Gastric Morphological Changes Research Articles

Changes in gastric morphology during long-term use of vonoprazan compared to proton pump inhibitors.

Changes in gastric morphology during long-term use of vonoprazan compared to proton pump inhibitors.

Хронический атрофический гастрит: факторы риска и их взаимосвязь с выраженностью морфологических изменений слизистой оболочки желудка

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

Amelioration of Alcohol Induced Gastric Ulcers Through the Administration of Lactobacillus plantarum APSulloc 331261 Isolated From Green Tea.

Gastric inflammation is an indication of gastric ulcers and possible other underlying gastric malignancies. Epidemiological studies have revealed that several Asian countries, including South Korea, suffer from a high incidence of gastric diseases derived from high levels of stress, alcoholic consumption, pyloric infection and usage of non-steroidal anti-inflammatory drugs (NSAIDs). Clinical treatments of gastric ulcers are generally limited to proton pump inhibitors that neutralize the stomach acid, and the application of antibiotics for Helicobacter pylori eradication, both of which are known to have a negative effect on the gut microbiota. The potential of probiotics for alleviating gastrointestinal diseases such as intestinal bowel syndrome and intestinal bowel disease receives increasing scientific interest. Probiotics may support the amelioration of disease-related symptoms through modulation of the gut microbiota without causing dysbiosis. In this study the potential of Lactobacillus plantarum APSulloc 331261 (GTB1TM), isolated from green tea, was investigated for alleviating gastric inflammation in an alcohol induced gastric ulcer murine model (positive control). Treatment with the test strain significantly influenced the expression of pro-inflammatory and anti-inflammatory biomarkers, interleukin 6 (IL6) and interleukin 10 (IL10), of which the former was down- and the latter up-regulated when the alcohol induced mice were treated with the test strain. This positive effect was also indicated by less severe gastric morphological changes and the histological score of the gastric tissues. A significant increase in the abundance of Akkermansia within the GTB1TM treated group compared to the positive control group also correlated with a decrease in the ratio of acetate over propionate. The increased levels of propionate in the GTB1TM group appear to result from the impact of the test strain on the microbial population and the resulting metabolic activities. Moreover, there was a significant increase in beta-diversity in the group that received GTB1TM over that of the alcohol induced control group.

Role of dietary polyphenols in the management of peptic ulcer.

Peptic ulcer disease is a multifactorial and complex disease involving gastric and duodenal ulcers. Despite medical advances, the management of peptic ulcer and its complications remains a challenge, with high morbidity and death rates for the disease. An accumulating body of evidence suggests that, among a broad reach of natural molecules, dietary polyphenols with multiple biological mechanisms of action play a pivotal part in the management of gastric and duodenal ulcers. The current review confirmed that dietary polyphenols possess protective and therapeutic potential in peptic ulcer mediated by: improving cytoprotection, re-epithelialization, neovascularization, and angiogenesis; up-regulating tissue growth factors and prostaglandins; down-regulating anti-angiogenic factors; enhancing endothelial nitric oxide synthase-derived NO; suppressing oxidative mucosal damage; amplifying antioxidant performance, antacid, and anti-secretory activity; increasing endogenous mucosal defensive agents; and blocking Helicobacter pylori colonization associated gastric morphological changes and gastroduodenal inflammation and ulceration. In addition, anti-inflammatory activity due to down-regulation of proinflammatory cytokines and cellular and intercellular adhesion agents, suppressing leukocyte-endothelium interaction, inhibiting nuclear signaling pathways of inflammatory process, and modulating intracellular transduction and transcription pathways have key roles in the anti-ulcer action of dietary polyphenols. In conclusion, administration of a significant amount of dietary polyphenols in the human diet or as part of dietary supplementation along with conventional treatment can result in perfect security and treatment of peptic ulcer. Further well-designed preclinical and clinical tests are recommended in order to recognize higher levels of evidence for the confirmation of bioefficacy and safety of dietary polyphenols in the management of peptic ulcer.

