Gastric Corpus Research Articles

The Effect of Dried Amnion Membrane Application in the Expression of Platelet Derived Growth Factors in the Healing Process of Stomach Stab Wound (Study on New Zealand Rabbit)

Background: Management of penetrating abdominal trauma, especially those affecting the stomach, keepsdeveloping. Although the technology in the field of surgery is getting more advanced, the risk of complications dueto leakage is still common. A lot of research is being done to improve the tissue healing process, including a varietyof surgical techniques and material uses. The amniotic membrane is a material that is widely used to help stimulatethe healing process. The amniotic membrane contains growth factors, one of which is platelet-derived growth factor(PDGF). PDGF is a major player in the wound healing process.Purpose: To investigate the differences in PDGF levels in gastric rupture repair with dry amniotic membrane asa biological dressing compared to primary repair of gastric rupture without using dry amniotic membrane.Method: This research was an experimental analytical study, using 42 samples of rabbits which were groupedinto 2 groups, namely the control and treatment groups. Stab wound of 2 cm by 0.5 cm wide with a depth entire gastricwall in gastric corpus was done and repaired with 4-6 interrupted suture using 5/0 polypropylene monofilament. Inthe control group, the wound was only sutured and the treatment group, dry amniotic membrane was applicatedbefore suturing. The expression of PDGF was examined from the suture tissue on day-7.Result: Intensity score was obtained in the treatment group with the highest score of 2 with a sample of 11(52.4%) as well as in the control group as many as 13 (61.9%) samples who had a score of 2. The extensionscore was obtained in the treatment group with the highest score of 1 with a total sample size of 10 (47.6%)while the control group had the highest score with a score of 0.5 as much as 14 (66.7%). After obtaining thePDGF intensity and extension values, then these two values are multiplied to get the PDGF expression. Fromthe results of the comparison test using the Mann Whitney test, it was found that the difference in PDGFexpression was significant between the treatment group and the control group with p = 0.008 (p <0.05).Conclusion: Applying dry amniotic membrane to the wound on the stomach will increase the expression ofPDGF in the wound area.

A novel method of grading gastric intestinal metaplasia based on the combination of subtype and distribution

BackgroundStudies have shown the value of subtypes and distribution of gastric intestinal metaplasia (GIM) for prediction of gastric cancer. We aim to combine GIM subtypes and distribution to form a new scoring system for GIM.MethodsThis was a cross-sectional study. No GIM, type I, II, and III GIM of gastric antrum and corpus scored 0–3 points respectively. Then the severity of the whole stomach was calculated in two ways: 1. The gastric antrum and corpus scores were added together, with a score ranging from 0 to 6, which named “Subtype Distribution Score of Gastric Intestinal Metaplasia (SDSGIM)”. 2. Direct classification according to a table corresponding to that of OLGIM. We compared the SDSGIM among benign lesions, dysplasia, and cancer and drew receiver operating characteristic (ROC) curve to determine the optimal cut-off value. According to the cut-off value and the classification from the table, the predictive ability of these two methods were calculated.Results227 patients were included. For SDSGIM, benign lesion group was significantly different from dysplasia or cancer group. Area under curve of ROC curve was 0.889 ± 0.023. The optimal cut-off value was 3. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of SDSGIM for malignancy were 89.5%, 78.0%, 74.6%, 91.2% and 82.8%. And those for the second classification method were 84.2%, 82.6%, 77.7%, 87.9%, and 83.3% respectively.ConclusionsThis study firstly combined GIM subtypes with its distribution forming a novel scoring system, which showed high prediction accuracy for malignant lesions.

Gastric Metabolomics Detects Helicobacter pylori Correlated Loss of Numerous Metabolites in Both the Corpus and Antrum.

