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

In histological examination of gastrectomy specimens from patients with duodenal ulcer, gastric ulcer, and early and advanced cancer, both chronic atrophic gastritis and intestinal metaplasia were identified in 54% of the cases with duodenal ulcer. At 90 to 100%, respectively, these mucosal changes were approximately twice as frequent with gastric ulcer and early and advanced gastric cancer. Mild dysplasia occurred in 54% of the cases with duodenal ulcer; occurred somewhat more frequently with gastric ulcer, in 75% of the cases; and in almost all cases with early and advanced gastric cancer, at 90% and 100%, respectively. Whereas 27% of the cases with duodenal ulcer, 62% with gastric ulcer, and 90% and 95% of the respective cases with early and advanced gastric cancer showed moderate dysplasia, only severe dysplasia in early gastric cancer (40%) and advanced gastric (81%) was clearly more frequent in comparison to duodenal ulcer (9%) and gastric ulcer (12%). In the cases with duodenal ulcer chronic atrophic gastritis and intestinal metaplasia were limited mostly to the antrum; with gastric ulcer and cancerous stomach disorders, they also occurred in other stomach sections. Mild and moderate dysplasia conformed to the same distribution pattern. Severe dysplasia, which was only detected in two ulcer cases, was not only substantially more frequent in cases with early and advanced gastric cancer, but also showed a clear topographic relationship to cancer localization in the stomach.
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PMID:Gastritis, intestinal metaplasia and dysplasia versus benign ulcer in stomach and duodenum and gastric carcinoma -- a histotopographical study. 46 Dec 33

Because of the higher risk of cancer in the gastric stump, an increased incidence of pre-cancerous conditions should be exspected also in the resected stomach. Therefore, a combined endoscopic and bioptic study was performed in order to investigate the incidence of dysplasias in the gastric stump after resection for benign conditions. Among 101 patients with gastric resection, 2 cases were excluded from this study because of preceeding gastric cancer and one because of cancer of the gastric stump. In 43 of the remaining 98 patients, a Billroth-I-resection (gastroduodenostomy) had been carried out. In the remaining 55 patients with a Billroth-II-resection (gastroenterostomy) 9 had an additional enteroanastomosis of Braun whereas in the residual 46 patients this enteroanastomosis was lacking. This distinction was made because of a facultative or obligatory bile reflux. The average age of the B-I-group was 68 years, of the B-II-group with enteroanastomosis 69 years, and the B-II-group without enteroanastomosis 62 years. A non-operated group matched for age served as control group. Biopsy particles from the anastomotic region were gained by endoscopy and cut in step sections. The classification of dysplasias (degree I-III) followed the criteria given by Nagayo as modified by Grundmann. Inflammatory reactive changes were separated from these. A few changes could not be classified definitely and were listed as unclassified dysplasia. While dysplastic changes of low degree were quite numerous in every group, the dysplasias of higher degree were only found in a small number of cases. In the 46 cases with B-II-resection without Braun's enteroanastomosis, there were 5 dysplasia II and 3 dysplasia II. In the 9 cases with B-II-resection and with Braun's enteroanastomosis, there was 1 dysplasia I and no dysplasia III. In the 43 patient with B-I-resection only 2 dysplasia II and no dysplasia III were found. In the control group of 98 patients matched for age there were only 5 cases with dysplasia I and 1 case with dysplasia III. Patients with higher degrees of dysplasia showed a higher age and a longer interval after operation. There was also a correlation between higher degrees of dysplasia and severe atrophic changes in the mucosa. Correlating the degree of dysplasia with the reason for gastric resection, most of the dysplastic changes occurred in patients resected for gastric ulcer, whereas cases resected for duodenal ulcer showed only 2 dysplasias I. The discussion refers to the few data about dysplasia of the gastric stump available from the literature. Atrophic and increased regenerative changes obviously play a role in the pathogenesis of these dysplastic changes. As a causative factor the role of bile reflux is discussed. A further diagnostic and therapeutic regimen for the different forms of dysplasia is proposed.
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PMID:Incidence of epithelial dysplasia after partial gastric resection. 46 Dec 34

