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Introduction: Helicobacter pylori is an important medical pathogen present in more than half of the world's population. Various treatment regimen are in use for the eradication of H. pylori, but due to the emergence of antibiotic resistance, its management is a big issue for clinicians. Methods: In this study all suspected cases that had visited District Headquarters Hospital Kohat were considered for screening of H. pylori infections. Preliminary information about their age, gender, general health conditions, occupation, etc. was taken for consideration. After recording initial signs and symptoms, samples were considered for H. pylori detection using stool antigen test and endoscopy. Fourteen-day proton pump inhibitor base triple and quadruple therapy were administered to each patient. Results: In total (n = 178), there were high numbers of positivity in patients aged below 30 years (82; 46.06%), most of whom belonged to rural areas. Conclusion: This study concludes that there were high numbers of positive patients aged below 30 years, and according to this study MEL (Metronidazole + Esomeprazole + Levofloxacin) is the most effective treatment regimen for the eradication of H. pylori. [ABSTRACT FROM AUTHOR]

Helicobacter pylori-(H. pylori) infection is one of the effective factors in the development of gastric premalignant lesions, and it is known that socioeconomic conditions are closely related to H. pylori infection. Our aim was to show whether there were differences regarding H. pylori infection and gastric histopathological findings between humans who had to manage an exhausting escape out of their own country and residents of a coastal town in the black sea region of Turkey. Endoscopic findings of Turkish and Afghan patients who underwent gastroscopy for various reasons, gastric biopsies, and their histopathological results (H. pylori, intestinal metaplasia, and gastric atrophy) and some biochemical parameters were retrospectively screened from the hospital online data system. A total of 222 patients, 41 Afghan and 181 Turkish, were included in the study. There were no significant differences regarding age and gender of the patients between the groups. The percentage of the patients with intestinal metaplasia and H. pylori infection was higher in the group of the Afghan patients than in Turkish patients. Afghan refugees had similar rates of atrophic gastritis (23.1% versus 21.5%; p=0.834), when compared to resident controls. Risk factors of gastric cancer include the presence of H. pylori infection, atrophic gastritis, and intestinal metaplasia. This study supports the knowledge that socioeconomic factors such as low economic conditions and poor health infrastructure are one of the major causes of widespread global H. pylori infection status. [ABSTRACT FROM AUTHOR]

Background. Despite some progress in addressing gastric cancer, a marked reduction in morbidity in all developed countries, the search for changes that precede carcinogenesis remains relevant and far from complete. The purpose of the study: to assess the content of aggressive and protective factors of gastric juice and oral fluid in comparison with morphological changes in patients with chronic atrophic gastritis. Materials and methods. The study included 56 patients: group I included 12 patients with atrophic changes of the gastric mucosa of varying severity, group II — 24 patients with atrophic changes diagnosed with intestinal metaplasia only in the antrum of the stomach, in group III group — 20 patients with intestinal metaplasia in the body and antrum of the stomach. The control group consisted of 16 healthy individuals. Assessment of the degree of atrophy and inflammation in the gastric mucosa was performed with the subsequent determination of integral indicators — stage and degree of atrophy according to the OLGA system and metaplasia — according to the OLGIM system. According to the morphometric study of sections using a light microscope XSP-139TP (“Ulab“, Ukraine) calculated indicators: nuclear-cytoplasmic ratio, the ellipticity of the nuclei. The content of glycoproteins, sialic acids, fucose, hexosamines was determined in gastric juice and oral fluid. Results. Morphometric study showed a significant decrease in the nuclear-cytoplasmic ratio to (0.12 ± 0.04) % in patients of group III. The coefficient of ellipticity of the nuclei of native cells decreased with the development of intestinal metaplasia: in group I it was equal to (0.76 ± 0.04) %, for group II it was (0.65 ± 0.11) %, and for group III — 0.41 ± 0.12) %. In patients with intestinal metaplasia in 82 % of cases with a 3-fold increase in the content of sialic acids in gastric juice was diagnosed with an increase in hexosamines by 35 %, while patients with only atrophic changes in the stomach showed a decrease in hexosamines 2 times compared to controls (p < 0.05). The spread of intestinal metaplasia in the stomach is associated with an increase in the amount of glycoproteins and hexosamines in the oral fluid of patients, while sialic acids in this biological fluid are increased in all study groups. There are direct relationships between the presence of intestinal metaplasia in the body of the stomach and the content of glycoproteins in both gastric juice (r = 0.446, p = 0.008) and in oral fluid (r = 0.378, p = 0.021). The relationship between the content of sialic acids in gastric juice with the degree and stage of gastritis by OLGA (r = 0.431, p < 0.01; r = 0.482, p < 0.01), the level of hexosamines in oral fluid with the coefficient of ellipticity of the nuclei (r = 0.447, p = 0,037). Conclusions. A comprehensive study of morpho-functional changes in the stomach and the ratio of aggressive and projective factors of oral fluid will determine the risk groups of patients with precancerous conditions. [ABSTRACT FROM AUTHOR]

Objective: Helicobacter pylori (Hp) is a risk factor for gastric cancer, and intestinal metaplasia (IM) is one of the precursor lesions of gastric cancer. The aim of this study was to examine the relationship between Hp and IM. Methods: A total of 550 patients who underwent upper gastrointestinal endoscopy between October 2018 and December 2019 were included in the study. The patient data of age, sex, endoscopic diagnosis, Hp positivity, IM, atrophic gastritis, and neoplasia were evaluated retrospectively. Results: There were 550 patients enrolled in the study: 228 males (41.5%) and 322 females (59.5%), with a median age of 37.0 years (interquartile range: 18.0-79.0 years). Hp was detected in 62.7% of the patients, IM in 17.1%, gastric atrophy in 9.1%, and gastric cancer in 2.9%. Among the patients with positive IM, 80 were Hp-positive and 14 were Hp-negative. The rate of IM was significantly higher in Hp-positive patients than in Hp-negative patients (p<0.001). In addition, the incidence of Hp-IM coexistence was significantly higher in patients over 50 years of age (p=0.002). Conclusion: There was a strong relationship between Hp and IM, and the relationship was correlated with age. Hp eradication is critical to prevent the development of IM, a precursor lesion of intestinal-type gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Activin A receptor type I (ACVR1) is involved in tumorigenesis. However, the underlying molecular mechanisms of ACVR1 in gastric cancer (GC) and its association with Helicobacter pylori remained unclear. Materials and methods: The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) database were utilized to explore the ACVR1 expression in GC and normal control and its association with survival. The ACVR1 was knocked out using CRISPR/Cas‐9; RNA sequencing analysis was performed in AGS cells with ACVR1 knockout and normal control. Functional experiments (CCK‐8, colony‐forming, and transwell assays) were conducted to demonstrate the role of ACVR1 in cell proliferation, invasion, and metastasis. H. pylori‐infected C57/BL6 models were established. ACVR1, p‐Smad1/5, and CDX2 were detected in AGS cells cocultured with H. pylori strains. The CDX2 and key elements of BMP signaling pathway were detected in AGS cells with ACVR1 knockout and normal control. In addition, Immunohistochemistry was performed to detect the ACVR1 and CDX2 expression in gastric samples. Results: ACVR1 expression was higher in GC than normal control from TCGA, GEPIA, and samples collected from our hospital (p < 0.05). ACVR1 promoted cell proliferation, migration, and invasion in vitro. Both cagA+ and cagA−H. pylori could upregulate the expression ACVR1 (p < 0.05). Downregulation of ACVR1 inhibited the H. pylori‐induced cell proliferation, migration, and invasion (p < 0.05). H. pylori increased the expression of p‐Smad 1/5 and CDX2. The CDX2 and key elements of BMP signaling pathway were downregulated in AGS cells with ACVR1 knockout. ACVR1 and CDX2 were upregulated in the stage of intestinal metaplasia (IM). Moreover, ACVR1 and CDX2 expressions were higher in H. pylori‐positive group than H. pylori‐negative group (p < 0.05). Conclusion: Our data indicate that H. pylori infection increases ACVR1 expression, promoting gastric IM via regulating CDX2, which is an essential step in H. pylori carcinogenesis. [ABSTRACT FROM AUTHOR]