Helicobacter pylori is a chronic bacterial pathogen that thrives in several regions of the stomach, causing inflammation that can vary by site and result in distinct disease outcomes. Whether the regions differ in terms of host-derived metabolites is not known. We thus characterized the regional variation of the metabolomes of mouse gastric corpus and antrum organoids and tissue. The uninfected secreted organoid metabolites differed between the corpus and antrum in only seven metabolites as follows: lactic acid, malic acid, phosphoethanolamine, alanine, uridine, glycerol, and isoleucine. Several of the secreted chemicals were depleted upon H. pylori infection in both regions, including urea, cholesterol, glutamine, fumaric acid, lactic acid, citric acid, malic acid, and multiple nonessential amino acids. These results suggest a model in which H. pylori preferentially uses carboxylic acids and amino acids in complex environments, and these are found in both the corpus and antrum. When organoid metabolites were compared to mouse tissue, there was little overlap. The tissue corpus and antrum metabolomes were distinct, including antrum-elevated 5-methoxytryptamine, lactic acid, and caprylic acid, and corpus-elevated phospholipid products. The corpus and antrum remained distinct over an 8-month infection time course. The antrum displayed no significant changes between the time points in contrast to the corpus, which exhibited metabolite changes that were consistent with stress, tissue damage, and depletion of key nutrients, such as glutamine and fructose-6-phosphate. Overall, our results suggest that the corpus and antrum have largely but not completely overlapping metabolomes that change moderately upon H. pylori infection.

Immunohistochemical differences in gastric mucosal damage between nodular and non-nodular gastritis caused by Helicobacter pylori infection.

In this study, the level of cell damage were analyzed immuno­histochemically to clarify the association between nodular gastritis and undifferentiated gastric cancer. Thirty patients of nodular gastritis were enrolled as the nodular gastritis group. Thirty patients of non-nodular gastritis were enrolled as the control group. They were evaluated according to the updated Sydney system and used for immunohistochemical staining (p53, Ki-67, E-cadherin, and 8-OHdG). The scores based on the updated Sydney system were significantly higher in the nodular group than in the non-nodular group for histologically assessed inflammation and activity in the gastric corpus (1.91 ± 0.77 vs 1.58 ± 0.60, p = 0.049, 0.83 ± 0.81 vs 0.44 ± 0.64, p = 0.032). On immunostaining, the detection of E-cadherin was lower in the nodular group for both the antrum (1.0 ± 0.62 vs 1.47 ± 0.85, p = 0.047) and the corpus (1.16 ± 0.81 vs 1.48 ± 0.71, p = 0.043) and the p53 labeling index of the gastric corpus was higher in the nodular group than in the non-nodular group (3.06 ± 1.94 vs 2.03 ± 1.99, p = 0.015). Nodular gastritis showed significant severe inflammation and immunohistochemical cell damage compared with non-nodular gastritis. These findings may play an important role in the oncogenesis of undifferentiated gastric cancer in nodular gastritis.

Helicobacter pylori and association between its positivity and anatomotopographic settlement in the stomach with the host age range.

Helicobacter pylori (H. pylori) is a Gram-negative, helically shaped flagellated bacterium. Major diseases associated with H. pylori infection include peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. The incidence of H. pylori in the anatomotopographic regions of the stomach, such as antrum, corpus, fundus, and incisura angularis, has been investigated. Do the rates of H. pylori in the settlements change over time according to the age ranges of the hosts? Does this change affect the diseases caused by or related to H. pylori? It is estimated that the outcomes, which have been obtained, may provide a new perspective in terms of understanding the etiopathogenesis of H. pylori-induced diseases. A comprehensive literature search of PubMed/MEDLINE databases had been conducted using a combination of terms, “Helicobacter pylori,” “Sydney System,” “stomach,” “pyloric antrum,” “gastric corpus,” “stomach cancer,” and “Helicobacter pylori and age.” There are very few articles examining the relationship between the topographic locations of H. pylori and host age range in the English language literature. Therefore, it is also purposed to emphasize the outcomes of our current research about the mentioned topic. In our opinion, similar studies should reveal the settlement and age range in the different geographic locations and societies as in our study. We believe that these findings will contribute to the efforts for understanding overtly of H. pylori-induced disease of the stomach.

Differences in image-enhanced endoscopic findings between Helicobacter pylori -associated and autoimmune gastritis.