The incidence and distribution of chronic gastritis, chronicatrophic gastritis and epithelial dysplasia I-III have been investigated in 50 resected stomachs of patients suffering from duodenal ulcer, gastric ulcer, early or advanced gastric cancer. Only in gastric cancer epithelial dysplasia III has been frequently observed, particularly in the neighbourhood of gastric cancer. Distribution of chronic-atrophic gastritis was similar to the distribution of dysplasia I and II. These mucosal lesions were detectable with the same frequency in patients with or without gastric cancer.
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PMID:[Histo-topography of gastric mucosa changes in benign and malignant stomach diseases]. 61 13

Being pepsinogen A (PGA) levels generally reduced and pepsinogen C (PGC) increased in gastric cancer patients, PGA/PGC ratio has been proposed as a useful marker of the tumour. We tested PGA, PGC and Gastrin (G) levels in patients with gastric cancer (39) and, as a control, in patients with epithelial dysplasia (21), chronic atrophic gastritis (57), gastric ulcer (11) or subjects lacking major or minor endoscopic and microscopic changes at gastroscopy (48). PGA and PGA/PGC levels were significantly reduced in gastric cancer patients (p less than 0.005 and p less than 0.0001 respectively with analysis of variance). Gastrin levels were also reduced in the same patients (p less than 0.005). We therefore adopted an index number (PGA x Gastrin) which was also dramatically reduced in gastric cancer (p less than 0.005); using an arbitrarily chosen cut-off, the "marker" showed very high sensitivity (76%), specificity (96%) and overall accuracy (74%, by Youden J test). We therefore suggest the use of the index number PGA x G in the diagnosis of gastric cancer, as the most useful gastrin presently available, to our knowledge.
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PMID:Pepsinogen A/pepsinogen C or pepsinogen A multiplied by gastrin in the diagnosis of gastric cancer? 175 13

To assess the evolution of gastric epithelial dysplasia (GED), a prospective multicenter study was based on a protocol of repeated endoscopies and biopsies. To date, 134 cases (0.4% of all patients endoscopically examined in the same period) have been diagnosed as having GED and 80 of those have had an "adequate" follow-up (at least three endoscopies). Mean follow-up time was 18 months. Gastric epithelial dysplasia was mild in 59% of cases, moderate in 25%, and severe in 10%. Six percent of the patients had lesions that were "indefinite for dysplasia." Chronic atrophic gastritis (40%), gastric ulcer (32%), gastrectomy (10%), and polyps (9%) were the most frequently associated lesions. The term "regression" was adopted for GED no longer detectable during follow-up and the term "progression" was used when more severe changes or cancer was detected. Mild GED regressed in 66% of cases, persisted in 15%, and progressed in 19% (three cases to moderate, one to severe, and five to cancer). Moderate GED regressed in 30% of patients, persisted in 30%, and progressed in 40% (one to severe GED and seven to cancer). Severe GED regressed in 12.5% of patients, persisted in 12.5%, and progressed to cancer in 75%. Of the five patients with lesions indefinite for dysplasia, two had no dysplastic changes at follow-up and three had cancer diagnosed. Ten of 21 cases of cancer (48%) were at the early stage. The diagnosis was reached within the first year of follow-up in 14 cases and after 1 year in seven (13 to 39 months). Fifteen of 21 cases of cancer were diagnosed in gastric ulcer patients. In conclusion, GED is an infrequent finding and its biologically neoplastic significance is confirmed by the results of the follow-up study: (1) in its mild form, it tends to regress but adequate subsequent check-ups are mandatory as it may associate with or evolve as cancer; (2) patients with moderate GED require strict follow-up since the lesion shows a higher cancer risk; (3) surgery is indicated for severe GED because gastric cancer develops in 75% of cases; and (4) patients with lesions indefinite for dysplasia should immediately undergo repeat endoscopy and biopsy. Such an approach allows gastric cancer to be detected at an early stage in a much higher percentage of cases than may be expected.
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PMID:Gastric epithelial dysplasia: a prospective multicenter follow-up study from the Interdisciplinary Group on Gastric Epithelial Dysplasia. 184 72

The beneficial effect of low-energy laser radiation on the natural course of disease, morphologic characteristics of gastric mucosa and key elements of systemic hemostasis was observed in 98 patients with precancer of the stomach (gastric ulcer and chronic atrophic-hyperplastic gastritis with epithelial dysplasia). A correlation between clinical response and normalization of morphologic appearance and homeostasis makes the above-mentioned treatment modality promising and worth further development.
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PMID:[The potentials of low-intensity laser radiation in treating precancerous diseases of the stomach]. 184 54