Purpose The aim was to compare the density of ghrelin-expressing cells (GECs) in morbid obese patients with or without intestinal metaplasia (IM). Materials and Methods The study included 48 patients out of 244 who underwent laparoscopic sleeve gastrectomy between 2015 and 2019. IM was detected in the sleeve gastrectomy specimens of 24 of these 244 patients. The study group consisted of all of the patients with IM. It was a case matched study. Matching factors were age and gender. Ghrelin was stained with a Leica semiautomatic immunohistochemical–staining machine. Stained preparations with ghrelin were subjected to light microscopic examination. Results The number of GECs in cases with IM was significantly lower than the cases without IM (p = 0.001). The number of GECs was significantly higher in cases with chronic inactive superficial gastritis than cases with chronic active superficial gastritis (p = 0.033). Conclusion We found that there was a decrease in the number of GECs in the corpus and fundus of the stomach in cases with gastric IM as a contribution to the literature. IM cause a decrease in the number of GECs in the gastric oxyntic glands. In addition, chronic active superficial gastritis is also associated with a decrease in the number of GECs. We can say that the common feature of all of these factors may be gastric mucosal damage. Consequently, damage to the gastric mucosa appears to reduce the number of GECs. [ABSTRACT FROM AUTHOR]

Indigenous Arctic Canadians have a higher prevalence of gastric neoplasms relative to North Americans of European ancestry. We investigated the hypothesis that low-dose methylmercury exposure from eating fish/whale increases the risk of gastric cancer in Arctic communities. We used intermediate endpoints from an established model of gastric carcinogenesis: intestinal metaplasia, atrophy, and severe chronic gastritis. During 2008–2012, we obtained gastric biopsies from participants of community-driven projects in 3 communities. In 2016, we collected hair samples to measure methylmercury levels and interviewed them about diet. In cross-sectional analysis, logistic regression estimated odds ratios for the estimated effect of hair-methylmercury concentration on the prevalence of each pathology outcome stratified by selenium intake. Among 80 participants, prevalence of intestinal metaplasia, atrophy and severe chronic gastritis was 17, 29 and 38%, respectively. Adjusted Odds of severe chronic gastritis and atrophy were highest at hair-methylmercury concentrations ≥1μg/g when estimated selenium intake was 0, and approached 0 for all methylmercury levels as estimated selenium intake increased. Gastric pathology increased with methylmercury exposure when selenium intake was low. Though limited by small numbers, these findings suggest selenium ingested by eating fish/whale may counter harmful effects of methylmercury exposure in Arctic populations. [ABSTRACT FROM AUTHOR]

Villous adenomas arising within intestinal metaplasia (IM) of the urinary tract are exceedingly rare with only 20 cases reported in the literature. Histologically most cases of IM do not have cytological atypia; however, in rare cases IM can show dysplastic changes ranging from low-grade to high-grade as seen in the gastrointestinal tract. We report a case of low-grade villous adenoma, arising in a background of cystitis cystica, occurring in the bladder neck of a 48-year-old male with a history of end-stage renal disease, secondary hyperparathyroidism, and kidney stones who never used tobacco.We review and summarize the literature for villous adenomas of the bladder. Moreover, given the background of cystitis cystica in our case, we affirm the possible pathogenic association with chronic irritation of the urothelium. In addition, we discuss the diagnostic challenges associated with villous adenomas of the urinary tract.

Barrett’s esophagus (BE) is a change in the distal esophageal mucosal lining, whereby metaplastic columnar epithelium replaces squamous epithelium of the esophagus. This change represents a pre-malignant mucosal transformation which has a known association with the development of esophageal adenocarcinoma. Gastroesophageal reflux disease is a risk factor for BE, other risk factors include patients who are Caucasian, age > 50 years, central obesity, tobacco use, history of peptic stricture and erosive gastritis. Screening for BE remains selective based on risk factors, a screening program in the general population is not routinely recommended. Diagnosis of BE is established with a combination of endoscopic recognition, targeted biopsies, and histologic confirmation of columnar metaplasia. We aim to provide a comprehensive review of the epidemiology, pathogenesis, screening and advanced techniques of detecting and eradicating Barrett’s esophagus.

Helicobacter pylori (H. pylori) infects about half of the world’s population and can lead to premalignant lesions and gastric cancer. Updated data about the correlation of histopathological diagnostics with endoscopic diagnostics are scarce. The objective of this study was to identify the concordance between endoscopic and histopathologic findings, with a focus on premalignant lesions. We performed a cross sectional, retrospective study over a 4-year period (2017–2021) on adult patients with dyspeptic symptoms and positive RUT (rapid urease test) in a single hospital centre, with a total of 133 patients infected with H. pylori being included in the study. Statistical associations between endoscopic appearance and histopathological results were found for atrophic antral gastritis (p = 0.001), intestinal metaplasia of the antrum (p = 0.018), gastric polyps (p < 0.001) and gastric corpus cancer (p = 0.012). Females were more likely to be diagnosed through endoscopy with gastric atrophy or intestinal metaplasia (p = 0.031), while chronic atrophic gastritis in corpus was more prevalent in patients older than 65 (p = 0.024). Overall, our study reveals only 21% concordance between Giemsa stain and RUT, highlighting the importance of combining rapid testing with endoscopic and histopathological diagnostic methods for a more accurate early diagnosis and prevention of gastric cancer.