Background and study aims The aim of this study was to elucidate the differences in image-enhanced endoscopy (IEE) findings between Helicobacter - pylori -associated and autoimmune gastritis. Patients and methods Seven H. pylori -naïve, 21 patients with H. pylori -associated gastritis and seven with autoimmune gastritis were enrolled. Mucosal atrophy in the corpus was evaluated using autofluorescence imaging and classified into small, medium and large. In a 2 × 2-cm area of the lesser curvature of the lower corpus, micromucosal pattern was evaluated by magnifying narrow band imaging and proportion of foveola (FV)- and groove (GR)-type mucosa was classified into FV > 80 %, FV 50 % to 80 %, GR 50 % to 80 %, and GR > 80 %, then a biopsy specimen was taken. Results Fifteen of 21 (71 %) H. pylori -associated gastritis patients exhibited medium-to-large atrophic mucosa at the corpus lesser curvature. All autoimmune gastritis patients had large atrophic mucosa throughout the corpus ( P < 0.001). All H. pylori -naïve patients had the FV > 80 % micromucosal pattern. Nineteen of 21 (90 %) H. pylori -associated gastritis patients had varying proportions of GR- and FV-type mucosae and five of seven (71 %) autoimmune gastritis patients showed FV > 80 % mucosa ( P < 0.001). Compared with patients who were H. pylori -naïve, patients with H. pylori -associated and autoimmune gastritis exhibited a higher grade of atrophy ( P < 0.001), but only patients with H. pylori -associated gastritis showed a higher grade of intestinal metaplasia ( P = 0.022). Large mucosal atrophy with FV > 80 % micromucosal pattern had sensitivity of 71 % (95 % CI: 29 %–96 %) and specificity of 100 % (95 % CI: 88 % to 100 %) for diagnosis of autoimmune gastritis. Conclusions IEE findings of the gastric corpus differed between H. pylori -associated and autoimmune gastritis, suggesting different pathogenesis of the two diseases.

Gastric foveolar elongation causes invisibility of regular arrangement of collecting venules in chronic active and inactive gastritis.

Helicobacter pylori (H pylori) infection is the most common cause of gastritis. The disappearance of regular arrangement of collecting venules (RAC) is well known as one of the main manifestations of H pylori-affected gastritis while the reason behind it remains obscure. The aim of this study was to investigate the relationship between invisibility of RAC and the length of gastric foveolae. 43 RAC-positive and 118 RAC-negative patients were enrolled. Gastric biopsy specimens were obtained from lesser and greater curvature of the corpus with RAC-positive or RAC-negative pattern. Histopathological evaluation was performed based on the updated Sydney System, and foveolar length was derived by a morphometric technique. The median gastric foveolar length in RAC-positive group (median [IQR], 138.54μm [120.50, 159.09]) was significantly shorter than that in the RAC-negative group (median [IQR], 260.96μm [217.40, 315.23], P<.05). The length of gastric foveolae in chronic active gastritis (RAC-negative, activity grades 1, 2, and 3) and inactive gastritis (RAC-negative, activity grade 0) was longer than that in normal group (RAC-positive, activity grade 0) (P<.05). The optimal cutoff value for gastric foveolae length of the corpus mucosa showing RAC-negative pattern was more than 181.53μm. The sensitivity and specificity of more than cutoff value for predicting the invisibility of RAC were 93.03% and 91.78%, respectively. The elongation of gastric foveolae caused the invisibility of RAC in gastric corpus mucosa in chronic active and inactive gastritis on gastroendoscopy.

Stimulation of Gastric Transit Function Driven by Hydrolyzed Casein Increases Small Intestinal Carbohydrate Availability and Its Microbial Metabolism.

Gastrointestinal (GI) functions affect gut nutrient flow and microbial metabolism. Dietary peptides modulate GI functions and improve small intestinal health, but the mechanism remains elusive. This study aims to investigate whether dietary peptides affect small intestinal microbial metabolism, and the underlying mechanisms. An ileal-cannulated pig model is adopted to explore the relationship between gut nutrient flow and microbial metabolism after treatment with hydrolyzed casein (peptides) or intact casein (Control)-based diet. The results demonstrate that hydrolyzed casein enhances microbial carbohydrate metabolism with higher Streptococcus abundance and higher lactate level in the ileum. Meanwhile, hydrolyzed casein increases ileal flows of nutrients, especially carbohydrate, leading to a higher carbohydrate availability in ileal digesta. To unveil the mechanisms, it is found that the hydrolyzed casein enhances the ghrelin signal and improves development of interstitial cells of Cajal and muscular layer in gastric corpus, indicating the enhanced upper GI transit function. In addition, hydrolyzed casein improves small intestinal health, as indicated by higher villus heights and luminal lactate concentrations in the jejunum and ileum. In conclusion, hydrolyzed casein stimulates upper GI transit function, enhances gut nutrient flow, and increases small intestinal carbohydrate availability and its microbial metabolism, which favor the small intestinal health.

