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)

131 patients operated on for gastric ulcer according to Gillroth II were investigated with gastroscopy and biopsy. The histology of the gastric mucosa was correlated with the time elapsed since resection. In most cases gastritis shows no difference between anastomosis and stump. In up to 12% gastritis in the stump was more pronounced that at the anastomosis. In the stump any form of gastritis can be seen even more than 20 years afer resection. Atrophic changes are more often to be found in the resected stomach and develop more rapidly than in the normal stomach. They probably result from the coincidence of the lost protective function of the mucous membrane after resection of the gastrin-producing antrum with the potentially damaging action of the contents of small intestine.
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PMID:[The histology of gastric mucosa in B II-stomach (author's transl)]. 50 60

The blood serum levels of gastrin and insulin and arterial blood levels of glucose were determined immediately before intravenous injection of 1 mg of glucagon, and 10, 20, 40 and 60 minutes later in 12 gastric ulcer patients, 14 duodenal ulcer patients and 12 controls using the radioimmunological and orthotoluidine methods respectively. Following glucagon administration the gastrin levels dropped in the controls and the gastrin patients, and increased in the duodenal patients by an average of 30%. Insulin levels increased in all three groups, but the increase was statistically significant in the two patients groups. Glucose levels in the blood also increased with no significant differences between the groups. It is suggested that the different effect of glucagon on gastrin levels may be due to gastrin-insulin interaction; the levels of the two hormones in the blood of duodenal patients were higher than in the other two groups studied.
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PMID:The effect of glucagon on the blood levels of gastrin, insulin and glucose in patients with gastric and duodenal ulcers. 52 17

In normal, duodenal ulcer, and gastric ulcer subjects the two main forms of gastrin, G17 and G34, were estimated by radioimmunoassay in fasting serum and after feeding. Two antisera were used: one showing high specificity for G17, the other specific for the common COOH-terminus of G17 and G34 and so allowing estimation of G34 by difference. Basal G17 was similar in gastric ulcer, duodenal ulcer, and normal subjects and the increases of G17 after feeding were also similar in these groups. In contrast, basal G34 was similar in normal and duodenal ulcer subjects but raised in gastric ulcer subjects. After a meal the G34 concentration in both gastric and duodenal ulcer patients was significantly higher than normal. It is concluded that the higher post-prandial gastrin responses in peptic ulcer that have been previously described are due largely to increased G34.
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PMID:Big and little gastrin responses to food in normal and ulcer subjects. 52 72

Recurrent peptic ulcer usually develops as the result of an ill-advised or poorly executed operation. The commonest surgical error is an incomplete vagotomy. Diagnosis is made best by endoscopy. Mandatory investigation includes determination of serum gastrin and calcium, and measurement of basal and maximal acid output. Management is surgical and depends on the initial ulcer operation. Decision-making is aided by the Hollander insulin test, the secretin infusion test and occasionally by a technetium scan. There is no place for procedures that do not reduce acid output. Emergency treatment of a complication should be followed by full investigation and the appropriate operation. Recurrent gastric ulcer should be treated by gastrectomy and excision of the ulcer.
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PMID:Symposium on peptic ulcer disease: 3. Practical management of recurrent peptic ulcer. 62 Mar 62

Gastric acid secretion basally and in response to intragastric meat extract instillation or to tetragastrin, and circulating gastrin concentration basally and after meat extract stimulation were studied in 67 patients with gastroduodenal ulcer, 30 patients after highly selective vagotomy or selective vagotomy for duodenal ulcer, 12 patients after antrectomy for or gastric ulcer and 10 control subjects. Circulating gastrin concentration increased significantly after meat extract stimulation in control subjects, patients with ulceration and patients after highly selective vagotomy, and acid secretion in each group was increased significantly above basal level. In patients after selective vagotomy, significant increase of circulating gastrin concentration was observed, but it was not associated with significant increase of acid secretion. After antrectomy, neither gastrin nor acid secretion increased significantly after meat extract stimulation. In conclusion, present study suggested that (1) gastric acid secretion in response to intragastric meat extract is chiefly affected by the responsiveness of oxyntic cells and release of antral gastrin and that (2) the presence of the antrum is almost essential for acid secretion after a test meal, and release of duodenal gastrin after antrectomy would not be so potent biologically as to result in an acid secretion.
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PMID:Gastric response to meat extract stimulation in patients with gastroduodenal ulcer and patients after vagotomy or antrectomy. 65 Oct 21

