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

Helicobacter pylori (Hp) is considered to be one of the causes of gastric mucosal injury. Using biopsy specimens from the gastric mucosa of patients with gastritis or gastric ulcer, the intramucosal mucus was quantified by computer image analysis to evaluate its relationship with Hp. In gastric mucosa positive for Hp, the mucus content within the gastric mucosa was significantly decreased. Ammonia was administered based on its assumed role in decreasing the mucus content of the gastric mucosa, and resulted in a decrease in rats to whom it was administered. Based on these results, cases of intractable gastric ulcer were studied. In these intractable cases, Hp was present significantly more often than in other cases and the intramucosal mucus content was significantly lower. These findings suggest that Hp may be a factor in the resistance of gastric ulcer to treatment.
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PMID:[Relation between Helicobacter pylori and intractable gastric ulcer--PAS positive intramucosal mucus as an index]. 157 1

To elucidate the role of Helicobacter pylori infection in the pathogenesis of gastric ulcer, we investigated the intracellular mucin content by measuring the periodic acid-Schiff-Alcian blue (PAS-AB)-stained substances, by means of computer, in the biopsy sample of gastric mucosa from patients with and without H. pylori infection. In the antral mucosa the intracellular PAS-AB-stained mucin content was significantly smaller in patients with infection than in patients without infection, whereas in the oxyntic gland mucosa the intracellular mucin content showed no significant change between patients with and without infection. In an animal study we investigated the effect of ammonia, which might be produced by H. pylori in the presence of urea. The ammonia, administered orally, caused a greater decrease of intracellular PAS-AB-stained mucin content in the gastric antral mucosa than in the body mucosa, in a dose-dependent manner. The results suggested that H. pylori infection had a different effect on the gastric mucosal intracellular PAS-AB-stained mucin and lowered specifically the antral intracellular PAS-AB-stained mucin content, possibly due to generation of ammonia by H. pylori.
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PMID:Different effect of Helicobacter pylori on the human gastric antral and body mucosal intracellular mucin. 170 31

In order to establish a reliable method for the production of gastric antral ulcer in rats, combined treatments with three factors: a vagal stimulant, a mucosal barrier breaker and a necrotizing agent were investigated. By the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (100-400 mg/kg, p.o.) and hydrochloric acid (0.15 and 0.35 N, 0.5-1.5 ml/100 g, p.o.) or ammonia solution (0.5-1.0%, 0.5-1.5 ml/100 g, p.o.), gastric lesions were prominently induced in sites of both the corpus and antrum on day 2. The largest antral ulcer was induced by the combination of 2-DG (200 mg/kg), aspirin (200 mg/kg) and ammonia solution (1%, 10 ml/kg); and the mean antral ulcer index (mm2) was 43.1 +/- 4.4 and the incidence was 100%. The antral ulcer was found to penetrate the muscularis mucosae and still observed on day 21 and day 28 after ulcer induction in a few cases. From these findings, it was indicated that this antral ulcer would be a useful model for studying the etiology and therapy of gastric ulcer disease.
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PMID:A reliable method for the production of antral gastric ulcer by a combination of 2-deoxy-D-glucose, aspirin and ammonia in rats. 174 89

Ammonia, released in the gastric mucosa by the action of Helicobacter pylori urease on transuded plasma urea, curtails the biosynthesis of mucus and/or causes the mucus to be disassembled at the mucosal surface. These changes facilitate colonisation by H pylori and may promote gastric ulcer formation.
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PMID:Hypothesis: Helicobacter pylori, urease, mucus, and gastric ulcer. 196 87