S1330 High Discovery Rate of Previously Undiagnosed Patients With Eosinophilic Gastritis and Duodenitis Using a Systematic Endoscopic Biopsy Protocol: Screening Data Analysis From ENIGMA, a Randomized Controlled Trial

INTRODUCTION: Eosinophilic gastrointestinal (GI) disorders (EGIDs) such as eosinophilic gastritis (EG) and duodenitis (EoD) are chronic inflammatory conditions characterized by aberrant accumulation and activation of localized tissue eosinophils and mast cells. Patients (pts) with EG/EoD present with non-specific, often debilitating GI symptoms including abdominal pain and cramping, early satiety, nausea and diarrhea. Non-specific symptoms, the absence of consensus diagnostic histopathologic guidelines, and the perception of rarity contribute to a delay in diagnosis of pts with EG/EoD. While the prevalence of EG/EoD is currently estimated to be ∼50,000 in the US, this may be an underestimate. We aimed to evaluate the prevalence of EG/EoD among symptomatic patients not previously diagnosed. METHODS: We reviewed screening data from ENIGMA, a multi-center, randomized, double-blind, placebo-controlled phase 2 trial assessing the safety and efficacy of AK002, an anti-Siglec-8 monoclonal antibody, in pts with EG/EoD. Adult pts were screened with a validated, daily 8-symptom EG/EoD questionnaire to capture moderate-severely symptomatic pts. Those who met symptom inclusion criteria underwent upper endoscopy (EGD) with gastric and duodenal biopsies as per protocol (12 total: 4 biopsies each from the gastric antrum, gastric corpus, and duodenum). Symptomatic pts meeting histologic definition of EG (≥30 eos/hpf in ≥5 hpfs) and/or EoD (≥30 eos/hpf in ≥3hpfs) were eligible for randomization. RESULTS: 113 pts entered screening for ENIGMA. 51 had no prior history of EG/EoD, 26 (51%) of whom met symptom criteria and underwent screening endoscopy. Of these 26 symptomatic pts, 15 (58%) met histologic criteria for EG/EoD, 13 of whom were randomized in the study. These 13 pts, previously given functional GI diagnoses, were clinically similar in constellation and magnitude of symptoms compared to the 52 randomized pts with previously established EG/EoD. CONCLUSION: There is growing evidence that EG/EoD is underdiagnosed, and that the true US prevalence may be higher than 50,000. Among moderate-severely symptomatic pts without known history of EG/EoD who entered screening for ENIGMA, 58% met histologic criteria for EG/EoD. EGD with multiple systematic gastric and duodenal biopsies of pts with chronic non-specific GI symptoms, including those with functional GI conditions, may demonstrate a higher prevalence of EG/EoD than is currently estimated.Figure 1.: Discovery Rate of Newly Diagnosed EG/EoD Patients in ENIGMA Screening 1) Consortium of Eosinophilic Gastrointestinal disease Researchers (CEGIR) sites; n = 62 entered screening 2) Primarily general gastrointestinal practices and professional GI research centers; n = 51 entered screening.Figure 2.: Similar Symptom Burden in Established and Newly Diagnosed EG/EoD Patients.Table 1.: Characteristics of Established and Newly Diagnosed EG/EoD Patients

S2948 Long-Term Proton Pump Inhibitor-Induced Gastric Microcystic Glandular Changes Leading to Gastric Wall Thickening

