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

In resected portions of the stomach we find chronic atrophic gastritis of the corpus only in 10% of the patients with duodenal ulcers, and chronic inflammatory changes are, contrary to patients with a gastric ulcer, less marked. The difference is statistically significant. Consistent with some other authors, we find that great progression of chronic inflammatory changes occurs in patients operated on account of duodenal ulcers in the course of the first three years after operation. From six cases of regression of chronic inflammatory changes after operation, in two cases undetected atrophic gastritis was involved which was present in a severe form in the body of the resected portion beyond the vicinity of the gastric ulcer. According to the author's findings regression of atrophic gastritis is possible. The high score of chronic inflammatory changes in the antrum of gastric resectates (3.54) and in the close vicinity of gastric ulcers (4.0) confirms the frequency of severe antral gastritis in peptic ulceration and the intensity of the focal inflammation in the vicinity of gastric ulcers.
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PMID:[Comparison of the degree of chronic gastritis in the resected gastric body with histologic findings in postoperative gastric biopsy]. 271 17

Fasting gastric juice pH and concentrations of vitamin C in gastric aspirate and plasma were measured in 73 patients undergoing endoscopy. Vitamin C concentrations were significantly lower in those with hypochlorhydria (pH greater than 4; n = 23) compared with those with pH less than or equal to 4 (p less than 0.005) and there was a significant correlation between gastric juice and plasma concentrations (p = 0.002). Patients with normal endoscopic findings had significantly higher intragastric concentrations of vitamin C than those with gastric cancer (p less than 0.001), pernicious anaemia (p less than 0.005), gastric ulcer (p less than 0.01), duodenal ulcer (p less than 0.05), or after gastric surgery (p less than 0.01). There was a strong trend (0.05 less than p less than 0.1) towards lower intragastric concentrations of vitamin C in patients with chronic atrophic gastritis. In vitro, vitamin C concentrations remained stable in acidic but fell significantly over 24 hours in alkaline gastric aspirate. Gastric secretory studies in five volunteers showed that vitamin C concentrations increased significantly after intramuscular pentagastrin. These findings suggest that the low fasting levels of vitamin C in hypochlorhydric gastric juice may be caused by chemical instability and that vitamin C may be secreted by the human stomach.
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PMID:Vitamin C in the human stomach: relation to gastric pH, gastroduodenal disease, and possible sources. 271 77

Chronic (atrophic) gastritis (AG) is common in active duodenal (DU) and gastric ulcer (GU) disease. In this case control study in consecutive prospective outpatients (571 cases and 1074 controls) who had undergone diagnostic upper gastrointestinal endoscopy and routine biopsies from both antral and body mucosa, we calculated the risk of coexisting active DU and/or GU in different gastritis of the antrum or body and according to grade (superficial gastritis, mild, moderate or severe atrophic gastritis). The risk of coexisting active gastroduodenal ulcer (ulcer in duodenum and/or stomach), as well as the risk of DU or GU, was dependent upon the presence and grade of gastritis in antrum and body mucosa. The risk of coexisting ulcer, as expressed as an age adjusted relative risk (RR) and calculated as odds ratio of gastritis in cases and controls, was significantly increased in the presence of superficial antral and body gastritis (RR = 8.5 (7.0-20.0) in men; RR = 5.8 (3.3-10.2) in women), as compared with the risk of ulcer in subjects with histologically normal mucosa (RR = 1). The risk of ulcer, and the risk of GU in particular, increased further with increasing severity of antral gastritis. In such patients with moderate or severe atrophic antral gastritis the RR of coexisting ulcer even exceeded 20 in men and 10 in women (RR = 25.6 (9.0-72.7) in men; RR = 11.7 (5.9-23.0) in women). On the other hand, the RR of ulcer, and the RR of DU in particular, was below 1 in the presence of atrophic gastritis in the gastric body, irrespective of the grade of gastritis in the antrum. We conclude that the type and grade of gastritis strongly predicts the risk of coexisting peptic ulcer, and that the risk of coexisting DU or GU increases with an increase in grade of AG of the antrum but decreases with an increase in grade of AG of the gastric body.
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PMID:Chronic gastritis and gastroduodenal ulcer: a case control study on risk of coexisting duodenal or gastric ulcer in patients with gastritis. 275 89