We examined the morphological changes in gastric mucosa and the generation of ammonia after exposure of the rat stomach to urea in the presence of urease, in attempts to investigate a pathophysiological role of urea, urease, and ammonia system in gastric ulcer diseases. Exposure of the stomach for 20 min to 2 ml urea (0.025-0.2%) together with urease (100 IU) induced histological damages in a concentration-related manner. Either urea or urease alone did not induce any histological change in the mucosa. Instillation of urea into the stomach generated ammonia in the presence of urease; the amount of ammonia was increased depending on the concentration of urea, and was closely associated with the severity of histological damage. The exposure of the stomach to ammonia (NH4OH: 0.01-0.1%) also produced histological damages in the gastric mucosa in a concentration-related manner. The characteristics of injury induced by 0.5-1.0% ammonia were stasis of microcirculation, disruption of the surface epithelial cells, and necrosis of the mucosa. These results demonstrated that ammonia generated from the hydrolysis of urea by urease in the stomach causes damages in the gastric mucosa.
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PMID:Generation of ammonia and mucosal lesion formation following hydrolysis of urea by urease in the rat stomach. 221 35

We examined the pathophysiological roles of the urea-urease-ammonia system in gastric ulcer disease using rats. Exposure of the stomach to ammonia (0.01-1.0%) decreased the transmucosal potential difference (PD) and histological injury in a concentration-dependent manner. Exposure of the stomach for 20 min to urea (0.025-0.2%) together with urease (100 IU) produced a decrease in PD and microscopic injury similarly, and the lesion was closely associated with the amount of ammonia produced. Urea and urease alone had no effect on the gastric mucosa. These results suggested the pathophysiological importance of urea, urease and ammonia in gastric ulcer disease.
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PMID:Effect of ammonia on the gastric mucosa in rats: pathophysiological importance of urease in gastric ulcer disease. 322 33

It is known that Helicobacter pylori (H. pylori) plays an important role in gastritis and peptic ulcer disease in the general population. Although upper gastrointestinal mucosal lesions have been one of the most common complications in patients with chronic renal failure, quite few reports are available regarding the prevalence of H. pylori and its influence on the upper gastro-intestinal tract. The present study was conducted to examine whether H. pylori is involved in the pathogenesis of upper gastrointestinal mucosal lesions in dialysis patients. The subjects consisted of 43 dialysis patients with upper gastro-intestinal tract symptoms. Thirty-four patients without any known kidney disease were used as controls. Gastric mucosa and gastric juice were obtained endoscopically. For the determination of H. pylori, culture of biopsy specimens from the gastric mucosa and histopathological examination with hematoxylin-eosin stain were used. Concentrations of serum gastrin and gastric juice ammonia were also measured. H. pylori was observed in 53.5% of the dialysis group and 64.0% of the controls. Gastro-duodenal lesions in H. pylori-positive dialysis patients included atrophic gastritis, superficial gastritis, erosive gastritis, and gastric ulcer. In the dialysis group, ammonia concentrations in the gastric juice were higher in patients with H. pylori than in those without H. pylori (489.1 +/- 35.8 mu g/ml vs 67.0 +/- 19.2 mu g/ml, p < 0.001). The former value was also higher than that seen in the H. pylori-positive controls (152.4 +/- 18.7 mu g/ml, p < 0.01). Serum levels of gastrin were significantly higher in patients with H. pylori than in patients without H. pylori (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of Helicobacter pylori in gastro-duodenal mucosal lesions in patients with end-stage renal disease under dialysis treatment]. 747 17