The aim of this work was to study the relationship between intestinal metaplasia and dysplasia in gastric ulcers and their tissue repair in 223 patients with 236 gastric ulcers found endoscopically and treated with H2 blockers. The average duration of follow-up for the men was 32.4 months (range, 12-87 months) and for the women 42.5 months (range, 12-88 months). In 112 patients (50.2%) with 118 gastric ulcers, intestinal metaplasia in the different types was observed. The data obtained allow us to state that severe dysplasia and gastric cancer can occur only in a restricted number of patients with intestinal metaplasia in gastric ulcers and/or gastric ulcer tissue repair (two in our study, more than 60 yr old), and only in the forms with sulphomucins, more precisely type III. In relation to the fact that gastric ulcers rarely become carcinoma, the intestinal metaplasia frequently observed should not be considered "precancerous", as such, but could become so in the presence of several factors which, excluding age, did not emerge from our study.
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PMID:Intestinal metaplasia and dysplasia in gastric ulcer and its tissue repair. 197 92

A follow up study with biopsy was initiated in 1982 to define the relations between variants of intestinal metaplasia and the evolution of chronic atrophic gastritis and gastric ulcer. All patients (58 with chronic atrophic gastritis and 66 with gastric ulcer) had intestinal metaplasia at the start of the study. In the six year period to 1988 a total of 241 biopsies were performed on the patients with chronic atrophic gastritis and 243 on the patients with gastric ulcer. Initially, 81% of the patients with chronic atrophic gastritis presented with type I intestinal metaplasia and 14% with type III intestinal metaplasia. During follow up type I was predominant, often associated with grades 2 and 3 active disease (81%) and 45% of these patients reverted to a non-intestinal metaplasia status by the third year of follow up. In contrast, type III metaplasia was more common in the absence of appreciable inflammation (78% of biopsy specimens), being persistent in five of seven patients in the third year of follow up, and was found to be associated with dysplasia in three of these patients. Similarly, the initial biopsy specimen showed type I metaplasia in most patients with gastric ulcer (82%) and type III in only 4%. Type I metaplasia was also predominant in these patients (80%), particularly in active disease (68%), gradually regressing with healing. In contrast, type III was associated with delayed ulcer healing and reactivation (75%; six of eight patients). We conclude that (a) type I is a short term reactive process which regresses with healing; (b) type III is related to prolonged injury and chronicity and may regress or progress to dysplasia; (c) persistent and more immature forms of metaplasia may carry an increased risk of malignancy.
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PMID:Variants of intestinal metaplasia in the evolution of chronic atrophic gastritis and gastric ulcer. A follow up study. 208 54

Two hundred and ninety-four patients with precancerous lesions of the stomach were followed and treated. The group included cases of gastric ulcer (101), polyps (78), atrophic-hyperplastic gastritis (81) and 34 patients who had undergone gastric resection for duodenal ulcer. Pathologic foci were surrounded by areas of epithelial dysplasia of varying degree in almost all patients. In the course of follow-up and treatment, dysplasia regressed in several cases and progressed to early cancer of the stomach in three. Recommendations for periodicity of check-ups of patients with chronic cancer of the stomach depending on degree of mucosal epithelium dysplasia were developed.
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PMID:[The ambulatory care of patients with precancerous diseases of the stomach]. 221 44

Quantitative analysis of dendritic cells (DC's) was carried out in tissue specimens of normal gastric mucosa (n = 15), gastric ulcer (n = 19), chronic atrophic gastritis (n = 28), and gastric carcinoma (n = 65) by ABC immunostaining with S100 protein antibody. Significant increases in DC number were observed in chronic atrophic gastritis with type III intestinal metaplasia and/or grade II, III dysplasia. The result suggests that DC's are potentially capable of presenting neoantigens associated with malignant transformation at the precancerous stage when malignant morphological changes have not yet taken place. Combined with routine diagnostic methods, the serial monitoring of DC density in gastric mucosa may be useful in the follow-up of premalignant lesions in the stomach and the diagnosis of early gastric carcinoma.
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PMID:S100 protein-positive dendritic cells and the significance of their density in gastric precancerous lesions. 224 39


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