histochemical examination for routine AB or Periodic acid schiff alcian blue (PAS-AB) in all esophageal biopsies with H&E section. This study aims to reveal the roles of H&E and AB staining methods in the assessment of intestinal metaplasia. 200 esophageal endoscopic biopsies were included in the study. Sections of the biopsies were re-evaluated blindly by two pathologists. H&E and PAS-AB stains were compared in terms of sensitivity, specificity, positive predictivity. In statistical analysis, a strong correlation was found between H&E and AB in the evaluation of intestinal metaplasia (Kendall, p = 0.00; r = 0, 81). In H&E evaluation, sensitivity is 79%, specificity 100%, positive predictivity 100%, negative predictivity 82.6%, while sensitivity is 100%, specificity 100%, positive predictivity 100%, negative predictivity 100% in PAS-AB stained sections. The main goal in the histopathological evaluation of intestinal metaplasia is to detect positive cases. Since absence of intestinal metaplasia means less importance, higher sensitivity and negative predictivity values should be preferred rather than 100% specificity and positive predictivity values observed in H&E sections. Considering these conditions, it seems rational to use an auxiliary histochemistry containing AB.

Мета: проаналізувати структурні зміни слизової оболонки шлунка та оцінити роль системи оксиду азоту в цих процесах у пацієнтів iз хронічним гастритом та кишковою метаплазією. Матеріали та методи. Морфологічне дослідження проводилося в 38 пацієнтів iз хронічним гастритом та атрофією, локальною (антральний відділ шлунка) або дифузною кишковою метаплазією. Концентрація оксиду азоту була визначена у вмісті шлунка та в крові всіх пацієнтів. Результати. Морфометричне дослідження показало помітне зниження (до (0,12 ± 0,04) %) ядерно-цитоплазматичного співвідношення в пацієнтів iз кишковою метаплазією порівняно з тими, хто мав атрофію. Еліптичність ядер клітин також зменшувалася з розвитком кишкової метаплазії та в пацієнтів без метапластичних змін дорівнювала (0,76 ± 0,04) %, у випадках локальної кишкової метаплазії — (0,65 ± 0,11) %, при дифузнiй метаплазії — (0,41 ± 0,12) %. Встановлено, що у хворих iз кишковою метаплазією, локалiзованою в антральному відділі, рівень оксиду азоту в шлунковому соку збільшується і на 24–65 % перевищує контрольну величину. Розглянуто можливий механізм загибелі клітин слизової оболонки шлунка внаслiдок апоптозу та некрозу в умовах гіперпродукції оксиду азоту. Висновки. Iнгібуючий ефект оксиду азоту на шлункову секрецію реалізується за рахунок його стимулюючого впливу на активність циклооксигенази та синтезу простагландинів.

Актуальность. Хронический атрофический гастрит (ХАГ) относится к предраковым заболеваниям желудка, на фоне которого часто наблюдаются кишечная метаплазия и дисплазия, а также чаще, чем у здоровых лиц, может возникать рак желудка. Цель исследования: изучить факторы риска ХАГ и их взаимосвязь с выраженностью морфологических изменений слизистой оболочки желудка. Материалы и методы. Под наблюдением находились 120 пациентов с ХАГ. Все больные проходили эндоскопическое (с функцией NBI), морфологическое обследование и анкетирование с помощью анкеты, которая была разработана для больных с ХАГ с целью изучения факторов риска. Результаты. Были определены значимые факторы развития предраковых изменений слизистой оболочки желудка, среди которых на первый план выступили показатели, которые характеризуют острый (r = 0,593) и хронический стресс (r = 0,544), употребление чрезмерного количества жареных (r = 0,636), копченых (r = 0,512) и маринованных (r = 0,591) продуктов, возраст (r = 0,639), ІІ группа крови (r = 0,651), онконаследственность (r = 0,533), наличие дуоденогастрального рефлюкса (r = 0,524) и патологии щитовидной железы (r = 0,522). По результатам эндоскопического и морфологического исследований выявлено уменьшение частоты Helicobacter pylori-инфицирования по мере роста перестроечных изменений слизистой оболочки желудка (атрофия — метаплазия — дисплазия). Выводы. Установлено возможное влияние таких факторов риска, как стресс, возраст, группа крови, наследственность, употребление чрезмерного количества жареных, копченых и маринованных продуктов, заболевания щитовидной железы и наличие дуоденогастрального рефлюкса на развитие ХАГ.

Background. Until now, the issue of the correlation between the cytokine balance and the progression of structural changes in the gastric mucosa remain completely uncertain. At the same time, the determination of the role of cytokine ba­lance as a component of gastric carcinogenesis will make it possible to substantiate new approaches to managing patients with atrophic gastritis. The purpose was to assess the level of pro- and anti-inflammatory cytokines, vascular endothelial growth factor (VEGF) at the stages of progression of structural changes in the gastric mucosa of patients with atrophic gastritis. Materials and methods. The study included 79 individuals with atrophic gastritis who underwent narrow band imaging endoscopic examination. The patients were divided into groups taking into account the revealed structural changes in the gastric mucosa: group I — 7 people with gastric mucosal atrophy without intestinal metaplasia (IM); group II — 16 individuals with gastric mucosal atrophy with IM limited by the antrum; group III — 45 people with diffuse IM against the background of gastric mucosal atrophy; group IV — 10 individuals with gastric mucosal dysplasia. In all patients, we assessed the level of interleukins (IL-8, IL-10, IL-18), tumor necrosis factor alpha (TNF-α), VEGF. Results. In patients of group IV, the concentration of IL-8 in the blood serum was 18.6 (11.3; 23.9) pg/ml that was significantly higher than in group I (by 5.0 times, p, Актуальність. До сьогодні питання взаємодії цитокінового балансу та прогресування структурних змін слизової оболонки шлунка (СОШ) залишаються остаточно не визначеними. Водночас визначення ролі цитокінового балансу як складової шлункового канцерогенезу дозволить обґрунтувати нові підходи до тактики ведення пацієнтів з атрофічним гастритом. Мета: оцінити рівень про- та протизапальних цитокінів, васкулоендотеліального фактора росту на етапах прогресування структурних змін СОШ у хворих на атрофічний гастрит. Матеріали та методи. У дослідження включено 79 хворих на атрофічний гастрит, яким проведено ендоскопічне дослідження в режимі NBI. Хворі були розподілені на групи з урахуванням виявлених структурних змін у СОШ: І група — 8 пацієнтів з атрофією СОШ без кишкової метаплазії (КМ); ІІ група — 16 хворих з атрофією СОШ із КМ, обмеженою антральним відділом шлунка; ІІІ група — 45 осіб з дифузною КМ на фоні атрофії СОШ; IV група — 10 пацієнтів з дисплазією СОШ. Усім хворим оцінювали рівень інтерлейкінів (ІЛ-8, ІЛ-10, ІЛ-18), фактора некрозу пухлини альфа (TNF-α), васкулоендотеліального фактора росту (VEGF). Результати. У хворих IV групи концентрація ІЛ-8 в сироватці крові становила 18,6 (11,3; 23,9) пг/мл і була вірогідно вище порівняно з пацієнтами І групи (в 5,0 раза; р

