Frequency of endoscopic findings of equine squamous gastric disease (ESGD) in rural horses and its association with Helicobacter pylori virulence genes

Equine gastric ulcer syndrome (EGUS) is a multifactorial disorder and one of the most common diseases in horses. The objective of this research was to detect one of the potential risk factors of equine squamous gastric disease (ESGD), the Helicobacter pylori specific gene, and tracing the presence of the duodenal ulcer-promoting gene (dupA) as a possible virulence marker. Gastric fluid together with faecal samples were collected from twenty rural horses from around Tabriz, Iran. Throughout the endoscopic examinations, the type, numbers, severity, and the location of the lesions were documented. Nine of twenty horses exhibited macroscopic lesions in the squamous mucosa that were later classified into grades 1, 2, 3, and 4. Only three of these horses exhibited H. pylori in their gastric fluid samples, whereas all faecal samples were H. pylori-negative. All the H. pylori-positive cases manifested severe forms of ESGD (grades 3–4). The age and sex were both unrelated to the lesion severity and ESGD status in this study. Research is required to further discuss the virulence aspects of dupA regarding ESGD.

Alterations in SLC4A2, SLC26A7 and SLC26A9 Drive Acid–Base Imbalance in Gastric Neuroendocrine Tumors and Uncover a Novel Mechanism for a Co-Occurring Polyautoimmune Scenario

Autoimmune polyendocrine syndrome (APS) is assumed to involve an immune system malfunction and entails several autoimmune diseases co-occurring in different tissues of the same patient; however, they are orphans of its accurate diagnosis, as its genetic basis and pathogenic mechanism are not understood. Our previous studies uncovered alterations in the ATPase H+/K+ Transporting Subunit Alpha (ATP4A) proton pump that triggered an internal cell acid–base imbalance, offering an autoimmune scenario for atrophic gastritis and gastric neuroendocrine tumors with secondary autoimmune pathologies. Here, we propose the genetic exploration of APS involving gastric disease to understand the underlying pathogenic mechanism of the polyautoimmune scenario. The whole exome sequencing (WES) study of five autoimmune thyrogastric families uncovered different pathogenic variants in SLC4A2, SLC26A7 and SLC26A9, which cotransport together with ATP4A. Exploratory in vitro studies suggested that the uncovered genes were involved in a pathogenic mechanism based on the alteration of the acid–base balance. Thus, we built a custom gene panel with 12 genes based on the suggested mechanism to evaluate a new series of 69 APS patients. In total, 64 filtered putatively damaging variants in the 12 genes of the panel were found in 54.17% of the studied patients and none of the healthy controls. Our studies reveal a constellation of solute carriers that co-express in the tissues affected with different autoimmune diseases, proposing a unique genetic origin for co-occurring pathologies. These results settle a new-fangled genetics-based mechanism for polyautoimmunity that explains not only gastric disease, but also thyrogastric pathology and disease co-occurrence in APS that are different from clinical incidental findings. This opens a new window leading to the prediction and diagnosis of co-occurring autoimmune diseases and clinical management of patients.

The Involvement of TRIB3 and FABP1 and Their Potential Functions in the Dynamic Process of Gastric Cancer

