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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed this study to evaluate the prevalence of reflux esophagitis and/or hiatal hernia in patients referred to a medical center and to examine the relationship between endoscopic reflux esophagitis and hiatal hernia. The study was carried out in 1,010 patients referred to Yong Dong Severance Hospital for upper gastrointestinal endoscopy because of symptoms related to the gastrointestinal tract from September 1994 to March 1996. The presence of hiatal hernia was defined as a circular extension of the gastric mucosa of 2 cm or more above the diaphragmatic hiatus. Reflux esophagitis was found in 5.3% of patients, hiatal hernia in 4.1%, duodenal ulcer in 7.2% and gastric ulcer in 8.2%. The prevalence rates of reflux esophagitis and hiatal hernia in males were significantly higher than those in females. Thirty-two percent of patients with reflux esophagitis had hiatal hernia. In patients without reflux esophagitis, hiatal hernia was found in only 2.5% (p<0.01). There was no significant association between the presence of hiatal hernia and the degree of esophagitis on endoscopy. Duodenal ulcer was the second most common endoscopic abnormality found in patients with reflux esophagitis. The prevalence rate of reflux esophagitis and/or hiatal hernia at a medical center is relatively low compared to peptic ulcer disease and other reports from the Western countries. Our study confirms the close association between reflux esophagitis and hiatal hernia.
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PMID:Reflux esophagitis and its relationship to hiatal hernia. 1040 66

Helicobacter pylori (H. pylori) infection is the cause of the frequent relapse of peptic ulcer disease. Successful eradication therapy of H. pylori is associated with a decline in the recurrence of peptic ulcer. In this paper, we discussed the significance of anti-ulcer therapy after H. pylori eradication therapy. In patients with duodenal ulcer, maintenance therapy for preventing ulcer recurrence is not necessary because the rate of ulcer recurrence after eradication therapy is very low. However, in patients with gastric ulcer, the rate of ulcer relapse and reflux esophagitis ranges between 5-10% in the Japanese population even after successful eradication therapy; therefore, maintenance therapy for 1 year may be permissible in patients with gastric ulcer even after successful eradication therapy.
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PMID:[Anti-ulcer therapy after eradication of Helicobacter pylori]. 1121 7

Little is known about the relationship between H. pylori infection and reflux esophagitis. To evaluate whether or not H. pylori plays a protective role in the pathogenesis of reflux esophagitis, the prevalence rates of reflux esophagitis depending on H. pylori status in consecutively diagnosed duodenal ulcer or benign gastric ulcer patients were evaluated. In addition, the incidence rates of reflux esophagitis depending on H. pylori status were evaluated for those patients who received follow-up endoscopy at least 6 months after eradication treatment. The prevalence rates of reflux esophagitis were 8.0% (2 patients) in the 25 H. pylori-negative duodenal ulcer group patients and 6.5% (36 patients) in the 555 H. pylori-positive duodenal ulcer group patients, and there was no statistical difference. Similarly, that of gastric ulcer patients was 9.4% (32 patients) in the 340 H. pylori-positive group patients, slightly higher than that in the 41 H. pylori-negative group patients 4.9% (2 patients), but without statistical significance. After eradication treatment the reflux esophagitis incidence rates were 2.5% (2 patients) in the 81 H. pylori-eradicated duodenal ulcer group patients and 7.7% (3 patients) in the 39 noneradicated duodenal ulcer group patients, and there was no statistical difference. Similarly, those of gastric ulcer patients were 6.8% (3 patients) in the 44 H. pylori-eradicated and 8.7% (2 patients) in the 23 noneradicated group patients again without statistical difference. These results suggest that H. pylori does not play a protective role in the pathogenesis of reflux esophagitis in patients with duodenal or gastric ulcer in Korea.
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PMID:No protective role of Helicobacter pylori in the pathogenesis of reflux esophagitis in patients with duodenal or benign gastric ulcer in Korea. 1176 66

BACKGROUND: Follow-up studies have shown that patients with ulcer disease are at risk of developing reflux esophagitis (RE) after successful eradication of Heliobacter pylori. It is still not clear whether this is induced by eradication of H. pylori or whether RE is already present at the time the ulcer is diagnosed. A cross-sectional study was done in consecutive patients suffering from active ulcer disease in order to assess coincidental RE. METHODS: Patients with an active duodenal or gastric ulcer were included in the study. Concomitant RE and the presence of hiatal hernia (HH) were scored. Biopsy specimens were taken for detection of H. pylori. RESULTS: In 375 patients (77%), an active duodenal ulcer was the only abnormality. In 43 patients (8.8%), duodenal ulcer and concomitant RE were present and 69 patients (14.2%) had a duodenal ulcer with concomitant HH. Patients with a duodenal ulcer were significantly younger than patients with concomitant RE or HH. From 374 patients (76.8%) with a duodenal ulcer, biopsy specimens were available for the detection of H. pylori. The majority of duodenal ulcer patients were H. pylori-positive. H. pylori was significantly more often present in patients with an active duodenal ulcer than it was in duodenal ulcer patients suffering from concomitant RE (P=0.04). In 218 patients (76%), a gastric ulcer was the only abnormality. Fifteen patients (5.2%) also had RE and 54 patients (18.8%) had a concomitant HH. There was no difference in H. pylori status in these three groups of patients. CONCLUSIONS: Given the low prevalence of concomitant RE, it is concluded that this condition is likely to occur in a large percentage of patients suffering from H. pylori-positive ulcer disease after successful eradication therapy.
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PMID:Reflux esophagitis and hiatal hernia as concomitant abnormality in patients presenting with active duodenal or gastric ulcer: cross-sectional endoscopic study in consecutive patients. 1202 Jun 29