Background: Seeking novel and effective therapies for gastric precancerous lesions (GPL) is crucial to reducing the incidence of gastric cancer. Ginsenoside Rb1 (GRb1) is a major ginsenoside in ginseng and has been proved to possess multiple bioactivities. However, whether GRb1 could protect against GPL and the underlying mechanisms have not been explored.Methods: We evaluated the effects of GRb1 on gastric precancerous lesions in rats on macroscopic, microscopic and ultramicroscopic levels. Then, an antibody array was employed to screen differential expression proteins (DEPs). Validation for the targeting DEP and investigation for the possible mechanism was conducted using immunohistochemistry, qRT-PCR, TUNEL apoptosis assay, immunoprecipitation and immunoblotting.Results: GRb1 was found to reverse intestinal metaplasia and a portion of dysplasia in the MNNG-induced GPL rats. The antibody array assay revealed seven DEPs in GPL rats as compared to control rats (5 DEPs were up-regulated, while two DEPs were down-regulated). Among the DEPs, β-catenin, beta-NGF and FSTL1 were significantly down-regulated after GRb1 administration. Our validation results revealed that enhanced protein expression and nuclear translocation of β-catenin were present in animal GPL samples. In addition, analysis of human gastric specimens demonstrated that β-catenin up-regulation and nuclear translocation were significantly associated with advanced GPL pathology. GRb1 intervention not only decreased protein expression and nuclear translocation of β-catenin, but interfered with β-catenin/TCF4 interaction. Along with this, declined transcriptional and protein expression levels of downstream target genes including c-myc, cyclin D1 and Birc5 were observed in GRb1-treated GPL rats.Conclusion: GRb1 is capable of preventing the occurrence and progression of GPL, which might be contributed by diminishing protein expression and nuclear translocation of β-catenin and interfering with β-catenin/TCF4 interaction.

Background: Oxidative stress status in different cancer types was investigated before, but not studied in gastric intestinal metaplasia to the best of our knowledge. Purpose of this study is to examine whether there is a difference between oxidative stress status in patients with intestinal metaplasia (IM) compared to individuals without IM, we compared the serum levels of disulfide (SS), total thiol (TT) and native thiol (NT). Methods: This was a prospective, non-randomized casecontrol study including 67 patients with histopathologically confirmed IM and 60 individuals demographically matched in terms of age, gender, BMI, smoking status, and chronic diseases as control group. Results: The mean NT TT and NT to TT (NT/TT) ratios were statistically significantly higher in IM group compared to controls ((351.71 ± 81.9 pmol/L vs. 271.82 ± 54.13 pmol/L, p= 0.000), (391.5 ± 92.69 pmol/L vs. 308.59 ± 55.53 iimol/L, p= 0.000) and (0.89 ± 0.6 vs. 0.87 ± 0.29, p= 0.022), respectively). The mean SS to TT (SS/TT) ratio was significantly lower in IM group than control group (0.050 ± 0.31 vs. 0.060 ± 0.014, P= 0.022). Median SS and mean SS/NT ratio was similar in both groups (16.3 (3.3-78) vs. 18.3 (10-32.7), p=0.271 and 0.055 ± 0.041 vs. 0.070 ± 0.019, p=0.068, respectively). In ROC analysis, cut off value of SS/NT for IM was found 0.062, in regression analysis, SS/NT <0.062 was found as an independently prognostic marker for IM (OR, 2.38; 95%CI: 1.168-4.865, P=0.017). Conclusions: SS/NT ratio lower than 0,062 was found as an independently prognostic marker for IM. This ratio could help to distinguish which patients should be followed closely for gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Untreated gastroesophageal reflux disease (GERD) can lead to Barrett's esophagus and an increased risk for esophageal adenocarcinoma. Magnetic sphincter augmentation (MSA) is a safe and effective modality for the treatment of GERD. Preliminary research on short-term outcomes after MSA demonstrated significant regression of Barrett's. Further investigation is required to evaluate the long-term effect of this treatment. Methods: A retrospective review of patients was conducted with biopsy-proven Barrett's esophagus who underwent MSA between 2007 and 2019. As a part of their preoperative evaluation, patients underwent esophagogastroduodenoscopy (EGD) with biopsies of the distal esophagus and gastroesophageal junction including any abnormal-appearing segments, pH testing, and a videoesophagram. Patients were categorized according to the length of Barrett's identified (ultrashort < 1 cm, short 1–3 cm, long > 3 cm). Improvement was defined as a decrease in length (e.g. long to short). Results: There were 87 patients identified for study inclusion. 55 patients were male. The median body mass index was 26.95. The median age was 61.81 (49.79–68.29). Mean follow-up time was 2.35 ± (1.57) years. 7 (8.0%) of these patients began with long segment Barrett's, 58 (66.7%) began with short segment disease, and 22 (25.3%) began with an ultrashort segment. Within this cohort, 74 (85.06%) had undergone postoperative biopsy. 7 out of 74 patients (9.46%) showed improvement in their intestinal metaplasia and 45/74 (60.81%) showed complete regression. Fisher's exact test showed a significant decrease in Barrett's length following MSA (p = 0.002). No patients progressed to dysplasia or neoplasia. There was a statistically significant decrease in the median Demeester score from 34.00 to 13.70 after surgery (p <.001). Conclusion: MSA reduces esophageal acid exposure and can lead to reduction or resolution of Barrett's esophagus. MSA is also effective at preventing progression of metaplasia to dysplasia or neoplasia. This effect remains consistent even after 2 years of follow-up. [ABSTRACT FROM AUTHOR]

Purpose: Intestinal metaplasia (IM) is a precancerous lesion that increases the risk of subsequent gastric cancer (GC) development. Previously, miR-1 has been shown to play an essential role in the initiation of bile acid (BA)-induced IM. The objective of the present study was to investigate the mechanism underlying miR-1 inhibition by BA in gastric cells. Methods: Ingenuity pathway analysis (IPA) was used to identify molecules acting upstream of miR-1. The effects of deoxycholic acid (DCA), FXR and SNAI2 on the expression of intestinal markers were assessed using quantitative real-time PCR (qRT-PCR) and Western blotting. The expression level of major molecules was detected by immunohistochemistry (IHC) in tissue microarrays. The transcriptional regulation of miR-1 was verified using luciferase reporter and chromatin immunoprecipitation (ChIP) assays. Results: We found that BA treatment caused aberrant expression of FXR and intestinal markers in gastric cells. Augmented FXR led to transcriptional activation of SNAI2, which in turn suppressed the miR-1 promoter. Moreover, we found that compared with normal tissues, the expression levels of both FXR and SNAI2 were increased and positively correlated with each other in IM tissues. Additionally, their expression showed an inverse correlation with that of miR-1 in IM tissues. Conclusions: Our findings indicate that FXR may be responsible for a series of molecular changes in gastric cells after BA treatment, and that the FXR/SNAI2/miR-1 axis exhibits a crucial role in BA-induced progression of IM. Blocking the FXR-oriented axis may provide a promising approach for IM or even GC treatment. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 <0.001). In the population under 40 years of age, the rates of gastric atrophy and intestinal metaplasia were 0.7% and 2.5%, respectively (p = 0.02), above the age of 40, these rates were determined as 10.8% and 18.4%, respectively. (p <0.001). Conclusion: According to the data of our center, the prevalence of H. pylori is high. In addition, the rate of intestinal metaplasia is relatively high in the male population over the age of 40. [ABSTRACT FROM AUTHOR]