The gastro‐esophageal reflux barrier: biophysical analysis on 3D models of anatomy from magnetic resonance imaging

The function and structure of the gastro-esophageal junction (GEJ) determine its efficacy as a reflux barrier. This study presents a novel methodology for the quantitative assessment of GEJ and proximal gastric morphology from magnetic resonance (MR) imaging. Based on this data we propose a new conceptualization of the hypothesis that a flap valve mechanism contributes to reflux protection. 3D models of the GEJ and proximal stomach were reconstructed from MR images in 12 healthy volunteers during respiration and on eating a test meal to maximum satiation. A rotating plane analysis measured the gastro-esophageal insertion angle and span of contact. An ellipsoid fit provided quantitative assessment of gastric shape and orientation relative to a fixed anatomical reference point. Position of the esophageal insertion on the 'gastric ellipse' was noted. An ellipsoid-cylinder model was designed to analyze the relationships among parameters describing the GEJ morphology. The insertion angle became more acute on expiration, but did not change with meal ingestion. In contrast the span of contact did not vary with respiration, but increased with gastric filling. Changes in gastric morphology with distension further augmented the span of gastro-esophageal contact in almost 70% of the studies. Novel MR imaging and biophysical analysis of the GEJ and proximal stomach provide a quantitative description of structures contributing to the reflux barrier. Changes in these parameters during respiration and on eating support the hypothesis that structural components of a functional 'flap valve' like mechanism contribute to reflux protection.

Short- and Long-Term Changes in Gastric Morphology and Histopathology Following Sleeve Gastrectomy in Diet-Induced Obese Rats

Sleeve gastrectomy (SG) has been used as a multipurpose surgical procedure for the treatment of morbid obesity. The aim of the study was to analyze gastric morphology and histology at two different time points after SG in rats. Thirty-five male Wistar rats were fed ad libitum during 3 months on a high-fat diet to induce obesity. Subsequently, 25 diet-induced obese rats underwent either SG (n = 12) or a sham operation (n = 13). The remaining ten obese animals encompassed the nonoperated control group (Co). Four weeks postoperatively, 15 rats (n = 5 rats/experimental group) were sacrificed, while the remaining 20 rats were sacrificed after 16 weeks (animals/group; Co = 5, sham = 8, SG = 7) to compare the gastric morphological and histopathological changes over time. Body weight and food intake were regularly recorded. For both time periods, the Co groups exhibited the highest body weight, while the rats undergoing the SG showed the lowest weight gain (P < 0.05). Initially, significant differences (P < 0.005) in food intake relative to body weight were observed between the Co rats and animals undergoing surgery, which disappeared thereafter. The actual total stomach size after both experimental periods in the SG group was similar to that of non- and sham-operated rats mainly due to a forestomach enlargement, which was more pronounced after 16 weeks. Traits of gastritis cystica profunda characterized by gastric foveolae elongation with hyperplasia and cystic dilatation of the glands were observed in the residual stomachs of the sleeve-gastrectomized rats. These findings were mostly observed after 16 weeks of performing the SG, although they were also detected occasionally following 4 weeks postoperatively. No intestinal metaplasia was observed. After SG gastric macro- and microscopic changes with functional implications in both the short and long term take place.

The effect of ciprofibrate on gastric secretion in the rat.

The potential of ciprofibrate to inhibit gastric secretion has been investigated in the rat. A significant gastric antisecretory effect was observed following a single oral administration of 300 and 500 mg kg-1 and following a single intraduodenal dose of 100, 300 and 500 mg kg-1. The toxicological significance of this finding is discussed in the light of a spate of recent publications linking changes in gastric morphology with hypergastrinaemia produced as a secondary effect of inhibition of acid secretion.