Background. The mechanisms of the functional interaction of the stomach and thyroid gland are based on the biological action of thyroid hormones. According to the European guidelines MAPS II, precancerous conditions of the stomach include atrophy and intestinal metaplasia of the gastric mucosa. The purpose of the work is to evaluate the structural and functional changes in the thyroid parenchyma in patients with precancerous conditions of the stomach. Materials and methods. The study was conducted in 44 patients with precancerous conditions of the stomach: 32 (72.7 %) women and 12 (27.3 %) men aged 33 to 76 years, on average (59.7 ± 1.7) years. Upper endoscopy was performed using the EVIS EXERA III system with an Olympus 190 gastroscope (Japan). According to the results of endoscopic examination, patients were divided into groups: group I — 11 people with atrophy of the gastric mucosa without intestinal metaplasia, group II — 13 individuals with atrophy of the gastric mucosa with intestinal metaplasia, limited by the antrum or body of the stomach, group III — 8 patients with diffuse intestinal metaplasia on the background of the gastric mucosa atrophy. The groups were representative by age and gender. All examined patients underwent a sonological examination of the thyroid gland with the ultrasound scanner Toshiba Xario (Japan) using a multi-frequency linear transducer with a frequency of 5–12 MHz. To assess the functional state of the thyroid gland, the levels of thyroglobulin and thyroid-stimulating hormone in the blood serum were determined by the enzyme immunoassay. Results. A significant increase in the frequency of diffuse and focal changes in the thyroid gland was found in patients with diffuse spread of intestinal metaplasia in the stomach (p < 0.05), which is confirmed by a correlation between the frequency of intestinal metaplasia of the body and antrum of the stomach with the presence of thyroid nodules (r = 0.44, p = 0.003; and r = 0.40, p = 0.006, respectively). At the same time, an increase in the frequency of focal hyperplasia of the gastric mucosa was associated with irregular contours of the thyroid gland (r = 0.41, p = 0.03) and an increase in the density of the thyroid capsule (r = 0.49, p = 0.04) that were the signs of a chronic inflammatory process. The spread of gastric intestinal metaplasia was accompanied by an increase in serum thyroglobulin by more than 3 times (p = 0.0134). Moreover, the level of thyroid-stimulating hormone significantly decreased as the precancerous changes in the gastric mucosa worsened (p = 0.0474), and the correlation between the level of this hormone and the presence of intestinal metaplasia in the stomach body (r = –0.46, p < 0.05) indicates the need for further study of the role of thyroid hormones in the development of precancerous conditions of the stomach. Conclusions. Patients with precancerous conditions of the stomach have a high frequency of structural changes in the thyroid parenchyma (81.8 %) of both diffuse (75.0 % of cases) and focal (43.2 %) nature. The spread of intestinal metaplasia in the gastric mucosa correlates with structural changes in the thyroid parenchyma, which is accompanied by a significant increase in thyroglobulin and a decrease in thyroid-stimulating hormone level in the blood serum. The frequency of structural changes in the thyroid gland increases with the development of precancerous changes in the stomach that is confirmed by a positive correlation between changes in the structure of the thyroid gland and the presence of xanthomas of the gastric mucosa, which are markers of precancerous conditions of the gastric mucosa (r = 0.52, p = 0.03).

Background. The study of the cytokine balance is important due to searching the general links of the pathogenesis of comorbidity in precancerous gastric lesions and thyroid diseases. The purpose was to determine the peculiarities of the cytokine balance in terms of the level of vascular endothelial growth factor (VEGF), tumor necrotizing factor (TNF) α, interleukins (IL) 8 and IL-18 in patients with precancerous gastric lesions depending on the changes in the structure of the thyroid gland. Materials and methods. Forty-five patients with precancerous gastric lesions were examined. Inclusion criteria were as follows: intestinal metaplasia in the body and/or antrum, atrophy in the body of the stomach. According to the results of an ultrasound examination of the thyroid gland, patients are divided into the groups: group I — 19 patients with nodular changes, group II — 18 patients with diffuse changes, and group III — 8 patients without changes. The control group included 10 healthy individuals. The level of IL-8, IL-18, TNF-α, VEGF was determined in the blood serum by the enzyme immunoassay using reagent kits of the Vector-BEST company, Novosibirsk, Russia. Results. 82.2 % patients with precancerous gastric lesions developed the changes in the structure of the thyroid gland (n = 37), 42.2 % (n = 19) had nodular changes in. The concentration of IL-8 in patients of group I was higher compared with group II, III and control group by 2.0 (p

Objective Esophageal white lesions (EWL) are commonly observed under upper endoscopy, while their clinical significance remains undetermined. The aim of this study was to identify the endoscopic characteristics of EWL and distinguish between different types of EWL. Methods Consecutive patients with upper gastrointestinal complaints and participants admitted for health check-up who underwent esophagogastroduodenoscopy from October 2018 to August 2019 in a tertiary hospital were prospectively screened. EWL were detected under endoscopy and biopsy was performed for histological analysis. Participants' characteristics, lifestyle, esophageal motility and reflux monitoring variables were analyzed. Results Of the 3641 consecutive participants screened, 303 of them aged 56.12 ± 10.95 years were found to have EWL (detection rate of 8.3%). More than one-third of them preferred hot drinks, eating pickled or spicy food, smoking and alcohol consumption and 5.3% had current or former upper gastrointestinal or head and neck cancers. The common endoscopic appearance of the EWL (2.9 mm ± 1.2 mm in diameter) included slightly elevated plaque, translucent white in color, with a clear border, round or oval in shape, and a scaly, rough or smooth surface. Histology showed low-grade intraepithelial dysplasia in 13 cases, leukoplakia in 10 and intestinal metaplasia in one. No significant differences were found between the histological findings and endoscopic manifestations of EWL. Conclusions EWL are not uncommon in daily endoscopic examination, with some of them being precancerous lesions. Conventional white-light endoscopy is insufficient to identify EWL, while histological assessment is important. Further studies using advanced endoscopic techniques with long-term follow-up are needed.