Background: Seeking novel and effective therapies for gastric precancerous lesions (GPL) is crucial to reducing the incidence of gastric cancer. Ginsenoside Rb1 (GRb1) is a major ginsenoside in ginseng and has been proved to possess multiple bioactivities. However, whether GRb1 could protect against GPL and the underlying mechanisms have not been explored. Methods: We evaluated the effects of GRb1 on gastric precancerous lesions in rats on macroscopic, microscopic and ultramicroscopic levels. Then, an antibody array was employed to screen differential expression proteins (DEPs). Validation for the targeting DEP and investigation for the possible mechanism was conducted using immunohistochemistry, qRT-PCR, TUNEL apoptosis assay, immunoprecipitation and immunoblotting. Results: GRb1 was found to reverse intestinal metaplasia and a portion of dysplasia in the MNNG-induced GPL rats. The antibody array assay revealed seven DEPs in GPL rats as compared to control rats (5 DEPs were up-regulated, while two DEPs were down-regulated). Among the DEPs, β-catenin, beta-NGF and FSTL1 were significantly down-regulated after GRb1 administration. Our validation results revealed that enhanced protein expression and nuclear translocation of β-catenin were present in animal GPL samples. In addition, analysis of human gastric specimens demonstrated that β-catenin up-regulation and nuclear translocation were significantly associated with advanced GPL pathology. GRb1 intervention not only decreased protein expression and nuclear translocation of β-catenin, but interfered with β-catenin/TCF4 interaction. Along with this, declined transcriptional and protein expression levels of downstream target genes including c-myc, cyclin D1 and Birc5 were observed in GRb1-treated GPL rats. Conclusion: GRb1 is capable of preventing the occurrence and progression of GPL, which might be contributed by diminishing protein expression and nuclear translocation of β-catenin and interfering with β-catenin/TCF4 interaction. [ABSTRACT FROM AUTHOR]

Background: Most patients undergoing esophagectomy will experience intermittent reflux of gastric and biliary content into the remnant esophagus postoperatively. The incidence of new or recurrent intestinal metaplasia following chemoradiation and surgery has not been well-described. Furthermore, post-resection guidelines do not exist regarding surveillance for metaplasia in the esophageal remnant. Methods: Patients undergoing Ivor Lewis esophagectomy after concurrent chemoradiation for a diagnosis of esophageal adenocarcinoma from 2006 to 2018 were identified. Pathology records were reviewed for the presence of intestinal metaplasia on pretreatment biopsies, surgical specimen, or post-resection biopsies. Results: In total, 619 patients met inclusion criteria, including 267 (43%) who had intestinal metaplasia noted either prior to or at the time of esophagectomy. The median duration of metaplastic disease prior to resection was 4.4 months. During a median follow-up time of 28 months (interquartile range, 12–60), intestinal metaplasia was noted in the remnant esophagus in 12 (2%) patients, 7 of whom had a prior history of metaplasia. Local recurrence of adenocarcinoma was also uncommon, and occurred in 37/577 (6%) of patients with complete resections, with similar event rates among those with and without a prior history of metaplasia (14/249 [6%] vs. 23/328 [7%], p = 0.614). Conclusions: Our findings suggest that despite several factors predisposing to mucosal damage following esophagectomy, occurrence of new intestinal metaplasia after trimodality therapy in our patient population appears to be rare, even among patient with a previous history of this pathologic finding, which may have significant implications for surveillance and cost-savings after resection. [ABSTRACT FROM AUTHOR]

Stomach pathologies develop in a complex interaction between the host's genetic background and H. pylori virulent genes. Thus, our study aimed to compare active chronic gastritis (ACG), and intestinal metaplasia (IM) with inactive chronic gastritis (ICG), according to interleukin polymorphisms of IL6-174 G/C, IL8-251 A/T, IL1β-511 C/T, and IL1RN VNTR taking into account patient gender and H. pylori genotypes. Interleukin polymorphisms were determined by RFLP-PCR and H. pylori genotype by PCR. IL6-174 GC and IL8-251 T allele showed a protective effect in women against ACG development and, conversely, IL8-251 polymorphism showed a risk for men. More virulent H. pylori strains were associated with the IL8-251 T allele and IL1β-511 T allele in the AGC, and the vacAm1 allele and cagE gene from H. pylori was associated with the IM. Analysis of the progression of gastric lesions must take into account host variability genetic associated with genes H. pylori due to the relation between the virulent H. pylori genes and more severe gastric lesions, besides the relevance to the gender to IL6-174 and IL8-251 polymorphisms. [ABSTRACT FROM AUTHOR]

Background and Aim: Improvement of atrophic gastritis and intestinal metaplasia (IM) is considered to reduce the gastric cancer risk, but whether it can be achieved by H. pylori eradication (HPE) remains controversial. To evaluate the effect of HPE, we observed the gastric mucosa for up to17 years after HPE and sex differences in gastric mucosa. Methods: In total, 172 patients (94 males, 78 females) with HPE were enrolled. Annual histological evaluations were performed for up to 17 years. The grades of mononuclear cells, neutrophils, atrophy, IM in the antrum and corpus were evaluated using the updated Sydney system. Results: Relative to the pre‐HPE period, atrophy had improved significantly 1 year after HPE in the antrum (1.50 ± 0.75 vs. 1.21 ± 1.25, P < 0.01) and corpus (0.59 ± 0.75 vs. 0.18 ± 0.52, P < 0.05). IM showed no significant change during 17 years after HPE at either biopsy site. Atrophy scores did not differ significantly between males and females. IM scores were significantly higher in males than in females before eradication (antrum, 0.67 ± 0.94 vs. 0.44 ± 0.77, P = 0.003, corpus, 0.20 ± 0.62 vs. 0.047 ± 0.21, P = 0.0027) and at most observation timepoints. Conclusions: During 17 years after HPE, atrophy, but not IM, improved significantly at the greater curvatures of the antrum and corpus. IM was significantly more severe in males than in females. Careful follow‐up after HPE based on sex differences in gastric mucosal characteristics is important. [ABSTRACT FROM AUTHOR]