Background: Dysregulated expression of TRIB3 and FABP1 have been previously observed in human cancer tissues. However, there are little information as to their expression change in dynamic gastric diseases and the functional roles.Methods: Tissues from a total of 479 patients, including 89 GS, 102 IM-GA, 144 EGC, and 144 AGC were collected. The protein expressions of TRIB3 and FABP1 were detected by immunohistochemical staining. Meanwhile, the potential functions of TRIB3 and FABP1 in GC were further analyzed by R software and some internet public databases, such as TCGA and DAVID.Results: During this multi-stage process that go through GS to EGC, the expression trend of TRIB3 and FABP1 protein was GS > IM-GA > EGC. Besides, the expression of TRIB3 protein continued to decrease in AGC, while the expression of FABP1 was abnormally increased. Hp infection was significantly associated with the decreased expression of TRIB3 and FABP1. In addition, the diagnostic efficiency of the combination of these two indicators to diagnose EGC was higher than that of a single indicator. Survival analysis showed that higher expression of TRIB3 or FABP1 could indicate a better prognosis of GC. The protein expressions of TRIB3 and FABP1 were significantly positively correlated. Moreover, CEACAM5 and PRAP1 were positively correlated with both TRIB3 and FABP1 expressions, while GABRP and THBS4 were negatively correlated. The macrophages M0 infiltration was positively correlated with both TRIB3 and FABP1 expressions.Conclusion: The protein expressions of TRIB3 and FABP1 gradually decreased with the gastric disease progress, and was positively correlated. Hp infection may reduce the protein expression of TRIB3 and FABP1. Combing TRIB3 and FABP1 expressions can improve the diagnostic efficiency for EGC. Either a high expression of TRIB3 or FABP1 indicates a better prognosis for GC. TRIB3 and FABP1 may interact with CEACAM5, PRAP1, GABRP and THBS4, and affect tumor immune microenvironment by regulating immune cells, and participate in the development and progression of GC.

Two Distinct Etiologies of Gastric Cancer: Infection and Autoimmunity

Gastric cancer is a leading cause of mortality worldwide. The risk of developing gastric adenocarcinoma, which comprises >90% of gastric cancers, is multifactorial, but most associated with Helicobacter pylori infection. Autoimmune gastritis is a chronic autoinflammatory syndrome where self-reactive immune cells are activated by gastric epithelial cell autoantigens. This cause of gastritis is more so associated with the development of neuroendocrine tumors. However, in both autoimmune and infection-induced gastritis, high risk metaplastic lesions develop within the gastric mucosa. This warrants concern for carcinogenesis in both inflammatory settings. There are many similarities and differences in disease progression between these two etiologies of chronic gastritis. Both diseases have an increased risk of gastric adenocarcinoma development, but each have their own unique comorbidities. Autoimmune gastritis is a primary cause of pernicious anemia, whereas chronic infection typically causes gastrointestinal ulceration. Both immune responses are driven by T cells, primarily CD4+ T cells of the IFN-γ producing, Th1 phenotype. Neutrophilic infiltrates help clear H. pylori infection, but neutrophils are not necessarily recruited in the autoimmune setting. There have also been hypotheses that infection with H. pylori initiates autoimmune gastritis, but the literature is far from definitive with evidence of infection-independent autoimmune gastric disease. Gastric cancer incidence is increasing among young women in the United States, a population at higher risk of developing autoimmune disease, and H. pylori infection rates are falling. Therefore, a better understanding of these two chronic inflammatory diseases is needed to identify their roles in initiating gastric cancer.

CD36 maintains the gastric mucosa and associates with gastric disease

The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd36−/−), with Cd36 deletion in parietal cells (PC-Cd36−/−) or in endothelial cells (EC-Cd36−/−). CD36 expresses on corpus ECs, on PC basolateral membranes, and in gastrin and ghrelin cells. Stomachs of Cd36−/− mice have altered gland organization and secretion, more fibronectin, and inflammation. Tissue respiration and mitochondrial efficiency are reduced. Phospholipids increased and triglycerides decreased. Mucosal repair after injury is impaired in Cd36−/− and EC-Cd36−/−, not in PC-Cd36−/− mice, and is due to defect of progenitor differentiation to PCs, not of progenitor proliferation or mature PC dysfunction. Relevance to humans is explored in the Vanderbilt BioVu using PrediXcan that links genetically-determined gene expression to clinical phenotypes, which associates low CD36 mRNA with gastritis, gastric ulcer, and gastro-intestinal hemorrhage. A CD36 variant predicted to disrupt an enhancer site associates (p < 10−17) to death from gastro-intestinal hemorrhage in the UK Biobank. The findings support role of CD36 in gastric tissue repair, and its deletion associated with chronic diseases that can predispose to malignancy.