INTRODUCTION: Long term (LT) proton pump inhibitor (PPI) induced gastric microcystic glandular mucosal changes could lead to significant gastric wall thickening which must be further evaluated to exclude underlying neoplastic process. CASE DESCRIPTION/METHODS: An 81-year-old male with GERD and Barrett’s esophagus (BE) on chronic omeprazole 40mg BID was evaluated by endoscopic ultrasound (EUS) for 1cm gastroesophageal junction (GEJ) sub epithelial lesion (SEL) seen on EGD and thickened gastric mucosa (2.6 cm) normalizing just proximal to GEJ identified on an otherwise negative CT abdomen done to evaluate for epigastric pain. EGD showed irregular carpet-like thickened gastric folds with cobble stoning sparing the gastric antrum. EUS showed a small cystic SEL at GEJ and marked diffuse thickening of gastric body mucosa (16 mm) with intact muscularis propria and absence of regional lymphadenopathy. Endoscopic biopsies revealed no H. pylori but gastric mucosa with microcystic glandular changes consistent with gastric mucosal trophic changes secondary to chronic PPI use. Due to BE however, patient was continued on PPI. DISCUSSION: PPIs remain the cornerstone for GERD treatment. Adverse effects from inappropriate PPI use are more clinically manifested in the elderly population. These include drug-drug interactions and increased risk of LT PPI adverse effects on digestive and extra-digestive organs (such as dementia, decreased bone density, and community acquired pneumonia). LT PPI use can lead to fundic gland polyp formation, small intestinal bacterial overgrowth, and collagenous colitis. Gastric trophic changes were found to occur secondary to LT PPI use in the form of parietal cell protrusion into the gastric lumen and fundic gland polyp formation resulting from increased serum gastrin level. Hypertrophic changes due to LT PPI induce gastric mucosal changes that can be appreciated endoscopically as gastric cobblestone-like lesions (GCLL). Sparing of the antrum in our patient of such changes can be explained by parietal cells being anatomically present in gastric fundic glands located primarily in the gastric fundus and body. Histopathology of gastric biopsies in these cases show fundic microcystic glandular change, parietal cell hyperplasia, and cytoplasmic vacuolation. A gastroenterologist should be familiar with such changes due to LT PPI use and, yet, must biopsy the gastric mucosa to exclude any underlying gastric infiltrative and neoplastic process.Figure 1.: Endoscopic view of gastric corpus showing thickened folds, carpet like polypoid lesions.Figure 2.: Radial EUS showing markedly thickened gastric mucosa and intact muscularis propria.Figure 3.: Histopathology of gastric corpus biopsies showing microcystic glandular conformation.

Helicobacter pylori-negative Gastric Cancer

&lt;i&gt;Helicobacter pylori (H. pylori)&lt;/i&gt;-negative gastric cancer is diagnosed when gastric malignancies are found in patients in &lt;i&gt;H. pylori&lt;/i&gt;-naïve stomachs. There are four types of noncardiac &lt;i&gt;H. pylori&lt;/i&gt;-negative gastric cancers. The signet ring cell-type poorly cohesive carcinoma is most common, followed by the chief cell-predominant type gastric adenocarcinoma of the fundic gland. Extremely well-differentiated adenocarcinoma of the corpus and well-differentiated pyloric gland cancers are rare outside Japan because of country-specific differences in diagnostic criteria. In endemic areas of &lt;i&gt;H. pylori&lt;/i&gt; infection, strict criteria are required for diagnosing an &lt;i&gt;H. pylori&lt;/i&gt;-naïve stomach. Both invasive and noninvasive &lt;i&gt;H. pylori&lt;/i&gt; tests should show negative results in a subject without a history of &lt;i&gt;H. pylori&lt;/i&gt; infection. Furthermore, the serum pepsinogen (PG) assay and endoscopic findings of the background gastric mucosa are required to discriminate subjects with past infections owing to spontaneous regression or unintended eradication of &lt;i&gt;H. pylori&lt;/i&gt;. There should be no gastric corpus atrophy (PG I ≤70 ng/mL and PG I/II ≤3.0). Gastroscopy should reveal a regular arrangement of collecting venules without gastric xanthoma, metaplastic gastritis, or advanced atrophy over the angle. On biopsy, there should be no gastric atrophy, intestinal metaplasia, neutrophils, or &lt;i&gt;H. pylori&lt;/i&gt; infiltration, and only a mild degree of mononuclear cell infiltration is permitted. The types and characteristics of noncardiac &lt;i&gt;H. pylori&lt;/i&gt;-negative gastric cancers are summarized in this review, along with current diagnostic challenges found in Korea.

Single-Cell Transcriptional Analyses Identify Lineage-Specific Epithelial Responses to Inflammation and Metaplastic Development in the Gastric Corpus