Gastric cancer is a leading cause of morbidity and mortality worldwide. Gastric intestinal metaplasia (GIM) has been described as a key histologic step in the development of gastric adenocarcinoma. However, not all people with GIM develop malignancy. We studied the factors associated with progression to dysplasia and advanced gastric neoplasia (aGN) in patients with baseline GIM. Retrospective cohort analysis of patients with baseline GIM and subsequent endoscopic evaluation at Cleveland Clinic Florida and Ohio Main Campus between 2005 and 2017. Demographic and exposure risk factors, as well as Kimura–Takemoto classification (KTc), were used as variables for hazards ratio (HR) and Kaplan–Meier survival-free analysis for aGN and any form of dysplasia progression. There were 708 patients identified with GIM; 29 patients (4.1%) progressed to any degree of dysplasia. From these, LGD was present in 12 cases (1.7%), HGD in 4 cases (0.6%), and gastric cancer in 13 cases (1.8%), for a total of 17 aGN cases. KTc was associated with dysplasia and aGN progression (p

ObjectiveGastric cancer (GC) is a leading cause of cancer-related mortality. Although microbes besides Helicobacter pylori may also contribute to gastric carcinogenesis, wild-type germ-free (GF) mouse models investigating the role of human gastric microbiota in the process are not yet available. We aimed to evaluate the histopathological features of GF mouse stomachs transplanted with gastric microbiota from patients with different gastric disease states and their relationships with the microbiota.DesignMicrobiota profiles in corpus and antrum tissues and gastric fluid from 12 patients with gastric dysplasia or GC were analysed. Thereafter, biopsied corpus and antrum tissues and gastric fluid from patients (n=15 and n=12, respectively) with chronic superficial gastritis, intestinal metaplasia or GC were inoculated into 42 GF C57BL/6 mice. The gastric microbiota was analysed by amplicon sequencing. Histopathological features of mouse stomachs were analysed immunohistochemically at 1 month after inoculation. An independent set of an additional 15 GF mice was also analysed at 1 year.ResultsThe microbial community structures of patients with dysplasia or GC in the corpus and antrum were similar. The gastric microbiota from patients with intestinal metaplasia or GC selectively colonised the mouse stomachs and induced premalignant lesions: loss of parietal cells and increases in inflammation foci, in F4/80 and Ki-67 expression, and in CD44v9/GSII lectin expression. Marked dysplastic changes were noted at 1 year post inoculation.ConclusionMajor histopathological features of premalignant changes are reproducible in GF mice transplanted with gastric microbiota from patients with intestinal metaplasia or GC. Our results suggest that GF mice are useful for analysing the causality of associations reported in human gastric microbiome studies.

Introduction: Gastric cancer is one of the most common causes of cancer-related deaths worldwide. Many epidemiological studies have shown several risk factors associated with the development of gastric cancer, including gastritis. The most common cause of gastritis is H. pylori infection. In the H.pylori-infected mucosa, there was a significant increase in VEGF levels. Several SNPs are thought to be involved in the etiology of malignancy, one of which is the VEGF-2578C>A polymorphism. Methods: A cross sectional study was conducted in Medan with 59 H. Pylori gastritis patients. Endoscopic examination was performed to assess the gastric mucosa. H.pylori status was determined by examination of Urea breath Test (UBT) and Campylobacter Like Organism (CLO) test followed by histopathological studies evaluating the presence of changes to pre-malignant lesions such as chronic atrophic gastritis, intestinal metaplasia, intestinal dysplasia. Genotype analysis was carried out using Polymerase Chain Reaction (RT-PCR). Data analysis was carried out by univariate and bivariate Result: Of the 59 patients with H. pylori gastritis, 35.8% of patients showed premalignant lesions. The majority of premalignant lesions had a CC genotype (37.9%, n = 11), but there was no significant relationship between the VEGF-2578 C>A polymorphism and the incidence of gastric premalignant lesions. Conclusion: Based on this study, the VEGF -2578C>A polymorphism was not associated with gastric premalignant lesions in H. pylori gastritis patients.. Keywords: Polymorphism VEGF, VEGF -2578C>A, Premalignant lesions, H. Pylori.

Helicobacter pylori (H. pylori) is an important risk factor of atrophic gastritis (AG), intestinal metaplasia (IM), and gastric cancer (GC). However, no report to date has described the endoscopic improvement of AG and IM after H. pylori eradication. Thus, the aim of this study was to evaluate the improvement of AG and IM after H. pylori eradication using endoscopic and histologic analyses. A total of 380 subjects were prospectively enrolled for up to 12 years and grouped by their H. pylori infection status: negative, non-eradicated, and eradicated. Endoscopic and histologic analyses of AG and IM were performed in the antrum and the corpus, by annual follow-up endoscopy. Endoscopic AG and IM in the antrum and corpus in the eradicated group improved compared to that in the non-eradicated group (AG, P = 0.002 and P = 0.005; IM, P = 0.038 and P = 0.048, respectively). Histologic AG and IM in the antrum and corpus in the eradicated group also improved compared to that in the non-eradicated group (all P

Primary adenocarcinoma of the seminal vesicle is very rare, with fewer than one hundred well-documented cases reported in the literature (1). These tumors have variable microscopic appearances, including cases with hobnail, polygonal and columnar neoplastic cells arranged in diverse architectural patterns (1). We recently received a radical cystoprostatectomy specimen from a 74-year-old patient with biopsy-proven muscle-invasive urothelial carcinoma.

