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)

To clarify the histogenesis of squamous cell carcinoma of esophagus, 307 esophagus resected from autopsied cases have been thoroughly examined. These specimens were dyed with Lugol solution and entirely blocked to study subserial sections. Among these specimens, two subclinically superficial squamous cell carcinomas were found. First case uncovered was that of a woman who had died of a carcinoma of uterus. Microscopic examination revealed a small carcinoma in situ, located in the cervical portion of the esophagus, though this lesion showed no associated dysplasia. The other case was that of an old man who had died of a massive hemorrhage from a gastric ulcer, associated with carcinomas of the lip, liver, and prostate. The esophageal lesion was an intramucosal carcinoma located in the mid esophagus that was encountered with moderate dysplasia. These examples are not only quite rare as being multiple primary carcinomas but they also suggest two possible types of cancer development of the esophagus: one that progresses from normal mucosa, and the other from dysplastic mucosa.
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PMID:[Two autopsy cases associated with a latent superficial carcinoma of esophagus]. 254 39

Total 39 cases of carcinoma stomach were noticed out of 142 malignant tumours of GIT (27.46 percent). Histologically maximum cases were of diffuse type (56.41 percent) followed by intestinal type (35.89 percent) and indolent mucoid carcinoma (7.69 percent) of the stomach. The surrounding epithelium showed lot of changes in the intestinal type of carcinoma stomach. About 78.57 percent showed intestinal metaplasia, 14.28 percent of these cases showed chronic gastric ulcer and severe dysplasia (carcinoma in situ) and another 14.28 percent revealed villous adenoma with carcinoma in situ. In contrast to this, in diffuse variety, only 13.63 percent cases revealed intestinal metaplasia, 27.27 percent showed basal cell hyperplasia, stratification of the epithelium of crypts and diffuse infiltration of mucosa by malignant cells and 4.54 percent showed atrophic gastritis also. In mucoid carcinoma all cases had basal cell hyperplasia and stratification of crypts. Hence these conditions should be taken as premalignant lesions of stomach and should be cured in proper time.
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PMID:Pre-cancerous lesions of stomach. 255 96

Over the period from January 1980 to March 1988 the frequency of dysplastic abnormalities associated wits 202 apparently benign gastric ulcers was determined and their course monitored. The relevant data were then evaluated separately for the various subgroups the ulcers were divided into on the basis of their natural history. No correlation was detected between natural history of gastric ulcer, dysplasia and onset of cancer. Though all dysplastic forms (mild, moderate and severe) may regress, all three showed a possibility of progression to EGC, obviously in increasing percentages: mild dysplasia: 2.53%; moderate dysplasia: 4.76%; severe dysplasia: 14.29%. The last of these three values appears to indicate a greater risk of cancer onset than in simple gastric ulcer and thus proves a useful marker for a more thorough monitoring of such patients.
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PMID:[Usefulness of long-term endoscopic follow-up of gastric ulcer. Study of related epithelial dysplasia]. 269 61

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

Atrophic gastritis with intestinal metaplasia is generally considered a precancerous lesion. We followed 261 patients with chronic atrophic gastritis and intestinal metaplasia, with and without gastric ulcer, every 12 months for 9 +/- 2 years by means of endoscopic and histological examination. In the presence of dysplasia, however, studies were carried out every 6 months in moderate cases, or every 3 months in severe cases. Patients with gastric ulcer received medical therapy for 8 weeks; if healing did not occur, treatment was continued. Only subjects with healed ulcers were admitted to the follow-up. To date, 205 subjects have been included in the study. Over a 10-year period, 16 patients with recurrent gastric ulcer and 12 patients with cancer in situ or in an early stage, were subjected to surgery. One case of advanced cancer was observed. Cancer has been found in five of 95 cases of atrophic gastritis with gastric ulcer (5.2%), and in 7 of 166 cases of atrophic gastritis without gastric ulcer (4.2%). The difference was not statistically significant. Our results confirm that gastric ulcer per se is not a high-risk condition, but it must be considered as an epiphenomenon on a background of epithelial atrophy.
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PMID:Gastric cancer in chronic atrophic gastritis. Associated gastric ulcer adds no further risk. 361 83