Chronic atrophic gastritis can lead to gastric metaplasia and increase risk of gastric adenocarcinoma. Metaplasia is a precancerous lesion associated with an increased risk for carcinogenesis, but the mechanism(s) by which inflammation induces metaplasia are poorly understood. We investigated transcriptional programs in mucous neck cells and chief cells as they progress to metaplasia mice with chronic gastritis. We analyzed previously generated single-cell RNA-sequencing (scRNA-seq) data of gastric corpus epithelium to define transcriptomes of individual epithelial cells from healthy BALB/c mice (controls) and TxA23 mice, which have chronically inflamed stomachs with metaplasia. Chronic gastritis was induced in B6 mice by Helicobacter pylori infection. Gastric tissues from mice and human patients were analyzed by immunofluorescence to verify findings at the protein level. Pseudotime trajectory analysis of scRNA-seq data was used to predict differentiation of normal gastric epithelium to metaplastic epithelium in chronically inflamed stomachs. Analyses of gastric epithelial transcriptomes revealed that gastrokine 3 (Gkn3) mRNA is a specific marker of mouse gastric corpus metaplasia (spasmolytic polypeptide expressing metaplasia, SPEM). Gkn3 mRNA was undetectable in healthy gastric corpus; its expression in chronically inflamed stomachs (from TxA23 mice and mice with Helicobacter pylori infection) identified more metaplastic cells throughout the corpus than previously recognized. Staining of healthy and diseased human gastric tissue samples paralleled these results. Although mucous neck cells and chief cells from healthy stomachs each had distinct transcriptomes, in chronically inflamed stomachs, these cells had distinct transcription patterns that converged upon a pre-metaplastic pattern, which lacked the metaplasia-associated transcripts. Finally, pseudotime trajectory analysis confirmed the convergence of mucous neck cells and chief cells into a pre-metaplastic phenotype that ultimately progressed to metaplasia. In analyses of tissues from chronically inflamed stomachs of mice and humans, we expanded the definition of gastric metaplasia to include Gkn3 mRNA and GKN3-positive cells in the corpus, allowing a more accurate assessment of SPEM. Under conditions of chronic inflammation, chief cells and mucous neck cells are plastic and converge into a pre-metaplastic cell type that progresses to metaplasia.

A modified Sydney system for the diagnosis of chronic gastritis in dogs

BackgroundThe Sydney system for assessing inflammatory lesions in the gastric mucosa is based on endoscopic and histological examinations. This study aimed to apply the Sydney system to diagnose gastritis in dogs. The study also compared the results of endoscopic and histological examinations conducted on gastric mucosal biopsy specimens. A total of 56 dogs with chronic vomiting were analyzed in the study. The physical appearance of the gastric mucosa was assessed through endoscopic examination, while the severity of the gastric inflammation, inflammation activity, glandular atrophy, and intestinal metaplasia were assessed by histopathological examination.ResultsThe endoscopic examination confirmed the presence of inflammatory lesions affecting the gastric corpus and pylorus in all the dogs, although the severity of these lesions differed between the individuals. Reflux gastritis was the most commonly observed gastric inflammation. In the histopathological examination of the gastric mucosal samples, inflammatory lesions were found in the gastric corpus of 53 dogs, while 55 dogs had lesions in the pylorus. This corresponds to a 96.4% agreement between the methods.ConclusionsThe Sydney system is a useful tool for macroscopic and microscopic assessment of changes in the gastric mucosa as it enables the determination of inflammation type and severity, which helps the canine gastroenterologists to reliably compare the results of the tests performed in different facilities. Besides, the use of the Sydney system in diagnosing lesions facilitates the selection and effective monitoring of treatment. However, despite a high rate of agreement between the results of endoscopic and histopathological examinations, it is recommended to use both these methods for the assessment of the gastric mucosa in dogs.

Upregulation of the TRPA1 Ion Channel in the Gastric Mucosa after Iodoacetamide-Induced Gastritis in Rats: A Potential New Therapeutic Target.

Acute gastritis is often untreatable by acid secretion-inhibiting drugs. Understanding the protective mechanisms including the role of Transient Receptor Potential Ankyrin1 (TRPA1) and Vanilloid1 (TRPV1) channels localized on capsaicin-sensitive afferents and non-neuronal structures might identify novel therapeutic approaches. Therefore, we characterized a translational gastritis model using iodoacetamide (IAA) and investigated TRPA1/V1 expressions. Wistar rats and CD1, C57Bl/6J mice were exposed to IAA-containing (0.05, 0.1, 0.2, 0.3, 0.5%) drinking water for 7 or 14 days. Body weight and water consumption were recorded daily. Macroscopic lesions were scored, qualitative histopathologic investigation was performed, TRPA1/V1 immunopositivity and mRNA expressions were measured. IAA induced a concentration-dependent weight loss and reduced water intake in both species. Hyperemia, submucosal edema, inflammatory infiltration and hemorrhagic erosions developed after 7 days, while ulcers after 14 days in rats. Trpa1 mRNA/protein expressions were upregulated at both timepoints. Meanwhile, TRPV1 immunopositivity was upregulated in the gastric corpus after 0.05% IAA ingestion, but downregulated after 0.2%, whereas Trpv1 mRNA did not change. Interestingly, no macroscopic/microscopic changes were observed in mice. These are the first data for the concentration- and duration-dependent changes in the IAA-induced gastritis in rats accompanied by TRPA1 upregulation, therefore, its therapeutic potential in gastritis should further be investigated.