Introduction: Helicobacter pylori infection is the major risk factor of atrophic gastritis and intestinal metaplasia. The vacA gene is one of the most virulence factors of H. pylori and genetic diversity in its s, m, i, and d regions is associated with gastric lesions severity. This study aimed to investigate the association of vacA s, m, i, and d regions with the risk of atrophic gastritis and intestinal metaplasia in a Casablanca population. Methodology: A total of 210 patients suffering from gastric lesions (chronic gastritis, atrophic gastritis, and intestinal metaplasia) were enrolled. The type of lesion was diagnosed by histological examination. Detection of H. pylori infection and genotyping of vacA regions were carried out by PCR. Results: The prevalence of H. pylori was 95%. The most common vacA genotypes were s2 (51.5%), m2 (77%), i2 (60.5%), and d2 (58.5%). VacA s1, m1, and i1 genotypes were associated with a high risk of intestinal metaplasia, while the vacA d1 genotype increases the risk of atrophic gastritis and intestinal metaplasia. The most common vacA combination was s2/m2/i2/d2 (52%), and it was more detected in chronic gastritis. The moderate virulent vacA combination (s1/m2/i1/d1) increases the risk of atrophic gastritis, while the most virulent vacA combination (s1/m1/i1/d1) increases the risk of intestinal metaplasia. Conclusions: Genotyping of vacA d region might be a reliable marker for the identification of vacA virulent strains that represent a high risk of developing precancerous lesions (atrophic gastritis and intestinal metaplasia). [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the accuracy and interobserver reliability of diagnosing and subtyping gastric intestinal metaplasia (IM) among general pathologists and pathology residents at a university hospital in Thailand, focusing on the challenges in the histopathologic evaluation of gastric IM for less experienced practitioners. The study analyzed 44 non-neoplastic gastric biopsies, using a consensus diagnosis of gastrointestinal pathologists as the reference standard. Participants included 6 general pathologists and 9 pathology residents who assessed gastric IM and categorized its subtype (complete, incomplete, or mixed) on digital slides. After initial evaluations and receiving feedback, participants reviewed specific images of gastric IM, as agreed by experts. Following a one-month washout period, a reevaluation of the slides was conducted. Diagnostic accuracy, interobserver reliability, and time taken for diagnosis improved following training, with general pathologists showing higher accuracies than residents (median accuracy of gastric IM detection: 100 % vs. 97.7 %). Increased years of experience were associated with more IM detection accuracy (p -value<0.05). However, the overall median accuracy for diagnosing incomplete IM remained lower than for complete IM (86.4 % vs. 97.7 %). After training, diagnostic errors occurred in 6 out of 44 specimens (13.6 %), reported by over 40 % of participants. Errors involved omitting 5 slides with incomplete IM and 1 with complete IM, all showing a subtle presence of IM. The study highlights the diagnostic challenges in identifying incomplete gastric IM, showing notable discrepancies in accuracy and interobserver agreement. It underscores the need for better diagnostic protocols and training to enhance detection and management outcomes. • Various diagnostic accuracy of gastric intestinal metaplasia (IM) is noted. • Increased years of experience are associated with more IM detection accuracy. • Diagnostic accuracy, agreement, and time generally improve after training. • Diagnostic accuracy for incomplete IM remains lower than for complete IM. • The subtle presence of IM can be easily overlooked. [ABSTRACT FROM AUTHOR]

Abstract Background In this study, we aimed to investigate the characteristics of the duodenal mucosal microbiota of patients with intestinal metaplasia (IM) and compare it with those of the gastric mucosal microbiota. Method We collected the duodenal and gastric mucosal samples from 10 adult patients with IM and 10 healthy controls (HC). The V3-V4 region of the bacterial 16S rRNA gene was examined by high throughput sequencing method. Results The diversity of the HC duodenal microbiota was higher than that of IM patient based on the Shannon and Simpson index while the Chao indices of IM duodenal mucosal microbiota was significantly higher than that of gastric mucosal microbiota of patients with IM. There was a marked difference in the duodenal microbiota structure between patients with IM and HC (ANOSIM, R = 1, P = 0.001). We also found that the Helicobacter pylori infection in gastric mucosa did not influence the structure of duodenal mucosal microbiota. The gastric mucosal microbiota structure significantly differed between patients with IM and HC who were H. pylori-negative (ANOSIM, R = 0.452, P = 0.042) or H. pylori-positive (ANOSIM, R = 0.548, P = 0.003), respectively. For duodenal mucosal microbiota, genera Lactococcus, Flavobacterium, Psychrobacter, Mysroides, Enhydrobacter, Streptococcus, and Leuconostoc were enriched in patients with IM. In contrast, genera Bacillus, Solibacillus, Lysinibacillus, Exiguobacterium, Oceanobacillus, and Paenibacillus were enriched in HC. Conclusion A marked dysbiosis duodenal mucosal microbiota in patients with IM was observed, and this dysbiosis might be responsible for IM pathogenesis.

An inflammatory process accompanied by the changes in mucosal microbiota is underlying the gastroduodenal diseases. Chronic inflammation of gastric mucosa is developed and supported by secretion of pro-inflammatory and anti-inflammatory cytokines by epithelial cells and immune cells induced by Helicobacter pylori and other microorganisms. Under the conditions of dysbiosis and immune dysregulation, gastric epithelial layer becomes like intestinal or colonic epithelium. The aim of this work was to determine diagnostic and prognostic value of cytokines in intestinal metaplasia of gastric epithelium. 204 patients with exacerbation of chronic gastritis, gastric ulcer, gastric polyposis and 40 healthy volunteers were included into the study, under their informed consent. The gastric biopsies were sampled by means of esophagogastroduodenoscopy (for histological and microbiological examination), along with drawing 5 ml of venous blood with serum separation (for enzyme immunoassay). Serum cytokine levels were studied by solidphase enzyme immunoassay. In statistical evaluation of the results, we have calculated sensitivity, specificity of indexes, logistic regression equations, characteristic curves were built with the definition of the index of consistency of the model by the area under the curves (AUC).Histological examination of gastric biopsies showed features of intestinal metaplasia in 61 patients (29.90%), colonic metaplasia was found in 40 cases (19.61%), being absent in healthy volunteers. The greatest sensitivity of intestinal metaplasia was observed for plasma levels of interleukin (IL)-6, IL-4, erythropoietin (EPO), tumor necrosis factor (TNF)α, IL-18, vascular endothelial growth factor (VEGF), interferon (IFN)α levels; in colonic metaplasia, for receptor antagonist IL-1β (IL-1ra), IL-8, EPO, IL-18, monocyte chemoattractant protein (MCP)-1, VEGF, IFNα, IL-1β, IL-6, IL-17. An increase in IL-6, EPO, IL-18, VEGF, IFNα were also common, thus indicative for changed functional activity of cytokines due to microbial contamination of gastric mucosa, tissue hypoxia with activation of angiogenesis, confirming a transition of intestinal metaplasia to gastric carcinogenesis. The greatest specificity in intestinal metaplasia was observed for IL-1β, IL-1ra, IL-8, IL-17, IL-2, IL-10; in colonic metaplasia, for IL-18, IFNα, IL-4, МСР-1, VEGF. In the intestinal metaplasia, the AUC interval was higher than 0.7 for IL-2, higher than 0.65, in VEG; in colonic metaplasia > 0.91, for IL- 18, VEGF, МСР-1, IFNα, having a significance level of < 0.001. The obtained prognostic models of intestinal metaplasia of gastric epithelium, according to the AUC index, had very good (Table 2, formula 1) and excellent quality (Table 2, 3, formula 2-11), confirmed by a high percent of cases which were correctly classified of metaplasia. Determination of serum cytokines in intestinal metaplasia of gastric epithelium is of diagnostic and prognostic value, and should be used for early diagnosis of precancerous conditions of the gastric mucosa, both as single indexes (IL-2, VEGF), and combined indicators, according to the calculated logistic regression equations.