Receptores tipo Toll, patogénesis y respuesta inmune a Helicobacter pylori

Helicobacter pylori colonize the gastric epithelial, most infected people are asymptomatic, 10 to 20% develop atrophic gastritis, peptic ulcer and less than 3% gastric cancer. These diseases are determined by the relationship between virulence factors of bacteria, host factors such as, genetic predisposition, and immune response. The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-kB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10. Chronic inflammation promotes gastric morphological changes, prevents apoptosis and allows angiogenesis generating neoplasic lesions and cancer. The aim of this review is to analyze the mechanisms proposed to date of the innate and adaptative immune response involved in H. pylori infection; remarking the mechanisms related in the elimination or persistence.

Unravelling a role for KCNQ1 in K+ recycling and gastric acid secretion

Unravelling a role for KCNQ1 in K⁺ recycling and gastric acid secretion

Gastric Morphological Changes Including Carcinoid Tumors in Animals Treated with a Potent Hypolipidemic Agent, Ciprofibrate

Oral administration of ciprofibrate, a potent hypolipidemic compound, to rats for 2 or more weeks at doses of 20 mg/kg/day or more resulted in hypertrophy and increased eosinophilia of the oxyntic cells in the gastric mucosa. Ultrastructural evaluation revealed small secretory canaliculi with small microvilli in these cells, changes consistent with the inhibition of acid secretion. After longer administration (e.g., greater than 2 months at 20 mg/kg/day), hyperplasia of the neuroendocrine cells (in particular, the enterochromaffin-like cells) was present in the fundic mucosa of the stomach. After life-time (2-year) administration at 10 mg/kg/day, neuroendocrine cell hyperplasia was accompanied by formation of malignant carcinoid tumors in the fundus of 5 of 59 male and 1 of 60 female rats. In contrast, administration of ciprofibrate to mice at 20 mg/kg/day for 2 months was not associated with oxyntic or neuroendocrine cell changes, a finding consistent with the lack of gastric carcinoid tumors in a 2-year mouse study. Similarly, no significant changes were induced in the marmoset stomach by doses as high as 100 mg/kg/day for 6 months. These findings are consistent with the hypothesis that the formation of gastric carcinoid tumors following ciprofibrate administration is a phenomenon that occurs specifically in those species such as the rat where this compound has significant gastric antisecretory activity.

Gastric Morphological Changes Leading to Carcinoid Tumours in Rats given Phenoxyisobutyrate Derivatives

Gastric Morphological Changes Leading to Carcinoid Tumours in Rats given Phenoxyisobutyrate Derivatives

Stump cancer following gastric surgery.

AbstractThis paper reviews the literature regarding the development of gastric cancer in the stomach remnant following gastric resection. Although there is as yet little supporting experimental evidence, clinical studies suggest that the risk of developing gastric cancer is increased, perhaps as much as 6‐fold, following partial gastrectomy for benign lesions. It also appears that the risk of developing cancer is greatest if the lesion for which the gastrectomy was originally performed was a gastric ulcer rather than a duodenal ulcer. The type of gastrectomy does not seem to influence this increased risk. Hypotheses are reviewed concerning the role of changes in gastric morphology following partial gastrectomy in the development of cancer.

The response to prednisolone in atrophic gastritis: a possible effect on non-intrinsic factor-mediated vitamin B 12 absorption.

The administration of prednisolone did not affect absorption of vitamin B(12) and gastric secretion of intrinsic factor in nine subjects with normal gastric mucosa, or in five with chronic superficial gastritis. No gastric morphological changes were observed in either group. In contrast, four of seven patients with pernicious anaemia showed improvement in absorption of vitamin B(12) during prednisolone administration for periods of two to 10 months. No consistent changes in gastric mucosal morphology were noted. An additional five patients were studied intensively during one month of prednisolone administration. In three, absorption of vitamin B(12) was restored to within the normal range between eight and 13 days after the commencement of the drug. The improvement was not paralleled by enhancement of secretion of intrinsic factor or other vitamin B(12) binders. Suppression of intrinsic factor antibodies in serum and gastric juice did not occur consistently in those patients showing a functional response.