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)

Lysolecithin was isolated and identified from the gastric contents of 5 patients with gastric ulcer and erosive and atrophic gastritis. The methods used involved methanolic extration, column chromatography on silica gel and sephadex gel filtration, followed by preparative thin layer chromatography. Identification of lysolecithin was verified in one sample by thin layer chromatography and elementary analysis. A method for quantitation of lysolecithin in human gastric fluid for routine clinical analysis is described, based on the procedure used for identification of this phospholipid. Further, a hemolysis test is proposed for screening gastric contents for lysolecithin concentrations above approximately 10 mg/100 ml. With the quantitative method, an average concentration of 66.1 mg of lysolecithin in 100 ml gastric content was found in the group of 5 patients. The screening test was positive in all 5 samples, but was negative with native gastric juice in 25 persons serving as controls. When the gastric fluid of the controls was concentrated, however, 9 samples gave a positive hemolytic reaction. From these 9 specimens, the lysolecithin concentration was found to average 0.9 mg/100 ml. These findings afford evidence that lysolecithin may be involved as a factor in the pathogenesis of gastric ulceration.
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PMID:[Isolation, identification and quantitative determination of lysolecithin in the human gastric juice]. 0 72

10 patients with benign gastric ulcer were treated with cimetidine 0-8 to 1-6 g/day for six weeks. Relief of symptoms was rapid. Endoscopy at the end of treatment showed that all the ulcers had healed. Healing was not associated with an improvement of acute atrophic gastritis nor with any change of gastric mucosal potential difference. No untoward clinical or laboratory effects were observed.
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PMID:Healing of gastric ulcer during treatment with cimetidine. 5 42

The half life time (T 1/2) of gastric emptying was measured in 53 patients suffering from atrophic gastritis or gastric ulceration, by use of a radiolabelled standardized test-meal. In healthy controls the T 1/2 was 58.8 +/- 9.1 min (median 59 min). In 35 gastric ulcer patients the T 1/2 of median 85 min was significantly slowed if compared to the normal value (2 p less than 0.01). After healing of the ulcer in 12 patients this value returned to normal. In 8 patients with diffusely atrophic gastritis the T 1/2 value was slowed significantly (median 123 min), if the gastritis was confined to the antrum, gastric emptying was accelerated (median 48 min).
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PMID:[Gastric emptying in patients with ulcus ventriculi (author's transl)]. 43 71

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

Anomalous DNA synthesis was seen in the stomach mucosa of mice with experimental stomach ulcer during different phases of the ulcerous process, using histoautoradiography. At the early stage of ulcer formation a decrease in the label index (LI) is seen. Formation of the ulcer, morphologically similar to the shronic one, is accompanied by growth of the number of DNA-synthesizing cells in its margins. Over a period of ulcer healing proliferative activity of epithelium decreases approximately to an initial level. Histoautoradiographic studies of bioptates of the stomach mucosa obtained under spot gastroscopy in patients suffering from the ulcerous disease allowed to reveal intensifying proliferative activity of epithelium in the ulcer margins. Similar changes in LI were found in gastritis, followed by the gland affection, and in atrophic gastritis.
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PMID:[Dynamics of DNA synthesis in the gastric mucosa in ulcer]. 51 92

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

Gastric juice was neutralized (nGJ) in vivo by 80 ml of a phosphate buffer containing radiolabelled vitamin B12 as dilution indicator. Unprocessed nGJ was analyzed in the double gel diffusion technique for the presence of serum proteins using monospecific antisera. Alpha1-Acid glycoprotein (AGP) was found in a high incidence (36 out of 38 subjects) in nGJ of gastric cancer patients. AGP was also observed less frequently in nGJ of patients with Billroth II resections (6/15), metaplasia (11/52), gastric ulcer (3/24), chronic atrophic gastritis (2/26) and chronic gastritis (3/63). AGP was absent in the control group (0/21), in patients with surface gastritis (0/38) and in subjects with normal acid secretion (0/45). Immunochemical studies demonstrated no identity of AGP with human "gastrointestinal tumor associated antigens." In 7 out of 17 AGP positive samples immunochemical differences between gastric and serum AGP were observed.
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PMID:Alpha 1-acid glycoprotein in gastric cancer juice. 80 43

