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Background: Currently, it is still unclear whether adding a mucoprotective agent to a proton pump inhibitor (PPI) results in better outcomes compared with using a PPI alone in patients with post‐gastric endoscopic submucosal dissection (ESD) ulcers. This study aimed to examine the efficacy of PPI alone versus combination treatment in healing of post‐gastric ESD ulcers, as well as on delayed bleeding and amount of blood transfused. Methods: A systematic search of MEDLINE, EMBASE, Cochrane, and ISI Web of knowledge databases, up until May 2017, for randomized trials comparing PPI alone versus PPI plus a mucoprotective drug in achieving ulcer healing in patients undergoing gastric ESD was performed. The primary outcome is scarring stage on endoscopic assessment at 4 or 8 weeks after gastric ESD. Results: From an initial 3071 citations, eight articles (n = 953 lesions from 934 patients) were analyzed. Patients receiving combination treatment achieved a scarring stage significantly more often than those on a PPIs alone at 4 or 8 weeks after ESD, (risk ratio = 1.36, 95% CI; 1.06–1.75). No study reported amount of blood transfused. There were no significant between treatment‐group differences in terms of delayed bleeding (risk ratio = 0.58, 95% CI; 0.17–1.99). Neither location of ulcer nor Helicobacter pylori infection was related to ulcer scarring stage. Conclusion: The limited evidences suggested combination treatment may be more effective in accelerating the process of ulcer healing in patients undergoing gastric ESD than the use of PPI alone, but does not appear to alter delayed bleeding risk. [ABSTRACT FROM AUTHOR]

Background and Aim Bleeding is the most common adverse event following colonoscopic endoscopic mucosal resection (EMR). We aimed to assess the clinical outcomes of a colon EMR according to the post-EMR ulcer status and determine the risk factors of delayed postpolypectomy bleeding (DPPB) based on the post-EMR ulcer status. Methods The medical records and endoscopic images of patients who underwent EMR of colon polyps with diameters of ≥ 5 mm were retrospectively reviewed by us. If any exposed vessels were observed on the post-EMR ulcer, the types of exposed vessels were classified into cut and uncut vessels. The coagulation injuries on the post-EMR ulcer were categorized as grades 1, 2, or 3. Results In total, 505 patients with 728 polyps were examined. Exposed vessels were present in 416 post-EMR ulcers, including cut vessels in 11 (1.5%) and uncut vessels in 405 (55.6%). With regard to coagulation injury, 113 (15.5%), 443 (60.9%), and 172 (23.6%) post-EMR ulcers had grades 1, 2, and 3 injuries, respectively. DPPB was observed in 20 lesions (2.7%). Multivariate analysis indicated that a polyp size > 10 mm (odds ratio [OR], 3.354; 95% confidence interval [CI], 1.229-9.154), cut vessels (OR, 18.913; 95% CI, 3.106-115.187), and grade 3 coagulation injury (OR, 16.796; 95% CI, 1.825-154.556) were associated with DPPB. Conclusions Cut vessels and severe coagulation injury on post-EMR ulcers, as well as larger polyp size, are risk factors for DPPB. Careful inspection of post-EMR ulcers and prophylactic hemostasis, if necessary, may improve the clinical outcomes of colonoscopic EMR. [ABSTRACT FROM AUTHOR]