Aim:Colorectal cancer (CRC) is one of the leading three cancers with high mortality. Colon polyps are precursors for CRC development. Helicobacter pylori is known to increase the risk of gastric cancer by intestinal metaplasia (IM) and glandular atrophy (GA), there are studies suggesting that it increases the risk of CRC by various mechanisms. Sydney criteria have been developed to provide a standardized approach to histopathological changes in gastric mucosa caused by H. pylori. The aim of this study was to evaluate H. pylori according to the Sydney criteria in patients with colon polyps and to contribute to the literature.Method:The study cohort included a control group (n=231) with normal colonoscopy findings and a patient group (n=600) who underwent upper gastrointestinal endoscopy and colonoscopy on the same day and had hyperplastic polyps, adenomatous polyps and malignant polyps. Age, gender, complications during endoscopy, number and localization of polyps, and histopathological results of gastric and colon biopsies were analyzed. The relationship between H. pylori, IM and GA and colon polyps were investigated with logistic regression model.Results:H. pylori was present in 609 (73.3%) of 831 patients. There was no statistically significant relationship between coexistence of H. pylori + IM and hyperplastic polyp and adenomatous polyp (p>0.05). It was found that IM did not increase the risk of CRC without H. pylori (p=0.15). There was a statistically significant relationship between CRC and H. pylori + IM (p=0.03). GA was detected in 70 patients (8.4%), and there was a statistically significant relationship between the presence of GA and CRC, regardless of the presence of H. pylori (p

Background/Aims Atrophic gastritis and intestinal metaplasia are sequential consequences of chronic Helicobacter pylori (H. pylori) infection. These conditions are well known to increase the risk of gastric adenocarcinoma development. Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is also a malignant consequence of H. pylori infection, but the relationship between gastric MALT lymphoma and atrophic gastritis-intestinal metaplasia has not been a focus of interest. We investigated the clinical characteristics of atrophic gastritis and intestinal metaplasia in patients with gastric MALT lymphoma. Materials and Methods A study was conducted by reviewing the electronic medical records of patients diagnosed as having gastric MALT lymphoma at an academic institute, the Yeouido St. Mary's Hospital, Seoul, Korea, between January 2001 and December 2018. Results Fifty-eight subjects were enrolled consecutively during the study period and analyzed retrospectively. The patients’ mean age was 56.9 years old. The male-to-female ratio was 1.15 (31/27). On histological examination, background atrophic gastritis and intestinal metaplasia were detected in 26.8% (15/58) of cases. Serum pepsinogen I, II and gastrin levels, as serological markers of atrophy, were evaluated in 28 subjects. Three (5.2%) of the 28 cases were compatible with serological atrophic gastritis (pepsinogen I/II ratio of

Objectives: In the USA, certain races and ethnicities have a disproportionately higher gastric cancer burden. Selective screening might allow for earlier detection and curative resection. Among a USA-based multiracial and ethnic cohort diagnosed with non-cardia gastric cancer (NCGC), we aimed to identify factors associated with curable stage disease at diagnosis. Methods: We retrospectively identified endoscopically diagnosed and histologically confirmed cases of NCGC at Mount Sinai Hospital in New York City. Demographic, clinical, endoscopic and histologic factors, as well as grade/stage of NCGC at diagnosis were documented. The primary outcome was the frequency of curable-stage NCGC (stage 0-1a) at diagnosis in patients with versus without an endoscopy negative for malignancy prior to their index exam diagnosing NCGC. Additional factors associated with curable-stage disease at diagnosis were determined. Results: A total of 103 racially and ethnically diverse patients were included. Nearly 38% of NCGC were stage 0-Ia, 34% stage Ib-III, and 20.3% stage IV at diagnosis. A significantly higher frequency of NCGC was diagnosed in curable stages among patients who had undergone an endoscopy that was negative for malignancy prior to their index endoscopy that diagnosed NCGC, compared to patients without a negative endoscopy prior to their index exam (69.6% vs. 28.6%, p=0.003). A prior negative endoscopy was associated with 94.0% higher likelihood of diagnosing curable-stage NCGC (p=0.003). No other factors analyzed were associated with curable-stage NCGC at diagnosis. Conclusions: Endoscopic screening and surveillance in select high-risk populations might increase diagnoses of curable-stage NCGC. These findings warrant confirmation in larger, prospective studies.

Zhongren Zhou,1 Irina Kalatskaya,2 Donna Russell,1 Norman Marcon,3 Maria Cirocco,3 Paul M Krzyzanowski,2 Cathy Streutker,3 Hua Liang,4 Virginia R Litle,5 Tony E Godfrey,5 Lincoln Stein21Department of Pathology & Immunology, Washington University, Saint Louis, MO, USA; 2Department of Adaptive Oncology, Ontario Institute for Cancer Research, Toronto, Ontario, Canada; 3Division of Gastroenterology, Department of Internal Medicine, St. Michael’s Hospital, Toronto, Ontario, Canada; 4Department of Statistics, George Washington University, Washington, DC, USA; 5Department of Surgery, Boston University School of Medicine, Boston, MA, USAPurpose: The incidence of esophageal adenocarcinoma (EAC) has increased by 700% in Western countries over the last 30 years. Although clinical guidelines call for endoscopic surveillance for EAC among high-risk populations, fewer than 5% of new EAC patients are under surveillance at the time of diagnosis. We studied the accuracy of combined cytopathology and MUC2 immunohistochemistry (IHC) for screening of Intestinal Metaplasia (IM), dysplasia and EAC, using specimens collected from the EsophaCap swallowable encapsulated cytology sponge from Canada and United States.Patients and methods: By comparing the EsophaCap cytological diagnosis with concurrent endoscopic biopsies performed on the same patients in 28 cases, we first built up the cytology diagnostic categories and criteria. Based on these criteria, 136 cases were evaluated by both cytology and MUC2 IHC with blinded to patient biopsy diagnosis.Results: We first set up categories and criteria for cytological diagnosis of EscophaCap samples. Based on these, we divided our evaluated cytological samples into two groups: non-IM group and IM or dysplasia or adenocarcinoma group. Using the biopsy as our gold standard to screen IM, dysplasia and EAC by combined cytology and MUC2 IHC, the sensitivity and specificity were 68% and 91%, respectively, which is in the range of clinically useful cytological screening tests such as the cervical Pap smear.Conclusions: Combined EsophaCap cytology and MUC2 IHC could be a good screening test for IM and Beyond.Keywords: Barrett’s esophagus, esophageal adenocarcinoma, cytology screening, MUC2 IHC, EsophaCap, intestinal metaplasia

Objectives: Gastric intestinal metaplasia have traditionally been associated with gastric adenocarcinoma. Gastric intestinal metaplasia is usually related to the Helicobacter pylori infection, older ages, smoking history, consumption of strong spicy foods, socioeconomic status and presence of IL10-592 C/A. The purpose of the present research study was to evaluate the simple laboratory parameters in subjects with gastric intestinal metaplasia Findings: From May 2018 and October 2018, a total of 541, 281 male and 260 female, consecutive cases with gastric intestinal metaplasia with the mean age of 58.5±15 years had been enrolled retrospectively with exclusion of the cases with a severe underlying disease, including a gastric cancer and gastric resection. The gastroscopy with the antral biopsy had been performed for all the cases and the biopsy samples had been evaluated for the presence of gastric intestinal metaplasia by Hematoxylin and Eosin and Helicobacter pylori status by Giemsa.The chi-squared test and independent t test were used for comparison. The mean serum urea level detected as 34.2.±16.1 mg/dL in the gastric intestinal metaplasia and 31.2±13.1 mg/dL in the control (95% CI from 32,3 to 34,6; p=0.013), while the mean serum creatinin level 0.84±0.28 mg/dL in the gastric intestinal metaplasia and 0.80±0.26 mg/dL in the control (95% CI from 0,80 to 0,85; p=0.042). Gastric intestinal metaplasia was detected mostly in elderly and male, regarding the multiple logistic regression (p

