Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is accumulating that Helicobacter pylori infection plays a major contributory role in peptic ulcer disease [Duodenal Ulcer (DU) and Gastric ulcer (GU)] and non-ulcer dyspepsia (NUD). We, therefore, studied prospectively 210 consecutive patients with upper gastrointestinal symptoms (62 DU, 38 GU and 110 NUD) to determine the prevalence of H. pylori infection and to investigate their association with histological gastritis. Using endoscopic biopsy of the gastric antrum for diagnosing H. pylori infection by Campylobacter-like Organism (CLO) test, histology or bacteriology, the overall prevalence of H. pylori was 63.3 per cent. When H. pylori infection was related to diagnosis, DU had the highest prevalence rate of H. pylori infection (66%), GU and NUD were less frequently associated with H. pylori infection (55% and 44% respectively). We found a close association between H. pylori infection and histologically antral gastritis, in that 72.7, 61.7, and 62.6 per cent of the DU, GU and NUD patients with antral gastritis (respectively) had H. pylori infection. In contrast, none of these patients seen with normal antrum had H. pylori infection. We also found that the prevalence of H. pylori in our patient series was not age related. Of the three procedures used to demonstrate H. pylori, the CLO test and histological staining method gave the highest yields of 84.9 and 79.6 per cent respectively, and bacteriology in only 44.3 per cent, we conclude that the prevalence of H. pylori infection in Thai patients with upper gastrointestinal symptoms is high. H. pylori infection commonly occurs in the patients with antral gastritis, suggesting a possible etiologic role for the bacterium in the histologic lesion.
 ...
PMID:Helicobacter pylori and peptic ulcer diseases: prevalence and association with antral gastritis in 210 patients. 129 55

Helicobacter pylori is known to be responsible for most cases of chronic gastritis, but its role in the outcome of gastric ulcer is unknown. The purpose of this study was to determine the prevalence of H. pylori infection before and after treatment of gastric ulcer, the micro-organism being untreated. The trial involved 26 patients with an acute episode of gastric ulcer, who had undergone endoscopy with biopsy of the antrum, the fundus and the ulcer rim at the initial examination and then 6 weeks and 1 year after the diagnosis. At day 0, 25 acute ulcers were associated with chronic H. pylori gastritis; one patient had neither gastritis nor H. pylori infection. The H. pylori count correlated with the activity of chronic gastritis and with the extension of intestinal metaplasia; it was not modified by the healing of gastric ulcer observed in 24/26 patients on day 360. These results confirm the existence of a close association between H. pylori, chronic gastritis and gastric ulcer. It also suggests that H. pylori is not directly involved in the healing or recurrence of gastric ulcer.
 ...
PMID:[Association of stomach ulcer and Helicobacter pylori. Prognostic implications]. 129 29

The effectiveness of a fluorescent analysis in the diagnosis of gastric cancer was studied in 280 patients. Fluorescence of a tumor was noted in 87% of cases. Dependence of fluorescence of a tumor on its sizes was revealed: in tumor diameter less than 1 cm, fluorescence was revealed in 94% of cases, more than 4 cm--in 76%. In infiltrative growth, only 74% of tumors were fluorescent. To define the possibility of the use of a fluorescent analysis in the differential diagnosis of gastric diseases, 490 patients with presumptive diagnosis of chronic gastritis, gastric ulcer disease, polyposis were examined. In diagnosis of +malignant polyps in 91.5% of cases, results of the fluorescent analysis concurred with the findings of histologic study. Probability of establishing the correct diagnosis by the data of fluorescent analysis in ulcer disease is equal to 87.5%, in chronic gastritis--86%.
 ...
PMID:[Use of the fluorescent analysis in early diagnosis of cancer of the stomach]. 138 May 85

The aim of this experience has been to evaluate the chief cell mass and serum pepsinogen I in gastric ulcer patients. Comparisons were also made with parietal cell mass and acid secretion. Chief cell mass and serum pepsinogen I are not only influenced by the localization of ulcer but, also, by the histological condition of fundic mucosa. In fact, the behaviour of serum pepsinogen I and chief cell mass in type I gastric ulcer is the same observed in case of fundic chronic gastritis without gastric ulcer. In case of gastric ulcer type I with superficial fundic gastritis it emerges normozymogenism with hyperpepsinogenemia++ I, with preatrophic fundic gastritis hypozymogenism with normopepsinogenemia, with atrophic fundic gastritis hypozymogenism with hypopepsinogenemia I. In type II and III gastric ulcer the chief cell mass and serum pepsinogen I behaviour as they do in duodenal ulcer with hyperpepsinogenemia although hypozymogenism is present.
 ...
PMID:[Chief cell mass in gastric ulcer: cyto-secretory correlations]. 139 Nov 49