We aimed to investigate the association between the triglyceride-glucose (TyG) index and gastric carcinogenesis, including precancerous conditions such as dysplasia, atrophic gastritis, and intestinal metaplasia. Patients who received an upper endoscopic assessment at a medical center were included. The enrolled patients were divided into four categories according to their TyG index quartile (Q). To evaluate the relationship between increase of TyG index and gastric cancer, we analyzed the patients who received a health checkup twice. Moreover, receiver-operating characteristic curve analysis was used to establish cut-off value of the TyG index for gastric cancer. Of 127,564 enrolled patients, 43,525 (34.1%) and 186 (0.1%) were diagnosed with precancerous conditions and gastric cancer, respectively. The odds ratios (ORs) of precancerous conditions given TyG index progressively increased across quartiles: using Q1 as the reference: Q2 (OR = 1.403, P

The esophagus and stomach, joined by a unique transitional zone, contain actively dividing epithelial stem cells required for organ homeostasis. Upon prolonged inflammation, epithelial cells in both organs can undergo a cell fate switch leading to intestinal metaplasia, predisposing to malignancy. Here we discuss the biology of gastroesophageal stem cells and their role as cells of origin in cancer. We summarize the interactions between the stromal niche and gastroesophageal stem cells in metaplasia and early expansion of mutated stem-cell-derived clones during carcinogenesis. Finally, we review new approaches under development to better study gastroesophageal stem cells and advance the field.

Background The ABC test measures serum pepsinogen and anti-Helicobacter pylori IgG antibody levels to predict precancerous conditions in the stomach and gastric cancer. However, a limitation of this test is that the gastric cancer risk is not negligible in patients with a negative result. Methods Based on their ABC results, 1157 patients were classified into Groups A (n = 392), B (n = 479), C (n = 247), and D (n = 39). In Group A, 24.2% of patients had atrophic gastritis and/or intestinal metaplasia and had thus been incorrectly assigned to Group A. Patients in Group A were then assigned to derivation (n = 236) and validation (n = 156) cohorts by 3:2 random sampling. Logistic regression analyses were performed to identify the factors discriminating between a correct (true) and incorrect (false) Group A classification. Results A 4-point discriminative model was constructed based on a high-negative H. pylori IgG antibody titer and the patient's age (50-64 and ≥65 years). The areas under the receiver operating characteristic curve for the derivation and validation cohorts were 0.868 and 0.894, respectively. In the validation cohort, the addition of a discriminative model score ≥2 to the ABC method showed a similar accuracy for predicting gastric cancer risk compared with the ABC method alone (93.8% vs. 92.4%). Conclusion The 4-point discriminative model may help identify patients with a normal serological test who are nonetheless at risk of developing gastric cancer.

Background The prevalence of duodenogastroesophageal reflux (DGER) and its effect on symptoms and oesophageal lesions in gastroesophageal reflux disease (GERD) is unclear. Aims To conduct a systematic review to determine the prevalence of DGER among patients with GERD, the effect of DGER on symptoms and oesophageal lesions, and the treatment of DGER. Methods We searched Pubmed and MEDLINE for full text, English language articles until October 2020 that evaluated DGER prevalence among patients with GERD, the effect of DGER on symptoms and oesophageal lesions, and the treatment of DGER. Results We identified 3891 reports and included 35 which analysed DGER prevalence in GERD, 15 which evaluated its effect in non-erosive reflux disease (NERD), 17 on erosive oesophagitis, 23 in Barrett's, and 13 which evaluated the treatment of DGER. The prevalence of DGER, when evaluated by Bilitec, among all GERD patients ranged from 10% to 97%, in NERD 10%-63%, in erosive oesophagitis 22%-80% and in Barrett's 50%-100%. There were no differences in the presence or degree of DGER among patients who were asymptomatic or symptomatic on proton pump inhibitors (PPI). The most commonly evaluated treatments for DGER were PPIs and DGER reduced post-PPI therapy in all studies. Conclusions The prevalence of DGER increased with more advanced oesophageal lesions and did not explain persisting symptoms among patients taking PPI therapy. PPIs appear to be effective in the treatment of DGER. DGER remains an important consideration in patients with GERD and future therapies deserve more study.

Objective To understand the protective effect of NF-κB signaling pathway inhibitor pyrrolidinedithiocarbamate (PDTC) on mice with chronic atrophic gastritis (CAG). Methods Helicobacter pylori (H. pylori) infection combined with high-salt diet was used to construct the CAG mouse model, and 100 or 200 mg/kg/day PDTC was intragastrically treated for 8 weeks. Then, hematoxylin and eosin (HE) and Alcian blue-periodic acid-Schiff (AB-PAS) staining were used to observe the pathology of gastric mucosa, while immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immuno sorbent assay (ELISA) and western blotting were determined to detect the expression of related molecules. Results The nuclear content of NF-κB p65 in the gastric mucosa of the CAG mice was increased accompanying by the structural disorder of the gastric mucosal epithelium, inflammatory cell infiltration, intestinal metaplasia, and increased MUC2 expression, but the symptoms were alleviated after PDTC treatment. In addition, the expressions of TNF-α, IL-1β, IL-6 and COX2 in the gastric mucosa and serum of CAG mice were higher than those control mice, which were reduced in CAG mice treated with either 100 or 200 mg/kg PDTC. Furthermore, 100 mg/kg and 200 mg/kg PDTC treatments reduced the serum PGE2 in CAG mice with the decreased PCNA and Ki-67 expression in gastric mucosa. The therapeutic effect of 200 mg/kg PDTC was significantly better than that of 100 mg/kg PDTC. Conclusion PDTC inhibited inflammation and the excessive proliferation of gastric mucosal epithelial cells, thereby exerting a potential therapeutic effect on CAG.