Background and Aim This study was conducted to determine the clinicopathologic factors affecting the stage of ulcerative early gastric cancer ( EGC), focusing on the relationships between cancer stage and degree of endoscopic ulcer depth and morphologic changes. Methods Medical records of 183 cases of ulcerative EGC who had received endoscopic examination two or more times with a minimum interval of one week, and who underwent either curative surgery or endoscopic treatment were retrospectively reviewed. Results Change in ulcer morphology at follow-up endoscopy was observed in 84 cases (45.9%) with improvement and exacerbation of ulcer in 65 (35.5%) and 19 (13.8%) cases, respectively. The presence of type III ulcer ( P < 0.01), and endoscopic findings suggesting submucosal cancer invasion (tumorous bank, fusion of converging folds, hardness or decreased flexibility) ( P < 0.01), and incomplete ulcer healing ( P = 0.036) were independently associated with a higher incidence of submucosal cancer invasion. The incidence of lymph node metastasis was 14.1%, and undifferentiated histology and presence of lymphovascular invasion were significantly associated with a higher incidence of lymph node metastasis ( P = 0.018 and P = 0.005, respectively). Conclusions Endoscopic resection with curative intent may be an acceptable option for EGC combined with endoscopic ulcer or ulcer scar, but should be restricted to cases showing significant improvement in the size and depth of ulcer at follow-up endoscopy, and which are not accompanied with deep ulcer more than the thickness of adjacent mucosal surface and prominent surrounding mucosal fold change. In addition, histologic criteria should meet the conditions of differentiated intramucosal cancer without lymphovascular invasion. [ABSTRACT FROM AUTHOR]

Background and Aim: To validate an early discharge policy in patients admitted with upper gastrointestinal bleeding (UGIB) due to ulcers. Methods: Patients with gastroduodenal ulcer or erosive gastritis/duodenitis were included in a previous study aiming to develop a practice guideline for early discharge of patients with UGIB. Variables associated with unfavorable evolution were analyzed in order to identify patients with low-risk of re-bleeding. After that, a one-year prospective analysis of all UGIB episodes was carried out. Results: A total of 341 patients were identified in the retrospective study. Variables associated with unfavorable evolution were: systolic blood pressure ≤ 100 mmHg, heart rate ≥ 100 bpm, and a Forrest endoscopic classification of severe. 10% of patients were immediately discharged; however, if predictive variables obtained in the multivariate analysis had been used, hospitalization could have been prevented in 34% of patients. A total of 77 patients were included in the prospective analysis. Although only 19.5% of patients were immediately discharged without complications, 29 patients (37.7%) were theoretically suitable for early discharge. Conclusions: Patients with UGIB who have clean-based ulcers and are stable on admission can be safely discharged immediately after endoscopy. Implementation of the clinical practice guideline safely reduced hospital admission for those patients. [ABSTRACT FROM AUTHOR]

Background and Aims: Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most significant causative factors of gastroduodenal ulcers. Recent reports have demonstrated that NSAIDs can also frequently induce ulceration and erosions of the small intestine. The aim of this study was to examine whether or not roxatidine (an H2 receptor antagonist), which is known to increase gastric mucus in addition to inhibiting gastric acid, might suppress indomethacin-induced small intestinal mucosal injury, through an increase in mucus in rats. Methods: Rats were given two p.o. doses of roxatidine, famotidine or cimetidine before and after the s.c. indomethacin injection. The injured area of the small intestine was analyzed. To examine effects of drugs on small intestinal mucus, rats were also given two p.o. doses of roxatidine, famotidine or cimetidine, and the ratio of the periodic acid Schiff (PAS)-positive area to the area of the mucosa in the small intestine was analyzed. In addition, we evaluated the involvement of nitric oxide (NO) and prostaglandins (PG) in the effect of roxatidine on small intestinal mucus. Results: Roxatidine significantly ameliorated indomethacin-induced small intestinal injury and increased the PAS-stained areas in the small intestinal mucosa, while cimetidine and famotidine had no significant effect. Pretreatment with N-nitro-L-arginine methyl ester but not with indomethacin, suppressed the effect of roxatidine on small intestinal mucus, suggesting that the effect is mediated by endogenous NO but not by PG. Conclusion: Roxatidine suppressed indomethacin-induced small intestinal injury in rats. One possible mechanism is an increase of small intestinal mucus, mediated by NO. [ABSTRACT FROM AUTHOR]