Aqueous ammonia in concentrations of 0.02 or 0.1% was continuously administered to rats to study its effect on the gastric mucosa histologically and cell kinetically. Furthermore, acetic acid ulcer, which is a model of chronic gastric ulcer, was experimentally induced in the stomachs of rats to assess the influence of 0.02% ammonia on the course of this ulcer. Male Donryu rats were divided into three groups given 0.02% ammonia, 0.1% ammonia or tap water. On several occasions (1, 3 and 5 days and 1, 4, 8, 12 and 24 weeks from the beginning of the experiment), the gastric mucosa in the fundic gland region and the antrum was examined histologically, and from the viewpoint of cell kinetics. The assessment in the 8th and 24th weeks employed the double labeling technique with bromodeoxyuridine and 3H-thymidine. The assessment on the other occasions used the flash labeling technique with bromodeoxyuridine. Both the 0.02% and 0.1% ammonia treatment groups showed a decrease in PAS-positive mucus and an enhanced cell cycling in the early stage of the experiment. After long periods of treatment, these groups showed a reduction in the gland height, a recovery in PAS-positive mucus and a suppression of cell cycle, suggesting direct toxicity of ammonia on the gastric mucosa. Although glandular atrophy was observed in these animals, infiltration of inflammatory cells was not observed. Thus, the relationship between ammonia and gastritis remained obscure. No ulcer developed in any group. Subsequently, we experimentally induced Ul-IV or Ul-V acetic acid ulcers in the stomachs of rats, according to the method of Okabe et al. (1971, 1972). These rats were divided into two groups given 0.02% ammonia or tap water. In the 4th and 8th weeks of the experiment, the stomachs of these rats were examined histologically and from the viewpoint of cell kinetics. The 0.02% ammonia treatment group showed a significant increase in the ulcer index (long diameter x short diameter; mm2) in the 4th and 8th weeks. This group also showed suppressed cell cycling of the regenerative epithelium and fibroblasts in the ulcer margin, suggesting direct toxicity of ammonia. Thus, healing of peptic ulcer was delayed by continuous administration of 0.02% ammonia.
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PMID:Influence of ammonia solution on gastric mucosa and acetic acid induced ulcer in rats. 751 30

The aim of the present study was to compare the gastric juice ammonia test to the CLO test for the diagnosis of H. pylori infection in culture-proven cases by receiver operating characteristic (ROC) curve analysis. We studied 75 subjects (44 with chronic gastritis, 10 with gastric ulcer, 6 with duodenal ulcer, 8 with gastric cancer, and 7 normal) by endoscopy with biopsy for tissue diagnosis, culture of H. pylori. CLO test, and by gastric juice ammonia determinations. The culture-positive group had significantly higher intragastric ammonia levels (13.7 +/- 5.8 mg/dl) than the negative group (4.9 +/- 2.4 mg/dl, P < 0.01). In ROC curve analysis, the gastric juice ammonia test showed higher true positive and lower false positive ratios than the CLO test (P < 0.05). In conclusion, the measurement of intragastric juice ammonia levels was considered to be simpler, quicker, and overall a more valuable method for diagnosing H. pylori infection.
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PMID:Gastric juice ammonia vs CLO test for diagnosis of Helicobacter pylori infection. 772 68

The effect of long-term administration of nipradilol (NIP, Hypadil Kowa, CAS 81486-22-8), a beta-blocker with a vasodilatory action, on esophageal varices was studied in 66 patients with compensated liver cirrhosis. Administration of NIP (6-12 mg/d) for 3-12 months produced progressive improvement of endoscopic findings over time (30% for C, 25% for F, and 40% for the R-C sign after 12 months). At the last examination (mean: 9 +/- 4 months), the improvement rates were 16.7%, 16.7% and 22.7%, respectively. No significant relationship was found between endoscopic improvement and the Child-Pugh score or the dose of NIP. Gastrointestinal bleeding occurred in five patients: one had bleeding esophageal varices, three had bleeding gastric varices, and one had a bleeding gastric ulcer. The systolic blood pressure was decreased significantly (4.6-12.3%) at 2 weeks as well as 1 and 2 months, and the heart rate showed a significant decrease throughout the study (10-18.4%). With the exception of the patients who had gastrointestinal bleeding, no symptoms of decompensation appeared, and there was no deterioration of laboratory parameters including ammonia. Adverse effects occurred in about 10% of the patients, most of which were related to bradycardia and/or hypotension, and they improved when the drug was withdrawn or the dose reduced. These results suggest that long-term administration of NIP is useful in the treatment of esophageal varices.
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PMID:Effect of long-term therapy with nipradilol on esophageal varices in patients with compensated cirrhosis. Results of a multicenter open study. 784 40


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