Chronic gastritis is a common inflammatory disease. In a number of patients, the inflamed gastric mucosa shows a gradual tendency to become atrophic (atrophic gastritis). Gastritis tends to be lifelong, and spontaneous healing is rare. With very few exceptions (e.g. in patients with autoimmune chronic corpus gastritis), gastritis is associated with the presence of the bacterium Helicobacter pylori. Inflammation and atrophy of the gastric mucosa result in impairment of gastric secretory functions (e.g. secretion of gastric acid, pepsin and gastrin). Such impairment is dependent on the topographic type of gastritis; i.e. whether the inflammation and atrophy occur in the antrum (chronic antral gastritis), corpus (chronic corpus gastritis) or in both the antrum and corpus simultaneously (chronic pangastritis). Gastritis of different topographic types associates with different gastric diseases. In patients with H. pylori-related antral or pangastritis, peptic ulcer disease, and in particular duodenal ulcer, is common (with an incidence exceeding 20% after 10 years' follow-up), as compared with peptic ulcer disease, which is very rare in patients with a normal stomach. Gastric ulcer may sometimes occur in patients with a rather atrophic stomach, but both gastric and duodenal ulcers are extremely rare in patients in whom the gastritis accompanies severe atrophic changes in the corpus mucosa. Routine biopsies from the antrum and corpus, and interpretation of the results in the light of the data on gastritis and its atrophic sequelae, allow the gastroenterologist to predict the risk and likelihood of peptic ulcer disease in patients with gastritis.
 ...
PMID:Natural history of gastritis and its relationship to peptic ulcer disease. 139 47

The development of gastric enterochromaffin-like (ECL)-cell hyperplasia in humans may be associated with extreme hypergastrinaemia, as occurs in Zollinger-Ellison syndrome (ZES) and pernicious anaemia (type A gastritis). More recently, endocrine cell hyperplasia has been found in all forms of chronic atrophic gastritis and even in cases of focal atrophy. Serum gastrin levels, non-antral gastric endocrine (argyrophil) cell growth, and the severity and type of concomitant gastritis were monitored in 66 unoperated and 8 antrectomized patients with poorly responsive peptic ulcer or reflux oesophagitis during up to 5 years' treatment with high-dose omeprazole, 40 mg daily. A small subgroup of patients (23%) had serum gastrin concentrations of more than four times the normal upper limit. These patients also had hyperplasia of the gastric argyrophil cells. More importantly, the same subgroup of patients had high-grade (atrophic) gastritis. Micronodular hyperplasia of argyrophil cells was significantly more frequent in biopsies showing atrophic gastritis (48%) than in biopsies showing only superficial gastritis (3.6%). It is concluded that, as previously demonstrated in untreated patients with gastric ulcer, the argyrophil cell hyperplasia observed during high-dose omeprazole therapy is related to the progression of chronic atrophic gastritis rather than to serum gastrin levels.
 ...
PMID:Inter-relationship between serum gastrin levels, gastric mucosal histology and gastric endocrine cell growth. 139 48

Sixty three children with dyspepsia (mean age 12 years, range one to 18, M/F 41/22) were Helicobacter pylori positive by histology of gastric antral biopsy specimens and were treated with a six week course of amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). The endoscopic diagnoses were: normal (16), nodular gastritis (19), oesophagitis (four), duodenal ulcer (13), and gastric ulcer (11). H pylori was eradicated in 54 (87%) and histological gastritis resolved in 51 and was improved in the other three. Repeat investigation was offered at six monthly intervals. Reinfection was found in three of 34 (9%) at six months, in none of 22 at 12 months, and in two of 18 (11%) at 18 months, yielding an 18 month cumulative relapse rate of 20%. Children with persisting infection despite treatment remained positive during follow up. Serum H pylori IgG concentrations fell after treatment (p < 0.001), and for individual children during follow up there was a progressive decline, but an increased concentration indicated recurrence. After eradication of H pylori by combined amoxycillin and tinidazole treatment, only a minority of children relapse during the ensuing 18 months.
 ...
PMID:Eighteen month follow up of Helicobacter pylori positive children treated with amoxycillin and tinidazole. 144 54