The presence of Campylobacter pylori was studied in biopsy material from gastric mucosa taken by guided biopsy during fiber gastroduodenoscopy from 101 patients with chronic gastritis (n = 50), peptic gastric ulcer (n = 28), peptic duodenal ulcer (n = 7), gastric cancer (n = 10) and gastric polyposis (n = 6). Campylobacter pylori was found in various quantity--moderate (++) and considerable ( )--in 64% of the patients with chronic gastritis, in 85.7% of the patients with peptic gastric ulcer and in 100% of the patients with peptic duodenal ulcer as well as in half of the patients with gastric cancer and polyposis. The quantity of Campylobacter pylori correlated with the severity of the inflammatory process and the degree of atrophy of the gastric antral mucosa. A tendency toward seasonal incidence of Campylobacter pylori infection of gastric mucosa was established: 78.69% of the patients examined during spring time (April-May) and 60.0% of the patients examined during winter time (January-February) had Campylobacter pylori infection. This explains to a certain extent the seasonal exacerbations of the pathological process in chronic gastritis and peptic ulcer. The development of a well expressed chronic atrophic gastritis is in direct relation with the greater quantity of Campylobacter pylori in the gastric mucosa. The study reveals the pathogenetic relations between the presence and quantity of Campylobacter pylori and the development and evolution of chronic gastritis and peptic gastric and duodenal ulcer.
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PMID:[Campylobacter pylori in patients with chronic gastritis and gastric and duodenal peptic ulcer]. 276 25

In view of the low incidence of hypertrophic pyloric stenosis, we present a case of this pathology in a male aged 74. Stenosis was of the diffuse type, associated with gastric ulcer and chronic atrophic gastritis. The patient was admitted to our Service with upper digestive tract hemorrhage after deterioration of the ulcer.
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PMID:Hypertrophic pyloric stenosis in the adult. 279 14

The aim of this double blind trial was to compare omeprazole 20 mg once daily with ranitidine 150 mg b.i.d. in treatment of benign gastric ulcer, evaluating both rates and histological aspects of the ulcer healing process. Eighteen patients were randomized, 9 to each treatment; one patient (ranitidine group) was excluded from the analysis because of malignant ulcer. Omeprazole appeared to be more effective than ranitidine in healing gastric ulcer. A more rapid relief of symptoms was observed in the omeprazole group than in the ranitidine group. Both drugs reduced chronic atrophic gastritis (with a trend in favour of omeprazole), while omeprazole showed a prompter activity on the components of acute inflammation.
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PMID:Histological aspects and healing rates of gastric ulcers treated with omeprazole 20 mg once daily or ranitidine 150 mg B.I.D. 279 47

Single biopsies of human gastric mucosa from controls and different groups of patients were used for enzymatic cell isolation by pronase and collagenase and subsequent count of parietal and nonparietal cells. This procedure was tested in regard to its validity and delivered the following cell numbers. Total gastric cells/mg wet weight gastric mucosa: normal gastric mucosa [controls (C), n = 95] 31,500 +/- (SEM) 1,490, chronic superficial gastritis (GI; n = 49) 36,300 +/- 2,770, chronic gastritis with beginning atrophy (GII; n = 36) 44,100 +/- 3,050 (p less than 0.025), chronic atrophic gastritis (GIII; n = 12) 40,100 +/- 5,760, duodenal ulcer (DU; n = 26) 29,340 +/- 2,280, gastric ulcer (GU; n = 23) 37,090 +/- 3,000, gastric resection according to Billroth I (BI; n = 7) 57,480 +/- 12,360 (p less than 0.005) and Billroth II (BII; n = 12) 52,560 +/- 6,730 (p less than 0.005). Parietal cells/mg wet weight gastric mucosa: 1,910 +/- 490 (C), 1,980 +/- 140 (GI), 1,700 +/- 200 (GII), 1,170 +/- 220 (GIII, p less than 0.025), 2,580 +/- 240 (DU, p less than 0.05), 1,690 +/- 150 (GU), 1,500 +/- 250 (BI), 1,360 +/- 320 (BII). Parietal cell concentration (density) did not differ in males and females and did not change with age. The method delivers relevant cell numbers, is suitable to detect qualitative differences and can be used for the interpretation of biochemical studies.
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PMID:Morphologically different biopsy specimens of the human gastric mucosa. I. The use of enzymatic cell isolation for quantitative determination of parietal cells. 301 1