Background and Aims Buried Barrett’s mucosa is defined as intestinal metaplasia that is “buried” under the normal-appearing squamous epithelium. This can occur in Barrett’s esophagus with or without previous endoscopic therapy. Dysplasia and neoplasia within buried Barrett’s mucosa have also been reported. However, endoscopic features of buried Barrett’s mucosa have not been described. At our tertiary referral center for Barrett’s esophagus, several endoscopic features have been observed in patients who were found to have buried Barrett’s mucosa on histology. These features are squamous epithelium which is (1) darker pink on white-light and darker brown on narrow-band imaging and/or (2) has a slightly raised or nodular appearance. It was also observed that either of these 2 features is frequently seen adjacent to a Barrett’s mucosa island. This study aimed to (1) evaluate the diagnostic accuracy of these endoscopic features, and (2) evaluate the frequency of endoscopically identifiable buried Barrett’s mucosa in patients with dysplastic Barrett’s esophagus, before and after endoscopic eradication therapy. Methods This was a retrospective analysis of a prospectively observed cohort of all cases of dysplastic Barrett’s esophagus referred to St Vincent’s Hospital, Melbourne. Endoscopy documentation software and histopathology reports of esophageal biopsy and EMR specimens between March 2013 and March 2019 were searched for terms “buried” or “subsquamous” Barrett’s mucosa. Endoscopic reports, images, and histopathology reports of suspected buried Barrett’s mucosa were then reviewed to apply the endoscopic features and correlate with the histologic diagnosis. Results In a cohort of 506 patients with dysplastic Barrett’s esophagus, 33 (7%) patients (73% male, median age at referral 70.5 years) had buried Barrett’s mucosa on histology. Twenty-seven (82%) patients had previous treatment for dysplastic Barrett’s esophagus; radiofrequency in 2 (6%), EMR in 4 (12%), and both modalities in 21 (64%). Six (18%) had no previous treatment. Histologically confirmed buried Barrett’s mucosa was suspected at endoscopy in 26 patients (79%). Endoscopic features were (1) darker pink or darker brown mucosa underneath squamous epithelium (24%), (2) raised areas underneath squamous mucosa (27%), and both features present concurrently (27%). These features were associated with adjacent islands of Barrett’s esophagus in 48%. Forty-four cases of buried Barrett’s mucosa were suspected endoscopically, and these were sampled by biopsy (50%) and EMR (50%). Buried Barrett’s mucosa was confirmed in 26 cases, with a positive predictive value of endoscopic suspicion of 59%. Eighteen cases of endoscopically suspected buried Barrett’s mucosa had no buried Barrett’s mucosa on histology; inflammation or reflux was identified in 12 (67%) patients. Dysplasia was identified within buried Barrett’s mucosa in 12 (36%) patients; 5 intramucosal adenocarcinoma, 1 high-grade dysplasia, and 6 low-grade dysplasia. Endoscopic features of buried Barrett’s mucosa were observed in 11 of 12 cases harboring dysplasia or neoplasia, compared with 15 of 21 cases of buried Barrett’s mucosa without dysplasia. Conclusions In this retrospective analysis of prospectively observed patients with dysplastic Barrett’s esophagus, buried Barrett’s mucosa was identified in 7%, including treatment-naive patients. The proposed endoscopic features of buried Barrett’s mucosa were seen in 79% of patients with histology confirmed disease. These endoscopic features may predict the presence of buried Barrett’s mucosa, which may contain dysplasia or neoplasia. An overlap between the endoscopic features of inflammation, reflux, and buried Barrett’s mucosa was observed. Future prospective studies are required to develop and validate endoscopic criteria for identifying buried Barrett’s mucosa.

Intestinal metaplasia (IM) in the esophagus is considered as a risk factor of subsequent intestinal-type adenocarcinoma based on the classical theory of metaplasia-dysplasia-carcinoma. IM rarely occurs in urinary tract and fewer studies have been reported with long-term follow-up in those patients with IM of bladder. Thus, the etiology, pathological characteristics and prognosis of IM of urinary tract remain unclear. In the past, IM was regarded as benign lesions in bladder and there might have no relationship between IM of bladder and potential malignancy. Recently, some studies suggested that IM of bladder might indicate a risk of progression to carcinoma and require active surveillance according to their findings. However, due to limited cases, there has not yet been any systematic review or consensus on the management of IM of bladder. Here we reported a patient diagnosed as pulmonary intestinal adenocarcinoma suspiciously secondary to IM of bladder, without primary gastrointestinal cancer or bladder adenocarcinoma. Receiving lung surgery and adjuvant chemotherapy, the patient had no recurrence after a follow-up of 27 months. Hence, the present case demonstrated that ectopic IM can be a driving factor of adenocarcinoma in other organs, such as pulmonary intestinal adenocarcinoma, and it requires a long-term follow-up with overall examinations.

Annotation. Barrett’s esophagus is an acquired condition that develops as a result of the replacement of normal stratified squamous epithelium in the lower part of the esophagus by columnar epithelium. Barrett’s esophagus is considered a complication of gastroesophageal reflux disease (GERD). It has been shown and proven that various endoscopic methods are successful in treating this condition. However, long-term success in preventing further metaplasia and dysplasia is incompletely studied. Biological welding – controlled action of high frequency current on living tissues. It is used to stop gastrointestinal bleeding, ablation of small intestinal metaplasia of the esophageal mucosa. The aim of this study was to evaluate the success of endoscopic treatments for Barrett's esophagus and the need for further surgery in patients with GERD complicated by Barrett’s esophagus. Patients with Barrett’s esophagus C1-3M2-4 (Prague classification 2004) and severe dysplasia without nodule, as well as confirmed GERD without esophageal hernia were included. A total of 98 patients were included in the study, of whom 89 were re-consulted and examined after primary Barrett's esophageal ablation. Endoscopic treatment was performed by argon-plasma coagulation (APC) and high-frequency welding of living tissues (HFW). In the dynamics of patients were re-examined. Patients with recurrent metaplasia and a high DeMeester index (˃100) underwent antireflux surgery – crurography (if necessary) and Nissen fundoplication with a soft and short cuff. Recurrence of small bowel metaplasia was recorded in 15 patients. 12 patients underwent a two-stage treatment: first a second session of esophageal ablation, and in the second stage - antireflux surgery. 2 patients refused surgical treatment and underwent only the second session of ablation. All patients received drug therapy – prokinetics and proton pump inhibitors. Three months after surgery, pH metry was performed again, which showed normalization of the DeMeester index, as a result of which patients had no complaints such as heartburn, chest pain, dysphagia, which significantly improved their quality of life. Esophagogastroduodenoscopy and biopsy of the mucous membrane of the lower third of the esophagus according to the Seattle protocol was also performed. After examination of the histological material of metaplasia zones were not recorded. It is concluded that antireflux surgery is required as part of Barrett’s esophageal treatment to prevent further dysplasia and the development of esophageal cancer.