Background and purpose: Identifying precancerous lesions for early detection of gastric cancer is greatly important in high risk areas for stomach cancer. In this study, we evaluated stomach biomarkers as a non-invasive method for recognition of gastric precancerous lesions. Materials and methods: In a cross-sectional study, patients with chronic dyspeptic symptoms who were candidate for endoscopy were selected from Sari gastroenterology clinic. After endoscopic and pathological evaluations, patients were divided into three groups: those with normal endoscopic findings and pathology, patients with chronic active gastritis, and those with intestinal metaplasia. Their serum samples were evaluated for PG1, PG2, PG1/PG2 ratio, Gastrin-G17, and Helicobacter pylori serology. Data analysis was done in SPSS V21. Results: A total of 63 patients were investigated of whom 19 were found with normal endoscopic results and pathology, 25 had chronic active gastritis, and there were 19 with intestinal metaplasia. Serum levels of PG1 and PG2 in patients with chronic active gastritis and intestinal metaplasia were higher than normal patients (p

Background. Chronic atrophic gastritis (CAG) is the pre-cancer diseases of stomach. There are often intestinal metaplasia and dysplasia, which could lead to gastric cancer development. The purpose was to study the different risk factors in patients with CAG, and their possible correlations with morphological gastric mucosal changes. Materials and methods. One hundred twenty patients with CAG were included in this study. They underwent an examination with magnifying narrow-band imaging endoscopy. Images resolution was evaluated, as well stomach endoscopic biopsies were analyzed to confirm diagnosis. The questionnaire was worked out and used in patients with CAG to evaluate risk factors. Results. It was found that acute stress (r = 0.593) and chronic stress (r = 0.544), large amounts of fried (r = 0.636), smoked (r = 0.512) and pickled foods (r = 0.591), age (r = 0.639), the A blood type (ABO blood group system) (r = 0.651), heredity (r = 0.533), duodenogastric reflux (r = 0.524), and thyroid disease (r = 0.522) were possible risk factors for CAG. According to examination with magnifying narrow-band imaging endoscopy and morphological results, the Helicobacter pylori incidence became rarer with the increase in gastric morphological changes (atrophy-metaplasia-dysplasia). Conclusions. The results show possible influence of risk factors, such as stress, age, the A blood type (ABO blood group system), heredity, large amounts of fried, smoked and pickled foods, as well as duodenogastric reflux and thyroid disease, in patients with CAG.

Copyright of Acta Medica Colombiana is the property of Acta Medica Colombiana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Gastric dysbiosis has been hinted as a potential cause of gastric cancer. However, changes in microbiome throughout the major stages of gastric carcinogenesis remain mostly unknown. To describe gastric microbiome at different stages, analysing for the first time dysbiosis specifically in patients with early gastric cancer (EGC). Cross-sectional study including patients (n = 77) with endoscopically and histologically confirmed normal stomachs (controls; n = 25), advanced atrophic gastritis with intestinal metaplasia (IM; n = 18) and EGC (n = 34). Endoscopic biopsies from antrum and corpus (n = 154) were analyzed. Next-generation sequencing was performed characterizing microbial communities down to the species level based on full-length 16SrRNA gene profiling. Significant differences were found in the microbiome profile between the groups. Firmicutes were more frequent (p =.012) and Proteobacteria were less frequent (p =.04) both in the IM and EGC when comparing to controls. Relative frequency of Helicobacter pylori, when present, was much higher in the controls (83%) when comparing to the other groups (IM 1%, EGC 27%; p =.006), being the dominant bacteria only in the controls. Dysbiosis was present already and more significantly at the IM stage, with two bacteria progressively increasing from controls to IM then to cancer: Gemella from 1.48 to 3.9% (p =.014); and Streptococcus from 19.3 to 33.7% (p =.04), being the EGC dominant bacteria. Our results confirm Helicobacter pylori dominancy in non-atrophic stomachs and progressive dysbiosis throughout gastric carcinogenesis. Gemella but particularly Streptococcus is significantly increased in patients with EGC. Specific modulation of these bacteria may change gastric cancer risk. [ABSTRACT FROM AUTHOR]

Introduction: Guidelines recommend endoscopy with biopsies to stratify patients with gastric premalignant lesions (GPL) to high and low progression risk. High-risk patients are recommended to undergo surveillance. We aimed to assess the accuracy of guideline recommendations to identify low-risk patients, who can safely be discharged from surveillance. Methods: This study includes patients with GPL. Patients underwent at least two endoscopies with an interval of 1–6 years. Patients were defined 'low risk' if they fulfilled requirements for discharge, and 'high risk' if they fulfilled requirements for surveillance, according to European guidelines (MAPS-2012, updated MAPS-2019, BSG). Patients defined 'low risk' with progression of disease during follow-up (FU) were considered 'misclassified' as low risk. Results: 334 patients (median age 60 years IQR11; 48.7% male) were included and followed for a median of 48 months. At baseline, 181/334 (54%) patients were defined low risk. Of these, 32.6% were 'misclassified', showing progression of disease during FU. If MAPS-2019 were followed, 169/334 (51%) patients were defined low risk, of which 32.5% were 'misclassified'. If BSG were followed, 174/334 (51%) patients were defined low risk, of which 32.2% were 'misclassified'. Seven patients developed gastric cancer (GC) or dysplasia, four patients were 'misclassified' based on MAPS-2012 and three on MAPS-2019 and BSG. By performing one additional endoscopy 72.9% (95% CI 62.4–83.3) of high-risk patients and all patients who developed GC or dysplasia were identified. Conclusion: One-third of patients that would have been discharged from GC surveillance, appeared to be 'misclassified' as low risk. One additional endoscopy will reduce this risk by 70%. [ABSTRACT FROM AUTHOR]

Background and Aims: The causes for the occurrence of goblet cells at the gastroesophageal junction (GEJ-GC) are unknown. The aim of our study was to compare the concurrent histologic changes of the stomach in (1) patients with GEJ-GC, but without Barrett's esophagus (BE) to those in (2) patients with BE and in (3) controls without GEJ-GC or BE.Methods: We used an electronic database of histopathologic records from 1.3 million individual patients, who underwent esophago-gastro-duodenoscopy (EGD) in 2009-2018. We compared the prevalence of Helicobacter pylori-positive gastritis (HpG), gastric intestinal metaplasia (G-IM), chronic inactive gastritis (CIG), and reactive gastropathy (RG) among the 3 patient groups, using odds ratios and their 95% confidence intervals.Results: Of all EGD patients, 4.0% harbored BE and 2.4% GEJ-GC. The average age of patients with GEJ-GC (60 ± 14) was significantly younger than the age of patients with BE (63 ± 12) and significantly older than the age of controls (55 ± 17). Female subjects were more common among GEJ-GC (54%) than BE (37%), but less common than among controls (63%). The 3 gastric histopathology changes associated with H. pylori were significantly more common in GEJ-GC than BE (for HpG 2.42, 2.29-2.56; for G-IM 1.82, 1.73-1.92; for CIG 1.31, 1.22-1.41). The corresponding differences between GEJ-GC and controls were less striking (for HpG 0.97, 0.93-1.01; for G-IM 1.15, 1.11-1.19; for CIG 0.90, 0.85-0.95). RG was slightly less common in GEJ-GC than BE (0.89, 0.86-0.92) and controls (0.94, 0.91-0.96).Conclusions: With respect to its demographic and histopathologic features, GEJ-GC likely represents gastric intestinal metaplasia as opposed to BE and should prompt gastric intestinal metaplasia screening and management. [ABSTRACT FROM AUTHOR]