In this revision article it was tried to focus on the role played by pepsinogen/pepsin since its discovery until its practical use. Pepsinogen determination as the gastric acid secretion has different basal or stimulated secretion levels in the peptic ulcer, gastritis, etc. The methods for pepsinogen determination are evaluated, verifying that, in spite of radioimmunoassay utilization another methods less sophisticated have been used successfully. The pepsinogen seric levels (PSL) after stimulation with Histalog, discriminate the patients suffering from duodenal ulcer from normal individuals, and they are higher among men than women. A parallelism is made between pepsinogen-I and II finding out pepsinogen-I higher level in smoking individuals. The pepsinogen-I is increased in the duodenal ulcer and II in the gastric ulcer and both of them bent to be characterized as a genetic marker for peptic ulcer. Finally, the main clinical applicability for PSL group I determination is the detection of atrophic gastritis considering its potential for gastric malignancy.
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PMID:[Pepsinogen I and duodenal ulcer]. 306 7

Factors in upper intestinal content that can produce acute injury to the gastric mucosa include lysolecithin and the bile acids. Both damage the gastric mucosal barrier by increasing mucosal permeability. The secondary and deconjugated bile acids are more toxic in this regard than are the primary or conjugated ones. The extent of injury is highly pH-dependent. Although the bile acids do not affect the gel properties of gastric mucus, they do produce significant inhibition of carbonic anhydrase activity and gastric bicarbonate secretion. In concert with other topical damaging agents, bile acids increase mucosal blood flow. However, gross mucosal lesions are rarely observed under these circumstances. Chronic exposure of acid-peptic-secreting mucosa to upper intestinal content results in the development of a severe atrophic gastritis within 6 months. The ability of atrophic mucosa to maintain an intraluminal pH gradient is impaired, and it ulcerates with great regularity when exposed to a highly acid environment. Clinically, excessive enterogastric reflux has been implicated in the pathogenesis of both benign gastric ulcer and the post-gastrectomy syndrome of alkaline reflux gastritis. The evidence to support this view for both disease entities is reviewed.
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PMID:Other causes of GI mucosal injury: upper intestinal content. 311 2

138 consecutive patients with endoscopically and histologically confirmed benign gastric ulcer were investigated in order to evaluate the relationship between aging and parameters relating to gastric ulcer pathophysiology and natural history: prevalence in dyspeptic patients referred to an endoscopic unit, recurrences, gastric acid secretory capacity, peptic activity, incidence of precancerous and neoplastic changes. On the basis of our results, different populations of gastric ulcer patients seem to be identifiable: (1) young patients (aged under 40), with low prevalence and recurrence rates, with acid capacity above normal range, high peptic activity and no risk for precancerous or neoplastic changes, (2) middleaged subjects (41-50), with high prevalence and recurrence rates, high peptic activity and acid activity within the normal range, atrophic gastritis, intestinal metaplasia, dysplasia and low incidence of cancer, and (3) elderly patients (aged over 50), with lower prevalence and recurrence rates, frequent association with chronic atrophic gastritis, impaired acid and peptic secretion, in whom one may observe either an association of the ulceration with cancer or evolution of dysplasia into neoplasia. These observations confirm that elderly and middle-aged gastric ulcer patients should undergo routine follow-up, and that pathophysiological data should be taken into account before deciding upon antiulcer therapy.
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PMID:Gastric ulcer and stomach aging: pathophysiology and clinical implications. 322 Feb 64


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