We measured gastric and duodenal mucosal prostaglandin concentrations in 69 patients with active or inactive duodenal or gastric ulcer disease and 26 non-ulcer controls. Each underwent endoscopy enabling us to obtain multiple biopsies from the gastric body and antrum and from the duodenal bulb and postbulbar duodenum for measurement of mucosal prostaglandin concentrations, as well as a single biopsy from each region for mucosal histology. Using a multivariate linear regression model, we found that neither gastric nor duodenal ulcer disease significantly affected gastric or duodenal mucosal prostaglandin concentrations. Mucosal prostaglandin concentrations were similar at the edge of the ulcer and in the adjacent non-ulcerated mucosa. Neither gender symptoms, smoking, use of H2-receptor antagonists, disease activity, nor Helicobacter pylori infection had an independent effect on mucosal prostaglandins in any region. Gastritis in the body of the stomach was associated with significantly higher prostaglandins, while older age was associated with significantly lower gastric and duodenal prostaglandins. Gastroduodenal mucosal prostaglandins are thus not altered in patients with active or inactive peptic ulcer disease, even when multiple demographic and histologic variables are taken into consideration.
 ...
PMID:Gastric and duodenal mucosal prostaglandin concentrations in gastric or duodenal ulcer disease: relationships with demographics, environmental, and histological factors, including Helicobacter pylori. 144 36

Gastroendoscopic biopsy specimens from 366 patients were stained with HE, Warthin-Starrys or Giemsa and mucin histochemical methods. Positive rate of Helicobacter pylori (HP) was 73.8% in chronic gastritis. Positive rates of HP in gastric ulcer disease were 88.2%, 91.9%, and 11.1% at the near and distant mucosa of ulcer and in duodenitis, respectively. Positive rates of HP in duodenal ulcer disease were 81.5%, 24.6% and 7.2% at the pyloric-antral area and at the near and distant mucosa of duodenal ulcer, respectively. The number of HP in active inflammation was higher than that in inactive inflammation (P < 0.05). The HP almost lived in the neutral mucin. There was no statistical significant difference between near and distant mucosa of ulcer (P > 0.05). HP might play an important role in the pathogenesis of chronic gastritis, and it might aggravate the peptic ulcer disease.
 ...
PMID:[A study on the pathogenicity of Helicobacter pylori in chronic gastritis and peptic ulcer disease]. 145 59

One hundred forty-five consecutive gastric biopsy specimens showing colonization by Helicobacter pylori (HP) were studied. Biopsy specimens were obtained from patients with the following conditions: gastric ulcer (GU; 76), active chronic gastritis (ACG; 52), GU with duodenal ulcer (DU; 10), and ACG with DU (7). The mean age of the patients in the ACG group was 8.6 years less than the patients in the GU group. Helicobacter pylori colonization and HP-induced epithelial degeneration (ED) were quantified by a grading system (grades 0 to 6) comprising both focal and global scores for bacterial density (HP grade) and severity of ED (ED grade). The ED grade was directly proportional to the HP grade in all biopsy specimens. Gastric ulcer biopsy specimens were associated with higher HP grades: HP grade more than 5 in 25 cases (32.9%) and ED grade more than 5 in 18 cases (23.6%) of GU compared with similar respective scores in 9 cases (17.9%) and 2 cases (3.8%) of ACG. The difference was due primarily to a higher global score of bacterial density and higher focal score of ED in the GU biopsy specimens. These results support the hypothesis that HP-positive ACG and HP-positive GU are lesions within a single disease spectrum. Heavy HP colonization and severe HP-induced epithelial damage are predisposing factors in ulcerogenesis. Because HP-positive ACG is probably a preulcerative state, eradication of the bacteria in HP-positive ACG might prevent subsequent GU.
 ...
PMID:Helicobacter pylori-related gastritis and gastric ulcer. A continuum of progressive epithelial degeneration. 146 50


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>