Impact of Helicobacter pylori Infection on Gastric Variceal Bleeding among Patients with Liver Cirrhosis

Background and Aims. Currently, it is well known that Helicobacter pylori- (H. pylori-) related peptic ulcer is one of the main causes of nonvariceal bleeding in cirrhotic patients. However, there is a lack of data to identify the exact effect ofH. pyloriinfection on variceal bleeding. This study was conducted to identify the impact ofH. pyloriinfection on gastric variceal bleeding in cirrhotic patients.Patients and Methods. 76 cirrhotic patients with gastric varices were included in this prospective study and divided into 2 groups: nonbleeding gastric varices (32 patients) and bleeding gastric varices (44 patients). The fasting serum gastrin level was measured. Mucosal biopsies from the gastric body and antrum were examined to determine the patterns of gastritis and the presence ofH. pylori.Results. The frequency ofH. pyloriinfection in the studied patients was 59.2%. There were significant differences between both groups regarding liver decompensation (P=0.001), red color sign over gastric varices (P=0.0011), prevalence ofH. pyloriinfection (P=0.0049), histological patterns of gastritis (P=0.0069), and serum gastrin level (P=0.0200). By multivariate analysis, Child C cirrhosis, red color sign over gastric varices, andH. pylori-induced follicular gastritis were independent risk factors for bleeding from gastric varices.Conclusion.H. pylori-induced follicular gastritis is considered as an additional risk factor for bleeding from gastric varices.

Topographic distribution of gastritis in heavy pigs investigated by a geographic information system approach

The aim of this paper was to determine the topographic distribution of gastritis lesions in pigs through an open source geographic information system (GIS) software analysis. The stomachs of 146 Italian heavy pigs were collected at slaughter and subjected to macroscopic pathological examination of the internal mucosa. A total of 623 lesions were either classified as hyperplastic or follicular (97%) with the remaining minority of lesions categorised as atrophic and simple. The hyperplastic gastritis lesions had an average surface of 77.8 cm² and were mainly located in an oval shaped area of the fundus region of the stomach near the <em>Curvatura ventriculi major</em>. The follicular gastritis lesions had generally a smaller surface (40.3 cm²) and were concentrated in two distinct small areas of the pyloric region. The GIS analysis provided the opportunity to produce useful maps showing the distribution and characteristics of gastritis in pigs.

Prevalence of Helicobacter pylori among patients with dyspepsia and correlation between endoscopic and histological diagnosis

Background: Dyspepsia is a prevalent complaint in general practice and gastrointestinal clinics. Helicobacter pylori have major causal relationship with gastro duodenal disease. The following study seeks to identify the prevalence of H. pylori based on histology and to correlate endoscopic findings with histopathology.Materials and Methods: This was a cross-sectional observational study conducted in GRP Polyclinic and Om Hospital and research centre from April 2015-September 2015. The upper gastrointestinal endoscopic findings were recorded and were correlated with histopathological findings. All the relevant data were collected and analysed using Statistical Package of Social Sciences version 16 for windows. Results: Endoscopy finding was divided into reflux esophagitis, antral gastritis, duodenitis, duodenal ulcer, gastric ulcer, and gastric cancer. Duodenal ulcer and gastric ulcer was noted more frequently in males than in females (55.0% vs. 45.0% and 58.2% vs. 41.8%), respectively, P < 0.001).Chronic follicular gastritis was the most common in gastric ulcer (41.7%), whereas chronic persistent gastritis was common in non-ulcerative disease. Chronic active gastritis and chronic follicular gastritis were more common in ulcerative diseases, whereas chronic persistent gastritis was more common in gastritis and duodenitis (P < 0.001). The overall prevalence of H. pylori infection was 68.1% with male preponderance. Chronic active gastritis had highest prevalence of H. pylori (84.8%), followed by chronic follicular gastritis (84.1%) and chronic persistent gastritis (p value < 0.001.Conclusion: Rate of H. pylori infected patients with dyspepsia was high. Ulcerative lesions were more common in males than in females with higher rate of infection with H. Pylori. Histological diagnosis of chronic active gastritis and chronic follicular gastritis was the most common pathologies in ulcerative lesions.

Helicobacter pylori Promotes the Production of Thymic Stromal Lymphopoietin by Gastric Epithelial Cells and Induces Dendritic Cell-Mediated Inflammatory Th2 Responses

ABSTRACT Helicobacter pylori colonizes the stomach and induces strong, specific local and systemic humoral and cell-mediated immunity, resulting in the development of chronic gastritis in humans. Although H. pylori-induced chronic atrophic gastritis is characterized by marked infiltration of T helper type 1 (Th1) cytokine-producing CD4+ T cells, almost all of the inflamed gastric mucosae also contain focal lymphoid aggregates with germinal centers. In addition, typical H. pylori-induced chronic gastritis in children, called follicular gastritis, is characterized by B-cell follicle formation in the gastric mucosa. The aim of this study was to examine whether thymic stromal lymphopoietin (TSLP), an epithelial-cell-derived cytokine inducing a dendritic cell (DC)-mediated inflammatory Th2 response, is involved in Th2 responses triggering B-cell activation in H. pylori-induced gastritis. Here, we show that H. pylori triggered human gastric epithelial cells to produce TSLP, together with the DC-attracting chemokine MIP-3α and the B-cell-activating factor BAFF. After DCs were incubated with supernatants from H. pylori-infected epithelial cells, the conditioned cells expressed high levels of costimulatory molecules, such as CD80, and triggered naïve CD4+ T cells to produce high levels of the Th2 cytokines interleukin-4 and interleukin-13 and of the inflammatory cytokines tumor necrosis factor alpha and gamma interferon. In contrast, after incubation of the supernatants with the neutralizing antibodies to TSLP, the conditioned DCs did not prime T cells to produce high levels of Th2 cytokines. These results, together with the finding that TSLP was expressed by the epithelial cells of human follicular gastritis, suggest that H. pylori can directly trigger epithelial cells to produce TSLP. It also suggests that TSLP-mediated DC activation may be involved in Th2 responses triggering B-cell activation in H. pylori-induced gastritis.