Background and Aim: Following endoscopic therapy, up to 20% of patients with non-variceal upper gastrointestinal hemorrhage experience rebleeding. The aim of the present study was to determine risk factors for recurrent hemorrhage in these patients. Methods: This was a retrospective cohort study of consecutive patients admitted to a tertiary care hospital between 1 July 1999 and 30 June 2004, with non-variceal upper gastrointestinal hemorrhage. Patients were evaluated for rebleeding within 30 days of successful therapeutic endoscopy. Using the hospital's endoscopic database, 236 patients were identified. Risk factors were identified using multivariable logistic regression with backward selection. Internal validation was carried out using bootstrapping. Results: Six risk factors were identified: failure to use a Proton pump inhibitor post-procedure ( P = 0.056), Endoscopically demonstrated bleeding ( P = 0.053), Peptic ulcer as the bleeding source ( P = 0.018), Treatment with epinephrine monotherapy ( P = 0.0026), post-procedure Intravenous or low molecular weight heparin use ( P = 0.0014), and moderate or severe Cirrhosis ( P = 0.032) (PEPTIC). The risk of rebleeding increased as the number of risk factors present increased. The observed rates of rebleeding were: 7.1%, 16.4%, 37.0%, 75.0% and 100% for zero, one, two, three or four risk factors, respectively (no patients had five or six risk factors present). The bias-adjusted area under the receiver–operator characteristic curve for the number of risk factors predicting rebleeding was 0.69. Conclusions: We have identified six easily remembered risk factors, which, when summed, predict recurrent hemorrhage following endoscopic therapy for non-variceal upper gastrointestinal hemorrhage. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori is the major causative factor of ulcer but the use of ibuprofen and other non-steroidal anti-inflammatory drugs have also been implicated in development of ulcer. The purpose of the present study was to determine the anti-ulcer effect of glucosamine. Methods: The protective effect of glucosamine on ibuprofen-induced peptic ulcer in male albino rats was studied with respect to changes in the volume of gastric juice, acid output, pepsin activity, activities of membrane bound ATPases, protein content, glycoprotein components and histopathology. Results: Oral administration of ibuprofen caused significant increase in the number of lesions in the gastric mucosa, increases in the volume of gastric juice and acidity, and decreased activity of pepsin. The levels of protein content and glycoprotein components (hexose, hexosamine and sialic acid) and ATPase activities were also observed. Oral pretreatment with glucosamine resulted in significant reduction in the number of lesions in the gastric mucosa and decreases in the volume of gastric juice and acidity. The pepsin activity was also maintained at near normalcy. Prior oral administration of glucosamine significantly prevented the ibuprofen-induced depletion of protein and glycoprotein components and maintained the activities of membrane bound ATPases as compared to untreated ulcer induced group of rats. Conclusion: The anti-ulcerogenic activity of glucosamine might be ascribable to its ability to neutralize the hydrochloric acid secreted into the stomach and to its capability to strengthen the mucosal barrier by increasing mucosal glycoprotein synthesis and to its free radical scavenging property. Histopathological investigations of the mucosal tissue also support the anti-ulcerogenic effect of glucosamine. [ABSTRACT FROM AUTHOR]

Activation of adenosine A2A receptors reduces the production of various pro-inflammatory cytokines and suppresses neutrophil activation. Water-immersion restraint is well known to cause gastric mucosal lesions due to stress. The pathogenesis of stress-induced gastric mucosal lesions is characterized by activation of inflammatory cells and production of inflammatory cytokines. Agonists of adenosine A2A receptors are known to be anti-inflammatory, but the effects of these compounds on the development of gastric mucosal lesions has not been reported. In the present study, the effect of a potent and selective adenosine A2A receptor agonist, ATL-146e, on water-immersion stress-induced gastric mucosal lesions was studied.Rats were subjected to water-immersion stress with or without pretreatment with a single intraperitoneal injection of a potent and selective agonist of the adenosine A2A receptor. The gastric concentrations of myeloperoxidase (MPO), as an index of neutrophil accumulation, and the pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were measured.The total length of gastric erosions (ulcer index) in control rats was 21.6 ± 3.23 mm and was reduced by 86% to 3.1 ± 0.83 mm by pretreatment with 5.0 µg/kg ATL146e (P < 0.001). The gastric content of MPO, TNF-α and IL-1β were all increased after water-immersion stress and reduced to near normal levels by ATL-146e.A specific adenosine A2A agonist inhibits stress-induced gastric inflammation and damage. A2A agonist compounds may be useful for preventing ulcers and appear to act by blocking gastric inflammation.© 2004 Blackwell Publishing Asia Pty Ltd [ABSTRACT FROM AUTHOR]