Analysis of Dieting with Gastritis in The Students of Muhammadiyah University Jakarta 2021

Gastritis is an inflammatory process or health problem caused by irritation and infection of the gastric mucosa and submucosa. Gastritis can attack all levels of society from all levels of age and gender. Diet is to provide an overview of the way or behavior taken by a person or group of people in choosing and using the food consumed every day which includes the regularity of eating frequency, meal portions, and the type of food and drink consumed based on social and cultural factors in which they live. According to Riskesdas 2013, the incidence of gastritis in several regions of Indonesia is quite high with a prevalence of 274,369 cases from 238,452,952 inhabitants, it was found that in the city of Surabaya the incidence of gastritis was 31.2%, Denpasar 46% while in Central Java the incidence of gastritis is quite high at 79.6%. Gastritis usually occurs due to irregular eating frequency so that the stomach becomes sensitive when stomach acid increases. It is better for people who have a history of gastric disease not to eat acidic and spicy foods because they can cause gastritis to recur.

The Effect of the Change in Lymph Flow Following Gastrectomy for Initial Disease on the Prognosis of Remnant Gastric Cancer

Background: Remnant gastric cancer (RGC) has been increasing for various reasons such as longer life span, medical progress, and others. It generally has a poor prognosis, and its mechanism of occurrence is unknown. The purpose of this study was to evaluate the clinicopathological features of and clarify the prognostic factors of RGC.Methods: Between January 2002 and January 2017, 39 patients with RGC following distal gastrectomy underwent curative surgical resection at the Okayama University Hospital; their medical records and immunohistochemically stained extracted specimens were used for retrospective analysis. Results: On univariate analysis, initial gastric disease, pathological lymph node metastasis, and pathological stage were the significant factors associated with a poor overall survival (OS) (p=0.0139, 0.0061, and 0.0158, respectively). Multivariate analysis of these 3 factors showed that only initial gastric disease caused by malignant disease was an independent factor associated with a poor prognosis (p=0.0141, odds ratio [OR]:4.151, 95% confidence interval [CI]:1.333-12.93). In addition, the presence of a left gastric artery (LGA), and tumor-infiltrating CD8+ T cell expression were higher in the benign disease group than in the malignant group (p<0.0001 and p=0.0485, respectively).Conclusion: The lymph flow change caused by lymph node dissection for malignant disease in initial surgery might have an effect on the suppression of tumor immunity and the poor prognosis of RGC.

TP6.2.15 Staging Laparoscopy and Peritoneal Cytology for Gastric and Gastro-oesophageal Junction Malignancy: an Audit from a Single Oesophagogastric Resection Centre

Aims AUGIS recommends staging laparoscopy in all gastric cancers and selected gastro-oesophageal junction (GOJ) cancers. We previously audited our practice of staging laparoscopy and peritoneal cytology and found that in a cohort of 158 consecutive patients, no tumours less than T3 with negative nodes had positive cytology, resulting in change in practice to selectively use peritoneal cytology in patients with a T-stage of 3 and above or N+ disease. Our aim was to assess the impact of this audit on current practice. Methods We retrospectively reviewed the notes of patients undergoing staging laparoscopy and oesophagogastroduodenoscopy (OGD) identified by MDT from January 2019 to December 2019. Patients who underwent resection on the same day were excluded. Results 63 patients underwent staging laparoscopy and OGD, 54 for GOJ and 9 for gastric disease. The majority were staged as T3 or T4a (81%). As a result of staging laparoscopy and OGD, 4 (6%) patients were changed from curative to palliative pathway, 2 (3%) of whom had positive cytology. No patients had positive peritoneal cytology for a T stage of 2 and below with no positive nodes, further demonstrating the safety of the recommendation. Conclusions Peritoneal cytology has a low yield in changing the clinical course of patients but can upstage up to 6% of patients. The re-audit backs up the previous guidance in the safety of using our current threshold for recommending peritoneal cytology and potentially prevents delaying treatment while waiting for cytology results.