Early detection of gastric cancer (GC) is a critical step for decreasing mortality. The aim of this study was to evaluate the performance of four prediction models for risk stratification in the screening of GC and precancerous lesions among a large, high-risk population in China. This study was a retrospective analysis of data from the Provincial Gastric Cancer Screening Program (Zhejiang, China) spanning the period between October 2016 and April 2019, in which 97,541 individuals from the urban areas of 10 cities in Zhejiang province, China participated in this program. Demographic and clinical characteristics data were collected, and serum pepsinogens I and II, gastrin-17, and anti-H. pylori IgG antibody were detected. Participants were asked to voluntarily undergo gastroscopy. The performance of the ABC method, new ABC method, Tu’s prediction model, and Li’s prediction model, which stratified participants into low-, medium- and high-risk subgroups, were evaluated using the area under the receiver-operating characteristic (ROC) curve (AUC) and Youden index. Among the participants, 6005 (3447 males and 2558 females, mean age of 58.35 years), voluntarily underwent gastroscopy. Overall, 72 (1.20%) GC cases (30 early and 42 advanced) and 2006 cases with precancerous lesions (270 atrophic gastritis, 1634 intestinal metaplasia, and 102 dysplasia/intraepithelial neoplasia) were identified. Notably, Li’s prediction model achieved the greatest AUC and Youden index values (0.708 and 0.319, respectively) for predicting GC, and exhibited the greatest ability to detect precancerous lesions, especially intestinal metaplasia. Li’s prediction model performs the best for risk stratification in the screening, detection, and diagnosis of GC and precancerous lesions, whereas the overall performance of the other three models is similar ( www.chictr.org.cn , ChiCTR2100043363).

AIM: The purpose of the study is to investigate the occurrence of the main forms of chronic gastritis, metaplastic and dysplastic changes in the gastric mucosa, the degree of their severity, and to assess their potential risk for the development of gastric cancer. MATERIALS AND METHODS: The study involved 2982 patients who underwent esophagogastroduodenoscopy with a standard biopsy of the gastric mucosa for morphological assessment and bacterioscopy. If autoimmune gastritis was suspected, an additional serological diagnosis was performed. When detecting intestinal metaplasia of the gastric mucosa as well as neoplastic changes according to the histological report, the description of this report was analyzed in order to identify possible equivalents in the macroscopic description of the mucous membrane. RESULTS: Out of 2982 histological studies of gastric mucosa biopsies, 1273 cases (42.7%) were found to contain H. pylori contamination. In 726 cases (24.3%), intestinal metaplasia. 66 biopsies (2.21%) showed the presence of low-grade intraepithelial neoplasia of the mucosa, 2 biopsies showed indeterminate neoplasia and 4 biopsies showed high-grade neoplasia. In 3 out of the total number of the samples, intravascular gastric adenocarcinoma was detected. In 168 cases (5.6%), gastritis was detected with predominant inflammation of the fundal region characteristic of autoimmune gastritis. In 286 biopsies (10.6%), inflammatory and/or atrophic changes and/or metaplastic changes were preserved, which, as a rule, did not have high activity and pronounced inflammation. In the remaining 1279 cases (42.9%), there was no significant inflammation or atrophic changes. The analysis of endoscopic findings showed that the detectability of intestinal metaplasia of the gastric mucosa without a biopsy study was 13.3%. DISCUSSION OF THE RESULTS: According to the results of the conducted research and analysis, it can be stated that at present, the correct diagnosis of chronic gastritis with the establishment of the etiological factor, prognosis and risks of stomach cancer development is practically not feasible within the modern health care system. This not only deprives a doctor of the opportunity to make a correct diagnosis and prescribe adequate treatment to a patient, but also makes almost all cascades of carcinogenesis, including early cancer, invisible.

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.

To care and treat patients with esophageal cancer, one must first understand the epidemiology of Barrett's esophagus (BE). BE is defined as the intestinal metaplasia occurring within the esophagus from normal squamous epithelium to abnormal specialized columnar epithelium. BE, while first described by Allison in 1948, was attributed to Norman Barrett in 1950, who reported a case of chronic peptic ulcer in the lower esophagus that was covered by columnar epithelium.

This position paper, sponsored by the Asociación Española de Gastroenterología [Spanish Association of Gastroenterology], the Sociedad Española de Endoscopia Digestiva [Spanish Gastrointestinal Endoscopy Society] and the Sociedad Española de Anatomía Patológica [Spanish Anatomical Pathology Society], aims to establish recommendations for performing an high quality upper gastrointestinal endoscopy for the screening of gastric cancer precursor lesions (GCPL) in low-incidence populations, such as the Spanish population. To establish the quality of the evidence and the levels of recommendation, we used the methodology based on the GRADE system (Grading of Recommendations Assessment, Development and Evaluation). We obtained a consensus among experts using a Delphi method. The document evaluates different measures to improve the quality of upper gastrointestinal endoscopy in this setting and makes recommendations on how to evaluate and treat the identified lesions. We recommend that upper gastrointestinal endoscopy for surveillance of GCPL should be performed by endoscopists with adequate training, administering oral premedication and use of sedation. To improve the identification of GCPL, we recommend the use of high definition endoscopes and conventional or digital chromoendoscopy and, for biopsies, NBI should be used to target the most suspicious areas of intestinal metaplasia. Regarding the evaluation of visible lesions, the risk of submucosal invasion should be evaluated with magnifying endoscopes and endoscopic ultrasound should be reserved for those with suspected deep invasion. In lesions amenable to endoscopic resection, submucosal endoscopic dissection is considered the technique of choice.