Our objective was to assess the complications of laparoscopic fundoplication in 77 patients older than 70 years of age. The indications for surgery were (1) complications of reflux esophagitis (n = 17), (2) large hiatal hernia (n = 10), (3) asthma and bronchitis (n = 7), (4) the need for other surgery (n = 13), and (5) a patient's desire to discontinue medical treatment that was controlling reflux esophagitis (n = 30). Operative time varied from 34 to 250 minutes (mean [standard deviation], 116 +/- 20). Hospital stay varied from 12 hours to 19 days (mean, 1.2). No patient needed conversion to open operation. Intraoperative complications were observed in 4 patients (5.2%): left pneumothorax in 2, major operative bleeding in 1, and minor spleen lesion in 1. The most common postoperative complications were gas-bloating syndrome and dysphagia. Gastric ulcer was diagnosed in two. Other postoperative complications included acute delirium, acute urinary retention, and acute ischemia of the lower extremity. One patient died of congestive heart failure. It is concluded that laparoscopic fundoplication is an effective procedure for treating geriatric patients with reflux esophagitis and may be performed with low morbidity and mortality rates.
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PMID:Complications of laparoscopic fundoplication in the elderly. 1259 50

The stomach is the main source of circulating ghrelin. Plasma concentrations of this hormone in patients with various upper gastrointestinal diseases remain undetermined. Thus we measured plasma ghrelin levels by radioimmunoassay in 225 subjects, including 134 Helicobacter pylori-infected and 91 uninfected subjects. They included 67 patients with chronic gastritis (CG), 26 with benign gastric polyp (BGP), 24 with gastric ulcer (GU), 24 with reflux esophagitis (RE), 18 with duodenal ulcer (DU), 28 with acute gastritis (AG), 23 with gastric cancer (GC), and 39 who had normal mucosa on upper endoscopy (N). Plasma pepsinogen I and II levels were also measured. The extent of gastritis was assessed endoscopically. Ghrelin levels differed significantly among the different disease groups. Plasma ghrelin concentrations were lowest in the CG group, followed by the GU group, and highest in the AG patients. There was a significant difference in the levels between differentiated and undifferentiated GC. Ghrelin concentrations in BGP, RE, and DU patients were comparable to those in the N group. Ghrelin circulating levels were lower in H. pylori-positive than -negative individuals, but the significant differences among disease groups were still observed in H. pylori-infected and uninfected populations. Ghrelin concentrations correlated positively with plasma pepsinogen I levels and I/II ratios and inversely with the extent of H. pylori-related gastritis. Plasma ghrelin levels varied widely in diverse conditions of the upper digestive tract, reflecting the inflammatory and atrophic events of the background gastric mucosa. Further investigation is warranted to unravel the mechanisms of the high circulating ghrelin levels in certain upper gastrointestinal diseases.
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PMID:Circulating ghrelin levels in patients with various upper gastrointestinal diseases. 1590 53

A total of 10,000 patients underwent upper gastrointestinal endosopy examination between August 1979 and October 1994 at Tikur Anbessa Hospital, Addis Ababa. The major indications were dyspepsia (59.4%), upper gastrointestinal bleeding (18%) and liver disease (10.8%). The other indications include dysphagia (2.2%), gastric outlet obstruction (2.1%), postoperative dyspeptic symptoms (1.9%), weight loss and/or anemia (1.4%), epigastric mass (0.6%) and odynophagia 0.2%. The mean age of the patients and their sex ratio was 36 years and 2:1, respectively. Twenty eight percent of the patients had normal findings. The commonest abnormal findings include duodenal ulcer (41%), esophageal varices (9%), acute gastritis (6%), duodenitis (3.4%), and reflux esophagitis (2.3%). Benign gastric ulcer was rare. The ratio of duodenal ulcer to gastric ulcer was 19.1%. Duodenal ulcer (45.6%), esophageal varices (15.6) and acute gastritis (5.7%) were found to be the commonest causes of upper gastrointestinal bleeding. The endoscopy or histology diagnosis of cancer in both the esophagus and stomach was 2.8% and 1.3%, respectively. The agreement between endoscopy and histology in the diagnosis of esophageal and gastric cancer was 80%. There was no major complication related to endoscopy or premeditation. Endoscopy is a fairly accurate and safe procedure and therefore should be available and applied widely for the diagnosis of upper gastrointestinal diseases in Ethiopia.
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PMID:Upper gastrointestinal endoscopy: a review of 10,000 cases. 1689 26