Helicobacter pylori Eradication Induced Constant Decrease in Interleukin- 1B Expression over More Than 5 Years in Patients with Gastric Cancer and Dysplasia.

Background/AimsHelicobacter pylori (Hp) suppresses gastric acid secretion by repressing the expression of the H+, K+-adenosine triphosphatase (H+, K+-ATPase) and stimulating interleukin-1 (IL-1β; encoded by IL-1B). This study was aimed at evaluating the expression of the H+, K+-ATPase and IL-1β after Hp eradication.MethodsTwo hundred twenty-one subjects were categorized as Hp-negative (n=84) or Hp-positive (n=137) according to the results of Hp tests (histology, CLO test, culturing, and serology). The mRNA expression levels of IL-1B and ATP4A (the gene encoding the α-subunit of H+, K+-ATPase) were measured in biopsy specimens from the gastric corpus using real-time polymerase chain reaction.ResultsThe Hp-positive group had significantly higher IL-1B mRNA levels than the whole Hp-negative group and the intestinal metaplasia (IM)-negative subgroup. After Hp eradication, the difference between the Hp-negative and Hp-eradicated groups disappeared, including in the IM-negative subgroup. The IL-1B mRNA level did not significantly change from the baseline level. Within the gastric cancer (GC)/dysplasia subgroup, the IL-1B mRNA levels at 1, 2, 3–4, and ≥5 years after Hp eradication were significantly lower than the baseline level. The difference in ATP4A mRNA levels between the Hp-negative and Hp-positive groups was not significant at baseline, and the changes in the ATP4A mRNA levels after Hp eradication compared to the baseline levels in the whole group and subgroups stratified by the presence of IM and GC/dysplasia were not significant.ConclusionsInfection with Hp has an effect on the level of IL-1B mRNA in IM-negative subjects. The continuous reduction in the IL-1B mRNA level in patients with GC/dysplasia after Hp eradication contributes to the prevention of metachronous GC after Hp eradication.

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

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

Nutrient-sensing components of the mouse stomach and the gastric ghrelin cell.

The ability of the gut to detect nutrients is critical to the regulation of gut hormone secretion, food intake, and postprandial blood glucose control. Ingested nutrients are detected by specific gut chemosensors. However, knowledge of these chemosensors has primarily been derived from the intestine, while available information on gastric chemosensors is limited. This study aimed to investigate the nutrient-sensing repertoire of the mouse stomach with particular emphasis on ghrelin cells. Quantitative RT-PCR was used to determine mRNA levels of nutrient chemosensors (protein: G protein-coupled receptor 93 [GPR93], calcium-sensing receptor [CaSR], metabotropic glutamate receptor type 4 [mGluR4]; fatty acids: CD36, FFAR2&4; sweet/umami taste: T1R3), taste transduction components (TRPM5, GNAT2&3), and ghrelin and ghrelin-processing enzymes (PC1/3, ghrelin O-acyltransferase [GOAT]) in the gastric corpus and antrum of adult male C57BL/6 mice. Immunohistochemistry was performed to assess protein expression of chemosensors (GPR93, T1R3, CD36, and FFAR4) and their co-localization with ghrelin. Most nutrient chemosensors had higher mRNA levels in the antrum compared to the corpus, except for CD36, GNAT2, ghrelin, and GOAT. Similar regional distribution was observed at the protein level. At least 60% of ghrelin-positive cells expressed T1R3 and FFAR4, and over 80% expressed GPR93 and CD36. The cellular mechanisms for the detection of nutrients are expressed in a region-specific manner in the mouse stomach and gastric ghrelin cells. These gastric nutrient chemosensors may play a role modulating gastrointestinal responses, such as the inhibition of ghrelin secretion following food intake.