1. Prostaglandin A-, prostaglandin E- and prostaglandin F-like substances were determined radioimmunologically in antral biopsy material obtained by endoscopy. 2. In patients with gastritis, the concentrations of prostaglandin (E+A)-like substances were six times as high and of prostaglandin F-like substances twice as high as in normal subjects. In chronic atrophic gastritis, the concentrations of prostaglandin (E+A)-like material was four times as high as in normal subjects whereas prostaglandin-F like material remained unchanged. In acute gastric ulcer, prostaglandin (E+A)-like material reached concentrations four times times higher than in normal subjects, accompanied by a fivefold increase of prostglandin F-like substances. After healing of the gastric ulcer, prostaglandins returned to normal values. 3. There was no correlation between gastrin and prostaglandins in all biopsy specimens.
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PMID:Concentrations of prostaglandin A-, E- and F-like substances in gastric mucosa of normal subjects and of patients with various gastric diseases. 84 56

Although many facts on epidemiology of gastric cancer and on the preceding atrophic gastritis are known, sufficient scientific foundations for planning primary prevention are lacking. It is suggested that with rising standards of living and hygiene and with dissemination of optimal nutrition according to physiologic aspects, incidence of gastric cancer will further decrease. 2. It is possible to identify some high risk groups: elderly persons with familial aggregation of stomach cancer, blood group A, pernicious anemia, atrophic gastritis and intestinal metaplasia, anacidity, and patients operated upon for benign epithelial neoplasms or gastric ulcer. Prophylactic supervision of this segment of the population seems mandatory but by this means, only a small percentage of all gastric cancer can be detected early. 3. Our knowledge is sufficient for the planning of intervention studies, e.g. long tome prophylactic application of ascorbic acid or vitamin A or intensive drug treatment of atrophic gastritis. Therefore we have started such a trial using carbenoxolon. 4. Screening methods for detection of early gastric cancer in asymptomatic persons have been evaluated in Japan. Their application in Europe cannot be generally recommended. The cost-benefit ratio is prohibiting. 5. Today, the main route to detect stomach cancer when curable is the thorough examination of persons with dyspeptic complaints. Radiological examination holds the first place and is supplemented by fibergastroscopy which enables aimed biopsy and cytologic examination of gastric juice. All other methods have only limited value in selected situations. 6. Without resignation we must realize that a solution of the problem cannot be expected in the near future. Further efforts are necessary in order to gain solid scientific foundations and to introduce research results into medical practice.
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PMID:[Scientific foundation of gastric cancer control (author's transl)]. 86 74

Samples of gastric contents from 152 patients with pyloric reflex were taken during gastroscopy after an overnight fast and examined for hemolytic activity. Hemolysis was induced by 97 specimens (64%). The hemolysis test was positive in 45% of patients with a histologically normal gastric mucosa, in 76% of patients suffering from chronic atrophic gastritis with intestinal metaplasia, in 83% with gastric erosions and in 67% with gastric ulcer. No lysolecithin was found in 9 of the 97 positive specimens. The other aspirates contained widely differing values up to 320 mg/100 ml. The average quantities of lysolecithin in gastric contents varied in the different patient groups from 20 to 60 mg/100 ml. These values are much higher than the mean value of 0.9 mg/100 ml quantified in patients without pyloric reflex during an earlier investigation. It is now widely accepted that pyloric reflex promotes gastritis. Furthermore, it has been shown on several occasions that bile constituents exert a damaging effect on the gastric mucosa barrier. The same is true of lysolecithin, which promotes (for example) acute cholecystitis under experimental conditions. These findings, together with the results of our investigation, seem to afford evidence that lysolecithins may exert a pathogenic influence in the development of different gastric lesions.
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PMID:[Hemolysis-inducing substances in gastric secretion, incidence-rate of lysolecithin]. 89 30


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