We evaluated the effects of the use of nonsteroidal anti-inflammatory drugs (NSAIDs) on endoscopic and histological findings in patients with rheumatoid arthritis (RA) before and after the eradication of Helicobacter pylori infection. Helicobacter pylori (H. pylori) eradication using lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week was conducted in 44 patients (mean age: 56.5 years) with RA. Using the updated Sydney system, endoscopic and histological findings of the greater curvature of the antrum, the greater curvature of the upper corpus, and the lesser curvature of the lower corpus were compared before and after eradication, for a mean follow-up period of 3.5 months. Overall, H. pylori eradication was successful in 32 patients (72.7%). Of these 32 patients, 23 were NSAID users. In the successful eradication group, (1) there was no significant change on endoscopic findings, including gastric erythema and erosion in all three regions irrespective of NSAIDs use; (2) of 17 active ulcers before eradication in NSAIDs users, all healed except for one duodenal ulcer that persisted, where one patient newly developed a gastric ulcer, one developed erosive duodenitis, and two developed reflux esophagitis, all in NSAID users; (3) neutrophil infiltration and chronic inflammation were significantly improved in all three regions after H. pylori eradication irrespective of use of NSAIDs, while atrophic change and intestinal metaplasia did not change. In the eradication failure group; (1) there was no significant change on endoscopic and histological findings in the three regions; (2) two of three ulcers present before eradication on NSAID users persisted even after eradication, and no new cases of gastric ulcer or erosive duodenitis occurred. In conclusion, over a mean follow-up period of 3.5 months, use of NSAIDs in Japanese patients with RA did not impair the healing process of gastric and duodenal ulcers nor did it affect the endoscopic and histological improvements associated with H. pylori eradication.
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PMID:Nonsteroidal anti-inflammatory drug use does not affect short-term endoscopic and histologic outcomes after Helicobacter pylori eradication in patients with rheumatoid arthritis. 1756 79

The proton pumpvinhibitor, lansoprazole, is reported to have acid secretion inhibiting effect as well as anti-inflammatory effects such as inhibition of cytokine secretion from inflammatory cells. Clinically, excellent efficacy of lansoprazole is reported for not only gastric ulcer but also gastroesophageal reflux disease (GERD). Since GERD is categorized endoscopically into erosive esophagitis and non-erosive reflux disease, it is important to make accurate assessment of any improvement in the inflammatory process when using endoscopic ultrasonography (EUS) capable of visualizing the submucosal structure. We report here our experience in assessing the effect of treatment with lansoprazole on esophageal wall structure using EUS in patients with GERD. At baseline (before treatment), EUS showed abnormalities in the mucosa, submucosa and muscularis propria caused by inflammation, thickening of the entire esophageal wall and changes in the contractile properties of esophageal smooth muscles reflecting the effects of inflammation on the entire wall of the lower esophagus in reflux esophagitis regardless of whether it is erosive or endoscopically-negative. Treatment with lansoprazole resulted in normalization of esophageal wall structure and improvement of motility, suggesting that lansoprazole improves not only mucosal inflammation but also submucosal inflammation in GERD.
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PMID:Lansoprazole-induced improvement of esophageal submucosal injury. 1819 2

A 75-year-old man underwent endoscopic hemostatic therapy for hemorrhagic gastric ulcer in September 2002. After healing of the gastric ulcer, he underwent Helicobacter pylori eradication therapy in February 2003. In August 2007, an irregular tumor was detected in the lower esophagus at annual checkup for gastric cancer screening using X-ray. Endoscopic examination showed that the lower margin of the tumor almost coincided with the esophagogastric junction and that a short segment of Barrett's epithelium existed near the tumor. Biopsies of the tumor showed moderately to poorly differentiated adenocarcinoma. Mild reflux esophagitis and minor hiatal hernia was also observed, and the previously treated gastric ulcer was not recurrent. Absence of H. pylori was confirmed by serum antibody and urea breath test. Surgical resection of the lower esophagus and proximal stomach was performed. The tumor invaded into the muscularis propria of the esophageal wall but had no evidence of lymph node metastasis. Based on macroscopic and pathological findings, the tumor was recognized as esophageal adenocarcinoma. Previous endoscopic examination did not detect any apparent signs of tumor in the esophagogastric junction. As far as we know, this is the first report documenting a newly developed esophageal adenocarcinoma after the successful eradication of H. pylori.
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PMID:Esophageal Adenocarcinoma Developing after Eradication of Helicobacter pylori. 2176 87


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