Helicobacter pylori Colonization Drives Urokinase Receptor (uPAR) Expression in Murine Gastric Epithelium During Early Pathogenesis.

(1) Background: Persistent Helicobacter pylori infection is the most important risk factor for gastric cancer. The urokinase receptor (uPAR) is upregulated in lesions harboring cancer invasion and inflammation. Circumstantial evidence tends to correlate H. pylori colonization with increased uPAR expression in the human gastric epithelium, but a direct causative link has not yet been established in vivo; (2) Methods: In a mouse model of H. pylori-induced gastritis, we investigated the temporal emergence of uPAR protein expression in the gastric mucosa in response to H. pylori (SS1 strain) infection; (3) Results: We observed intense uPAR immunoreactivity in foveolar epithelial cells of the gastric corpus due to de novo synthesis, compared to non-infected animals. This uPAR induction represents a very early response, but it increases progressively over time as do infiltrating immune cells. Eradication of H. pylori infection by antimicrobial therapy causes a regression of uPAR expression to its physiological baseline levels. Suppression of the inflammatory response by prostaglandin E2 treatment attenuates uPAR expression. Notwithstanding this relationship, H. pylori does induce uPAR expression in vitro in co-cultures with gastric cancer cell lines; (4) Conclusions: We showed that persistent H. pylori colonization is a necessary event for the emergence of a relatively high uPAR protein expression in murine gastric epithelial cells.

THE ROLE OF GASTRIC LOCALIZATION AND THE GASTRITIS SCORE OF HELICOBACTER PYLORI IN THE DEVELOPMENT OF EROSIVE ESOPHAGITIS

Objective: The interactions between Helicobacter pylori (Hp) and gastroesophageal reflux disease (GERD) are a complex issue. The aim of this study was to investigate the correlation between Hp infection and the gastric localization of Hp and reflux esophagitis (RE) in adult patients. Material and Method: Two hundred thirty-nine patients with RE were compared with 229 age and sex matched participants in a control group. Biopsy specimens obtained from the gastric antrum and corpus were histologically evaluated. Results: The prevalence of Hp infection was significantly lower in the patients with RE than in the control group (Odds ratio 1.56, 95% CI 1.08-2.27; p=0.02, p&lt;0.05). Hp colonization in the corpus and gastrit scores in the corpus were significantly lower in the esophagitis group (p=0.01, p&lt;0.05), but there was no significant difference in Hp colonization in the antrum and gastrit scores in the antrum. It was found that Hp colonization and gastrit score in the corpus showed a negative correlation with esophagitis development. Conclusion: This study demonstrated that the prevalence of Hp infection and corpus gastritis score were significantly lower in patients with erosive reflux esophagitis than in the control group. Furthermore, it demonstrated that Hp colonization and corpus gastritis score were negatively correlated with esophagitis development.&nbsp;

A Gastric Cancer Following Sleeve Gastrectomy with Transit Bipartition Surgery

Gastric cancer is still a major cancer worldwide and more than one million cases of gastric cancer are diagnosed each year. It is known that stomach cancer is increasing, especially after surgical interventions to the stomach. Due to obesity and diabetes, the most common diseases of our age, obesity and metabolic surgery have been performed widely in recent years. Here in, It is aimed to report an interesting case of gastric cancer located on the stapler line in a short time after Sleeve Gastrectomy with Transit Bipartition operation. A 60-year-old male patient consulted to the general surgery outpatient clinic with complaints of intermittent epigastric pain and bloating. Sleeve Gastrectomy with Transit Bipartition operation was performed 3 years ago for morbid obesity and Type 2 diabetes. During endoscopy, a mucosal irregularity was detected in the gastric corpus. Histopathological examination of the biopsies revealed mucinous adenocarcinoma (signet ring cell type). Total gastrectomy was performed and the patient was discharged without any problem. We conducted a literature review of the studies published in English on PubMed, Medline and Google Scholarly databases on the development of cancer after Sleeve Gastrectomy with Transit Bipartition operation. Although we found many cases with gastric cancer in the follow-up only after Sleeve Gastrectomy, we did not find any cancer in the follow-up after Sleeve Gastrectomy with Transit Bipartition operation. Due to this feature, this case is the first case reported in the literature. In the postoperative follow-up of patients who have undergone Sleeve Gastrectomy with Transit Bipartition operation, we should be careful about gastric cancer, and we should not refrain from examination on the slightest suspicion.