The presence of atrophic gastritis (AG) and intestinal metaplasia (IM) is associated with an increased risk of gastric cancer (GC). Thus, the development of new strategies to improve AG/IM is essential for reducing the incidence of GC.We aimed to evaluate the efficacy of rebamipide for improving AG/IM.This was a prospective, randomized, pilot study from a single tertiary referral center. Fifty-three (rebamipide, n = 34 vs. placebo, n = 19) patients, who underwent endoscopic resection for gastric dysplasia or early GC, were analyzed. We obtained tissue samples from the antrum and corpus of the stomach, at the time of screening and 1-year later. The histologic grading of inflammation was performed by histopathologists RESULTS: The AG grade in the antrum improved significantly after rebamipide treatment (pre-administration, 1.870 ± 0.932 vs. post-administration, 1.430 ± 0.986; P = 0.013). Additionally, the severity of IM in the antrum was significantly improved (pre-administration, 1.750 ± 0.963 vs. post-administration, 1.370 ± 1.032; P = 0.038). The rebamipide subgroup analysis revealed that patients with no Helicobacter pylori (HP) infection showed significant improvements in AG in the antrum (pre-administration, 1.880 ± 1.040 vs. post-administration, 1.250 ± 0.894; P = 0.028) and IM in antrum (pre-administration, 1.840 ± 1.012 vs. post-administration, 1.180 ± 0.912; P = 0.020).This study demonstrated that the administration of rebamipide improves AG and IM in the antrum, especially in patients with HP non-infection (KCT0001915).

Introduction: Barrett’s esophagus is an acquired condition that develops as a result of transformation of normal stratified squamous epithelium in the lower part of the esophagus into columnar epithelium. Barrett’s esophagus is considered to be a complication of gastroesophageal reflux disease (GERD). Various endoscopic techniques have been shown to be successful in the treatment of this condition. However, long-term success in preventing further esophageal dysplasia is not clear. Biological welding consists in the application of controlled high-frequency current on living tissues and has been used to stop gastrointestinal bleeding, similarly to the APC technique which involves ablation of small intestinal metaplasia of the esophageal mucosa. Aim: The goal of this study was to evaluate the effectiveness of endoscopic techniques in the treatment of Barrett’s esophagus and verify the need for a subsequent surgical intervention in patients with GERD complicated by Barrett’s esophagus. Material and methods: Patients with Barrett’s esophagus C1-3M2-4 (Prague classification from 2004) and high dysplasia without nodules, as well as patients with confirmed GERD without hiatal hernia, were included in this study. Endoscopic treatment was performed with the use of argonoplasmic coagulation (APC) and high-frequency welding of living tissues (HFW). After the examination the patients were re-examined. Patients with recurrence of metaplasia and high DeMeester score (˃ 100) underwent antireflux surgery – crurography and Nissen fundoplication with creation of a soft and short cuff.Results: A total of 89 patients were included in the study, 81 of whom were reexamined after ablation of Barrett’s esophagus.In 12 patients, a recurrence of intestinal metaplasia resembling the small intestine was identified. Implementation of two-stage treatment was required for 9 patients – it involved a second procedure of ablation of the esophagus, followed by antireflux surgery. Surgical treatment was refused by 3 patients, who underwent only the second ablation procedure. All patients received drug therapy, consisting of prokinetics and proton pump inhibitors. Esophageal pH monitoring was repeated 3 months after surgery, showing normalization of the DeMeester score. As a result, the patients experienced no complaints such as heartburn, chest pain or dysphagia, which significantly improved their quality of life. Esophagogastroduodenoscopy and biopsy of the mucous membrane of the lower third of the esophagus were performed in accordance with the Seattle Protocol. After examining histological specimens, no regions of metaplasia were identified. Conclusion: Antireflux surgery is required as a part of the treatment for Barrett’s esophagus, which prevents further dysplasia and development of esophageal cancer.

Background Advances in endoscopic imaging enable the identification of patients at high risk of gastric cancer. However, there are no comparative data on the utility of standard and magnifying narrow-band imaging (M-NBI) endoscopy for diagnosing Helicobacter pylori (H. pylori) infection, gastric atrophy, and intestinal metaplasia. Aim To compare the diagnostic performance of standard and M-NBI endoscopy for H. pylori gastritis and precancerous conditions. Methods In 254 patients, standard endoscopy findings were classified into mosaic-like appearance (type A), diffuse homogenous redness (type B), and irregular redness with groove (type C). Gastric mucosal patterns visualized by M-NBI were classified as regular round pits with polygonal sulci (type Z-1), more dilated and linear pits without sulci (type Z-2), and loss of gastric pits with coiled vessels (type Z-3). Results The diagnostic accuracy of standard and M-NBI endoscopy for H. pylori gastritis was 93.3% and 96.1%, respectively. Regarding gastric precancerous conditions, the accuracy of standard and M-NBI endoscopy was 72.0% vs 72.6% for moderate to severe atrophy, and 61.7% vs. 61.1% for intestinal metaplasia in the corpus, respectively. Compared to type A and Z-1, types B+C and Z-2+Z-3 were significantly associated with moderate to severe atrophy [odds ratio (OR) = 5.56 and 8.67] and serum pepsinogen I/II ratio of ≤ 3 (OR = 4.48 and 5.69). Conclusion Close observation of the gastric mucosa by standard and M-NBI endoscopy is useful for the diagnosis of H. pylori gastritis and precancerous conditions.