Follow-up of patients operated on for gastric ulcer--137 with selective gastric vagotomy (SGV), pyloroplasty and ulcer excision (1967-1976) and 72 with proximal gastric vagotomy (PGV) and ulcer excision (1974-1984)--was supplemented with data from recent clinical, endoscopic and biopsy studies in 78 of the patients. Ulcer recurred in 27/137 SGV and 7/72 PGV cases (20.3 and 9.9%). Four patients died of gastric cancer 5-7 years after SGV. Of the endoscopically reexamined patients, 1/42 with SGV and 1/36 with PGV were found to have asymptomatic ulcer. The incidence of gastric stasis with food retention was 35.7% in the SGV, and 8.3% in the PGV group, and the respective incidences of severe gastric mucosal inflammation with fibrinous deposits were 42.9% and 2.7%. Mild or moderate dysplasia was shown in biopsies from 16.6% of the SGV and 8.3% of the PGV group. The high dysplasia incidence, especially after SGV, and the four gastric cancer deaths in that group indicate a need for long-term follow-up evaluation of possibly increased gastric cancer risk following vagotomy.
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PMID:An endoscopic study of ulcer recurrence and mucosal changes following vagotomy and excision of gastric ulcer. 363 May 28

One hundred and forty-four patients with apparently benign gastric ulcer were endoscopically followed up in order to evaluate the outcome of the lesion. Particular attention was given to: (a) detect possible delay in diagnosing gastric cancer; (b) ascertain the frequency of association with epithelial dysplasia; (c) establish the role of markers, such as serum pepsinogen group I (PGI), and gastric juice CEA in predicting gastric ulcer evolution. Endoscopic and bioptic check-ups were carried out during the first year at 3, 6 and 12 months after endoscopic healing of the ulcer, and then at every symptomatic recurrence. Ten patients (6.9%) were found to present histological evidence of malignancy (within 3 months in six cases, between 6 and 12 months in three cases, and after 41 months in the rest). Four cases were early gastric cancers, and six had shown dysplastic changes of the mucosa at the edge or scar of the ulcer. Serum PGI levels were not significantly different in gastric cancer patients, while gastric juice CEA levels were sharply increased compared to those of gastric ulcer patients: nine out of ten patients had values above normal range. These data suggest that: (a) there may be some delay in diagnosing gastric carcinoma, and gastric ulcer patients should be controlled routinely more than once; (b) the presence of dysplasia indicates the need for prolonged follow-up, because of the high risk of association with or evolution into gastric cancer, and because of the higher number of early gastric cancer detections that this protocol allows; (c) further support in monitoring patients "at risk" may be afforded by gastric juice CEA determination.
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PMID:Early and advanced gastric cancer during follow-up of apparently benign gastric ulcer: significance of the presence of epithelial dysplasia. 369 32

There have been recent findings of gastric cancer in patients treated with cimetidine but too soon after treatment for that drug to have had a pathogenetic role. Ranitidine has been shown to induce slight changes in the gastric mucosa. In 117 patients with gastric ulcer followed-up in some cases for 24 months, five cases of cancer were detected, one after more than a year of follow-up. The numbers were too small to allow any conclusion to be drawn regarding relationships with medication. No significant differences in incidence of gastric epithelial dysplasia between control patients and patients treated with cimetidine or ranitidine were found. No dysplastic lesions were seen during a brief follow-up of 19 duodenal ulcer patients and a few gastric ulcer patients treated with pirenzepine but the data is too limited to allow conclusions to be drawn.
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PMID:The risk of gastric dysplasia in medical long-term treatment of peptic ulcer disease. 385 10

A study on alterations occurring in gastric mucosa in cases of stage I stomach cancer identified chronic gastritis involving gland atrophy of varying degree as the basic background feature, with intestinal metaplasia and dysplasia being common manifestations of precancerous lesion development. Malignant transformation of hyperplastic polyps and adenomas occurs in areas in which dysplasia of metaplastic epithelium tends to spread. Stomach cancer development from gastric ulcer seems unlikely. Morphological factors should be considered, when groups of high risk for stomach cancer development are identified among cases of chronic gastric diseases.
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PMID:[Clinico-morphological characteristics of background diseases in stage I stomach cancer]. 402 59

Reflux of upper intestinal content to the gastric remnant after gastric resection is common and may cause damage to the gastric mucosa, resulting in gastritis, gastric ulcer, and possibly dysplasia. Different surgical procedures have been proposed to prevent reflux, among them Roux-en-Y diversion. In this study we have compared antrectomy followed by gastroduodenostomy (BI) with antrectomy followed by Roux-en-Y anastomosis with regard to enterogastric reflux. Reflux was recorded by cholescintigraphy, using a new method for quantification. In all patients biopsy specimens were taken for histopathological evaluation at gastroscopy. Twenty-seven patients were studied, 11 with gastroduodenostomy and 16 with Roux-en-Y diversion. All patients in the gastroduodenostomy group had reflux, compared with four in the Roux group (p less than 0.001). Under the light microscope all patients in the BI group showed a moderate to severe degree of inflammation compared with only seven in the Roux-en-Y group (p = 0.028). Our results show that Roux-en-Y drainage effectively diminishes reflux and may be an explanation for the lower extent of mucosal damage in these patients.
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PMID:Enterogastric reflux after gastric surgery. A comparison between gastroduodenostomy and Roux diversion. 404 37


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