Gastroesophageal sphincter pressure and serum gastrin concentration were determined in the fasting state and after the intake of a protein food in 6 normal subjects, 6 patients with gastric ulcer, and in 6 patients with duodenal ulcer. No significant differences in the fasting state were found. After the food intake, gastroesophageal sphincter pressure increased significantly over basal values in normals and in patients with duodenal ulcer, but in patients with gastric ulcer a decrease in pressure was noted. Serum gastrin rose in all subjects studied after the food stimulation, but it was significant only in the gastric and duodenal ulcer group. In two normals and two patients with duodenal ulcer the ingestion of a potato meal of similar weight to that of the protein meal showed no change either in serum gastrin or in sphincter pressure. In one additional normal subject and one duodenal ulcer patient the constant intravenous infusion of Aminosol for 2 h produced no change in serum gastrin or sphincter pressure. These results indicate that the effect of protein food on sphincter pressure is different for gastric or duodenal ulcers, and, furthermore, that this effect is mediated by proteins in the gastrointestinal tract.
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PMID:Gastroesophageal sphincter pressure and serum gastrin: reaction to food stimulation in normal subjects and in patients with gastric or duodenal ulcer. 72 10

Gastroesophageal sphincter pressure and serum gastrin concentration were determined in the fasting state and the intake of a protein food in 6 normal subjects, 6 patients with gastric ulcer, and in 6 patients with duodenal ulcer. No significant differences in the fasting state were found. After the food intake, gastroesophageal sphincter pressure increased significantly over basal values in normals and in patients with duodenal ulcer, but in patients with gastric ulcer a decrease in pressure was noted. Serum gastrin rose in all subjects studied after the food stimulation, but it was significant only in the gastric and duodenal ulcer group. In two normals and two patients with duodenal ulcer the ingestion of a potato meal similar in weight to the protein meal showed no change either in serum gastrin or in sphincter pressure. In one additional nromal and one duodenal ulcer, the constant intravenous infusion of Aminosol during 2 hours produced no change in serum gastrin or sphincter pressure. These results indicate that the effect of protein food on sphincter pressure is different for gastric or duodenal ulcers; furthermore, that this effect is mediated by proteins in the gastrointestinal tract.
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PMID:Gastroesophageal sphincter pressure and serum gastrin: reaction to food stimulation in normal subjects and in patients with gastric or duodenal ulcer. 75 81

In a double-blind trial 16 persons with gastric ulcer and 35 with duodenal ulcer were treated as out-patients with 1200 mg proglumide daily or 1320 mg magnesium tricilicate daily (as an "active placebo") for four weeks. The ulcers were assessed by endoscopy before and after treatment. The gastric ulcers disappeared in 75% of patients receiving proglumide (six of eight subjects) but in only 25% of those on the placebo (two of eight). There was no significant effect of proglumide on duodenal ulcers (17 in the proglumide and 18 in the placebo groups). Proglumide failed to affect either basal or maximally stimulated acid secretion, nor was there any change in the serum gastrin level. There were no side effects during proglumide administration. This underlines its therapeutic value in the treatment of gastric ulcer, in comparison with cimetidine or carbenoxolone.
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PMID:[Effective out-patient treatment of gastric ulcer with proglumide: preliminary results (author's transl)]. 76 39

Direct immunofluorescence technique with rhodamine-labelled rabbit anti-gastrin IgG conjugate was used for systematic mapping of the G-cell distribution in 16 resected stomachs (8 gastric ulcer patients and 8 duodenal ulcer patients with uraemia). Along the anatomical border of the proximal part of the antrum there was in both groups of patients a tranzitional zone with a low G-cell number per unit mucosa until the cells abruptly disappeared in the body of the stomach. The proximal end of the duodenum contained considerably fewer G cells than the antrum, and the number was equal in both groups. Within the antrum there was in the duodenal ulcer group a gradual increase in G-cell number from the proximal to the distal end, whereas in the gastric ulcer group no significant difference was found in different parts of the antrum. When corresponding antral parts were compared between the two groups, the only significant difference was that the distal part contained more G cells in the duodenal ulcer patients. In both groups the antral G-cell number showed no difference in circumferential distribution.
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PMID:Immunohistochemical investigation of gastrin-producing cells (G cells).The distribution of g cells in resected human stomachs. 79 81

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


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