Objective: We aimed to find the frequency of gallbladder carcinoma and the relationship between dysplasia and metaplasia, which are among predisposing factors for carcinoma.Material and Methods: In this study, the histopathological results of 815 patients who underwent cholecystectomy between 2016-2019 in Ahi Evran Training and Research Hospital, Department of General Surgery were retrospectively analyzed.Results: Of the patients who underwent cholecystectomy, 591 (72.5%) were female and 224 (27.5%) were male. The average age was 50.5 years for women and 54.1 years for men. The general average age was 51.5 years. Cholecystectomy was performed laparoscopically in 698 (85.6%) patients while in 117 (14.4%) patients the operation was either started as open cholecystectomy or the decision to convert to open cholecystectomy was made later during the operation for different reasons. Gallbladder carcinoma was detected in two (0.24%) patients, one 62-year-old male and one 67-year-old female. The rate of gallbladder carcinoma was 0.4%for male patients and 0.1%for female patients. Metaplasia in the gallbladder was detected in 16 (1.96%) patients, 15 of which were female and one was male. The average age of these patients was 43.6 years. Dysplasia was detected in only a 48-year-old male patient (0.12%).Conclusion: Chronic irritation caused by the presence of gallstones leads to metaplasia which is a precancerous lesion. Therefore, we think that patients with gallstones should be evaluated for surgery or close follow-up, even if they do not have symptoms., Amaç: Çalışmamızda kliniğimizde yapılan kolesistektomileri retrospektif olarak tarayarak safra kesesi karsinomu sıklığını ve karsinom predispozan faktörleri arasında yer alan displazi ve metaplazi arasındaki ilişkiyi bulmayı amaçladık.Gereç ve Yöntemler: Bu çalışmada Ahi Evran Eğitim ve Araştırma Hastanesi Genel Cerrahi Anabilim Dalında 2016-2019 yılları arasında kolesistektomi ameliyatı yapılan 815 hastanın histopatolojik sonuçları retrospektif olarak incelenmiştir.Bulgular: Kolesistektomi yapılan hastaların 591’i (%72.5) kadın 224’ü (%27.5) erkekti. Yaş ortalaması kadınlarda 50.5 yıl, erkeklerde 54.1 yıl olarak bulundu. Genel yaş ortalaması 51.5 yıl idi. Kolesistektomi ameliyatı 698 (%85.6) hastaya laparoskopik olarak yapılmış, 117 (%14.4) hastada ise ya açık olarak başlanmış ya da sonradan farklı sebeplerle açık kolesistektomiye geçilmişti. Biri 62 yaşında erkek, diğeri 67 yaşında kadın olmak üzere iki (%0.24) hastada safra kesesi karsinomu saptandı. Erkek ve kadın cinsiyete göre safra kesesi karsinomu oranı sırasıyla %0.4 ve %.0.1 idi. Safra kesesinde metaplazi 16 (%1.96) hastada saptandı. Hastaların 15 tanesi kadın, bir tanesi erkekti. Bu hastaların yaş ortalaması 43.6 yıl idi. Sadece 48 yaşında bir erkek hastada displazi saptandı (%0.12).Sonuç: Safra taşı varlığının neden olduğu kronik irritasyon, prekanseröz bir lezyon olan metaplaziye yol açmaktadır. Bu nedenle safra taşı olan hastaların semptomları olmasa dahi ameliyat için değerlendirilmesinin ya da yakın takibinin uygun olacağını düşünmekteyiz.

Objective: Helicobacter pylori infection is a well-established risk factor for gastric cancer, which is more common in developing countries where poor sanitation and domestic overcrowding are common. We tried to analyze the impact of the pandemic on Helicobacter pylori infection during COVID 19 related curfew and stay-at-home order. Material and Methods: Between 1-30 June 2020 (during stay-at-home order), a total of 172 dyspeptic patients who underwent upper gastrointestinal system endoscopy at our institution following stay-at-home order during COVID pandemic were included in this study along with a control group covering 192 dyspeptic patients who underwent endoscopy between 1-20 June 2019. Results: When we analyzed gastric biopsy specimens, those who faced stay-at-home order had similar rates of intestinal metaplasia (22% versus 29%; p=0.15) and atrophic gastritis (24% versus 29%; p= 0.396) compared to recent year's data. On the other hand, the rate of H.pylori infection was higher compared to pre-COVID period (59% vs. 46%, p

BACKGROUND AND AIM Gastrointestinal (GI) lesions may have subtle morphological changes. Linked color imaging (LCI) combines narrow-band wavelength light and white light imaging (WLI) in appropriate balance to enhance lesion detection. We compared the detection rates of upper GI lesions using LCI and WLI. METHOD Patients were randomized in a 1:1 ratio to receive tandem gastroscopy with WLI inspection followed by LCI, or vice versa. Endoscopic examination was performed using the EG-L590ZW gastroscope and the LASEREO endoscope system (Fujifilm Co., Tokyo, Japan). Histology was reported by a specialist GI pathologist blinded to the technique of lesion detection and was used as the gold standard for diagnosis. RESULTS Ninety patients (mean age 66.8 years, 51.5% male patients) were randomized to either LCI examination first followed by WLI (LCI-WLI), or vice versa (WLI-LCI). An 18.9% of gastroscopies in the study were for surveillance of previously known gastric cancer precursors. Ten patients (11.1%) had a history of Helicobacter pylori infection. There was no significant difference in the time taken for examination under LCI (311 ± 96 s) and WLI (342 ± 86 s) (P = 0.700). LCI detection rates were higher than WLI detection rates for gastric cancer precursors such as atrophic gastritis (2.19% vs 0.55%) (P

Background: Gastric disorders are responsible for a great deal of mortality and morbidity and are one of the most common encountered problems in clinical practice. H. Pylori infection is responsible for majority of acid peptic disease and is also a known carcinogen. Intestinal metaplasia is considered a precancerous lesion. We studied the incidence of H. pylori infection and mucin histochemistry of different gastric lesions. Methods: This study was conducted for a period of 1 year, in 50 gastric specimens received for histopathological study in the Department of Pathology, AMCH. Slides were stained with routine H&E and Giemsa for H. pylori detection. PAS/AB stain (at pH 2.5 & pH 1.0) was done to study mucin histochemistry. Results: Out of 50 cases, 58% cases were malignant and 42% cases were benign. H. Pylori was seen in 42% cases. IM was observed in 40% of gastric lesions. IM was more common in malignant lesions. On subclassification, Type 1 and 2 IM were seen almost equally in both benign and malignant gastric lesions, but Type 3 IM was more common in malignant lesion. Incidence of IM was higher in intestinal than diffuse adenocarcinoma. A statistically significant association was seen between H. Pylori infection and IM. Conclusion: Routine detection of H. pylori by special stains and mucin study in all gastric biopsy specimens helps in early detection of precancerous gastric lesions.

Benign tumoral bladder tumors in children are extremely rare. The inflammatory condition determined by the presence of glandular cystitis and intestinal metaplasia, coexisting or separately, can be a determinant factor for the development of these bladder masses. Both entities have been suggested to represent a precursor for bladder adenocarcinoma. We present the case of an autistic adolescent that presented with a polypoid bladder mass and urinary tract infection. We performed a cystoscopic examination and biopsy of the tumor and due to the large dimensions and preliminary histological results we decided to perform a laparotomy and excision of the mass and bladder wall that was attached to. Post operatory evolution and follow-up showed no recurrence or progression of the dysplasia towards adenocarcinoma.