Abstract Non-steroidal anti-inflammatory drug (NSAID) toxicity in the upper gastrointestinal tract is the most common serious drug-induced toxicity reported to drug regulatory authorities. In the last two decades, the rediscovery of H. pylori, development of potent ulcer-healing drugs and specific Cox-II inhibitors have opened new horizons in the management of NSAID toxicity. A Working Party composed of gastroenterologists and rheumatologists in the Asia-Pacific region met in Cairns, Australia, in 1999 to review the literature and develop appropriate guidelines. Recommendations were made based on the latest existing evidence. The importance of clinical events as study endpoints was emphasized. While differences exist between NSAIDs and aspirin, most studies have shown that advanced age, history of peptic ulcer disease, serious concomitant illnesses and coprescription of NSAID/aspirin with anticoagulants and steroids are high risk factors. These patients should be considered for prophylactic anti-ulcer therapy. Helicobacter pylori infection may aggravate the toxicity of NSAIDs and, in selected cases, should be treated before NSAID/aspirin is prescribed. Proton pump inhibitors and misoprostol are the most promising agents in preventing gastric and duodenal ulcers. When NSAID/aspirin needs to be continued in patients who develop an NSAID-related ulcer, proton pump inhibitors offer the best healing effect. With the discovery of cyclo-oxygenase isoforms (Cox-I and Cox-II), preferential and specific Cox-II inhibitors have been developed. While early clinical data have suggested promising anti-inflammatory effects and improved safety profile in the gastrointestinal tract, several key issues on long-term safety remain unresolved. The use of potent anti-ulcer therapy, treatment of H. pylori infection and the development of Cox-II inhibitor will change the scenario of NSAID/aspirin-related gastrointestinal toxicity in the next millennium. [ABSTRACT FROM AUTHOR]

Background: The main etiology of gastroduodenal ulcer are NSAID and Hp. The role if Hp infection to the patients who use NSAID is still controversy. We compare the prevalence of Hp infection among ulcer and non ulcer patients in those who used NSAID and who didn’t use. Material & Methods: A retrospective study had been done from 1995 - 1988 to 248 patients who were proven to have ulcer and non ulcer by endoscopic examination. Infection of Hp was tested by CLO and histopathology. Base on the history of NSAID consumption, the patients were divided into NSAID users group and non users group. Result: Between 1995 and 1998, 248 patients were studied, they consisted of 95 ulcer patients (50 GU, 40DU, 5 GU+DU) and 163 non ulcer patients. Age ranged from 16-78 years old. The median age of GU;DU and NU wee 61;49 and 44 yrs respectively. Among 95 ulcer patients, 67.4% were NSAID user and 32.6% were non users, the prevalence of Hp among NSAID users and non users were 20.3% and 81.7% respectively (p<0.01).Among 163 non ulcer patients 36.8% were NSAID users and 63.2% were non users, the prevalence of Hp among NSAID users and non users were 33.1% and 60.2% respectively (p<0.05). Ninety percent of 50 GU patients were NSAID users, the prevalence of Hp among them was 11.1%. The prevalence of Hp among GU patients who didnít use NSAID was 4/5(80%). Among 40 patients with DU,35% were NSAID users and 65% were non users, the prevalence of Hp among users and non users were 42.9% and 92.3% respectively (p<0.01). All patients with GU+DU were NSAID users, 40% of them had Hp positive. Conclusion: The prevalence of Hp among NSAID users was lower than non users. In NSAID users group who had ulcer the prevalence of Hp was lower than those who had non ulcer. This finding support that Hp infection may not increase the risk of ulcer in patient who use NSAID. [ABSTRACT FROM AUTHOR]