Objective: To identify whether bile reflux on endoscopy and other related variables are risk factors for precancerous gastric lesions and gastric cancer (GC). Methods: A multicenter, cross‐sectional and observational study was conducted in five centers in China from June to October 2019, 1162 patients were recruited and divided into the chronic gastritis (CG), the precancerous lesion (low‐grade intraepithelial neoplasia and intestinal metaplasia), and GC groups (including high‐grade intraepithelial neoplasia). All participants underwent detailed interviews, endoscopy and biopsy, and completed questionnaires. Odds ratio and 95% confidence interval were calculated with multivariate logistic regression models with or without adjustment for Helicobacter pylori infection. Results: We recruited 668 patients with CG, 411 with precancerous lesions and 83 with GC. By comparing the CG and precancerous lesion groups, independent risk factors for cancerous gastric lesions were the grade of bile reflux, patient's age, dietary habits and family history of GC. Similar results were obtained when comparing the CG and GC groups. In addition, bile reflux was confirmed as an independent risk factor for progression from precancerous lesions to cancer. Conclusions: Bile reflux on endoscopy as well as age, dietary habits and a family history of GC were independent risk factors for the development of precancerous gastric lesions and GC. [ABSTRACT FROM AUTHOR]

Copyright of Turkiye Klinikleri Journal of Internal Medicine / Türkiye Klinikleri İç Hastalıkları Dergisi is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Helicobacter pylori infection changes gastric microbiota profiles. However, it is not clear whether H. pylori eradication can restore the healthy gastric microbiota. Moreover, there has been no study regarding the changes in gastric microbiota with aging. The objective of this study was to investigate the changes in gastric corpus microbiota with age and following H. pylori eradication. Changes in corpus mucosa-associated microbiota were evaluated in 43 individuals with endoscopic follow-up > 1 year, including 8 H. pylori-uninfected and 15 H. pylori-infected subjects with no atrophy/metaplasia by histology and pepsinogen I/II ratio > 4.0; 17 H. pylori-infected subjects with atrophy/metaplasia and pepsinogen I/II ratio < 2.5; and 3 subjects with atrophy/metaplasia, no evidence of active H. pylori infection, negative for anti-H. pylori immunoglobulin G (IgG) antibody testing, and no previous history of H. pylori eradication. Successful H. pylori eradication was achieved in 21 patients. The gastric microbiota was characterized using an Illumina MiSeq platform targeting 16S ribosomal DNA (rDNA). The mean follow-up duration was 57.4 months (range, 12–145 months), and median follow-up visit was 1 (range, 1–3). Relative abundance of Lactobacillales and Streptococcus was increased with atrophy/metaplasia. In H. pylori-uninfected subjects (n = 8), an increase in Proteobacteria (Enhydrobacter, Comamonadaceae, Sphingobium); a decrease in Firmicutes (Streptococcus, Veillonella), Fusobacteria (Fusobacterium), Nocardioidaceae, Rothia, and Prevotella; and a decrease in microbial diversity were observed during the follow-up (p trend < 0.05). In 10 of 21 subjects (47.6%), H. pylori eradication induced restoration of microbial diversity; however, a predominance of Acinetobacter with a decrease in microbial diversity occurred in 11 subjects (52.3%). The presence of atrophy/metaplasia at baseline and higher neutrophil infiltration in the corpus were associated with the restoration of gastric microbiota after successful eradication, whereas a higher relative abundance of Acinetobacter at baseline was associated with the predominance of Acinetobacter after H. pylori eradication (p < 0.05). To conclude, in H. pylori-uninfected stomach, relative abundance of Proteobacteria increases, relative abundance of Firmicutes and Fusobacteria decreases, and microbial diversity decreases with aging. H. pylori eradication does not always restore gastric microbiota; in some individuals, gastric colonization by Acinetobacter species occurs after anti-Helicobacter treatment.

Background: Stomach diseases are an important sector of gastroenterology, including proliferative benign; premalignant; and malignant pathologies of the gastric mucosa, such as gastritis, hyperplastic polyps, metaplasia, dysplasia, and adenocarcinoma. There are data showing quantitative changes in chaperone system (CS) components in inflammatory pathologies and tumorigenesis, but their roles are poorly understood, and information pertaining to the stomach is scarce. Here, we report our findings on one CS component, the chaperone Hsp60, which we studied first considering its essential functions inside and outside mitochondria. Methods: We performed immunohistochemical experiments for Hsp60 in different samples of gastric mucosa. Results: The data obtained by quantitative analysis showed that the average percentages of Hsp60 were of 32.8 in normal mucosa; 33.5 in mild-to-moderate gastritis; 51.8 in severe gastritis; 58.5 in hyperplastic polyps; 67.0 in intestinal metaplasia; 89.4 in gastric dysplasia; and 92.5 in adenocarcinomas. Noteworthy were: (i) the difference between dysplasia and adenocarcinoma with the other pathologies; (ii) the progressive increase in Hsp60 from gastritis to hyperplastic polyp, gastric dysplasia, and gastric carcinoma; and (iii) the correlation of Hsp60 levels with histological patterns of cell proliferation and, especially, with tissue malignancy grades. Conclusions: This trend likely reflects the mounting need for cells for Hsp60 as they progress toward malignancy and is a useful indicator in differential diagnosis, as well as the call for research on the mechanisms underpinning the increase in Hsp60 and its possible roles in carcinogenesis. [ABSTRACT FROM AUTHOR]

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 < 0.05), group II (by 3.6 times, p < 0.05) and group III (by 3.4 times, p < 0.05). According to the results of the Kruskal Wallis test, the probability of a difference in the IL-8 level between the groups was 0.0260. The level of VEGF in the blood serum of patients with gastric mucosal dysplasia was significantly increased compared to that in people with gastric mucosal atrophy without IM (by 1.8 times, p < 0.05) and those with gastric mucosal atrophy with IM (by 1.7 times, p < 0.05). Changes in the cytokine balance towards proinflammatory cytokines were most pronounced in patients of groups III and IV; according to the results of the Kruskal Wallis test, the probability of a difference in the IL-8/IL-10 ratio between the groups was 0.0207. Conclusions. With the progression of structural changes in the gastric mucosa of patients with atrophic gastritis, an increase in the level of proinflammatory cytokines (IL-8, IL-18 and TNF-α) in the blood serum does not induce the secretion of anti-inflammatory cytokines (IL-10). According to the results of the ROC analysis, the diagnostic criteria for the formation of the risk group for detecting dysplastic changes in the gastric mucosa are VEGF level of more than 341.4 mU/ml (sensitivity — 90.0 %, specificity — 77.2 %) and the level of ILL-8 above 14.4 pg/ml (sensitivity — 80.0 %, specificity — 78.3 %). [ABSTRACT FROM AUTHOR]