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)

Antral somatostatin-immunoreactive cells (D cells) were counted pre- and postoperatively in 20 patients with duodenal ulcer and in 8 patients with gastric ulcer. Counts were obtained either over a 2-yr postoperative period (duodenal ulcer patients) at intervals of 0.5, 1, and 2 yr or over a greater than or equal to 4-yr postoperative period (gastric ulcer patients) at intervals of 1-2 yr. In patients with a normal population of gastrin-immunoreactive cells (G cells), the D cells were within the normal range (mean value 0.53% in duodenal ulcer patients and 0.67% in gastric ulcer patients). High G-cell values were accompanied by high D-cell values (e.g., in gastrin-cell hyperplasia) and low G-cell values were accompanied by low D-cell values. The G-cell to D-cell ratio was 8:1 and 6.6:1 in duodenal and gastric ulcer patients, respectively. After selective proximal vagotomy and pyloroplasty, the following observations were made: the relation of number of G cells to number of D cells remained unchanged; the postoperative rise in G-cell population was accompanied by a rise in D-cell population; hypertrophy of the D cells was apparent as was postoperative hyperplasia, with a postoperative increase in D-cell size. Morphologic coupling of the gastrin-somatostatin system in the antrum is assumed. This is constant in ulcer disease both before and after vagotomy.
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PMID:Behavior of somatostatin-immunoreactive cells in the gastric mucosa before and after selective proximal vagotomy and pyloroplasty in treatment of gastric and duodenal ulcers. 286 91

Gastrin, a polypeptide hormone secreted by G (gastrin)-cells in the antroduodenal mucosa, is not only a potent stimulant of gastric acid secretion but also exerts trophic actions on the parietal, chief and enterochromaffin-like cells in the oxyntic mucosa. Gastrin plays a crucial role in the pathogenesis of hypergastrinaemic peptic ulcer disease, i.e. in the Zollinger-Ellison syndrome, antral G-cell hyperfunction and retained excluded antrum after subtotal gastrectomy. In patients with normogastrinaemic duodenal ulcer disease the feedback mechanism between gastric acid and gastrin secretion is impaired, while in gastric ulcer patients gastrin secretion is appropriately regulated by gastric acid. Antisecretory drugs may exert varying effects on gastrin secretion. Potent antisecretory drugs, such as omeprazole, increase serum and antral gastrin concentrations, whereas histamine H2-receptor antagonists, such as cimetidine, ranitidine, famotidine and roxatidine, have little influence on gastrin. Interestingly, antisecretory doses of prostaglandin E2-analogues, such as enprostil and arbaprostil [15(R)-15-methylprostaglandin E2], inhibit gastrin secretion, while gastrin is not influenced by prostaglandin E1-analogues, e.g. misoprostol. Somatostatin and the somatostatin-analogue SMS 201-995 reduce serum gastrin levels and gastric acid secretion.
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PMID:The significance of gastrin in the pathogenesis and therapy of peptic ulcer disease. 306 68

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85

In the present paper the gastric secretory and motor responsiveness to a gastrin-like peptide, caerulein, was assessed in rats with a chronic gastric ulcer induced by 'isolation', 48 h after completing prolonged treatments (30 and 60 days) with cimetidine (80 and 160 mg/kg), pirenzepine (8 and 16 mg/kg) and sulglycotide (160 mg/kg) administered orally as a single daily dose. After a 30 day pretreatment with both doses of cimetidine, gastric acid secretion was inhibited and the pylorus spasmogenic activity induced by caerulein was enhanced. The gastric effects of the peptide were not modified by pirenzepine pretreatment while an antisecretory action was shown by sulglycotide after the completion of prolonged treatment (60 days). The ulcers were significantly reduced by cimetidine (low dose) and sulglycotide after 30 day pretreatment. The effects are more likely to be related to the treatment than to the presence of the drugs on gastric receptors.
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PMID:The effect of long-term treatment with antisecretory and antiulcer drugs on gastric secretory and motor responsiveness to caerulein in rats with chronic ulcers. 309 49

Low doses of insulin (less than 1.25 IU/kg body weight) stimulate gastric acid secretion in the rat, whereas higher doses (greater than 2.5 IU/kg) release gastrin and cause gastric ulcers but do not increase acid secretion. In this study we have characterized the ulcerogenic properties of insulin in the rat. A dose of 5 IU/kg subcutaneously proved to be maximally effective. Ulcer formation was rapid, and the maximum 90% incidence was reached after 5 h. Both glucose administration and food intake protected against the ulcerogenic effects of insulin. The effects of anti-ulcer drugs and of vagotomy on insulin-induced ulcers were also studied. Animals were divided into seven groups: 1) saline, 2) omeprazole, 3) ranitidine, 4) sucralfate, 5) bilateral vagotomy, 6) unilateral vagotomy, and 7) antrectomy. Medical treatment was continued for 6 days before insulin administration, operations having been performed 6-8 weeks earlier. Insulin was injected subcutaneously in a dose of 5 IU/kg. Five hours later stomachs were inspected for ulcers. Neither the antrectomized rats nor those treated with omeprazole or ranitidine had ulcers. In the saline- and the sucralfate-treated groups the gastric ulcer incidence was 83% and 80%, respectively, with a mean of six and seven ulcers per rat. Ulcers were evenly distributed between the two sides of the stomach. Rats that had undergone bilateral vagotomy (which abolishes gastric acid secretion and causes hypergastrinemia) responded to insulin with an ulcer incidence of 5%. In the unilaterally vagotomized rats there were only 2 ulcers on the denervated compared with 37 on the innervated side.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-induced gastric ulcers in the rat. 331 Jan 98

The relationship of gastric secretion in response to a single injection of insulin and in response to a histamine infusion, before and after partial gastrectomy, was analysed in 58 patients. The aspirated gastric juice was corrected for gastric outlet loss and enterogastric reflux. Gastrectomy drastically reduced the stimulated gastric secretion by a similar proportion for the two secretagogues, thereby implying that antral gastrin plays no greater part in one than in the other. Gastric outlet losses were also reduced after gastrectomy, but as a fraction of gastric contents, both gastric outlet loss and enterogastric reflux more than doubled; the possible relationship of these findings to the aetiology of gastric ulcer is discussed.
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PMID:Gastric outlet loss and enterogastric reflux after gastrectomy. 334 38

Mucosal atrophy of the gastric antrum (type B atrophic gastritis) is generally accepted as predisposing to the development of the intestinal type of gastric cancer. Since bombesin stimulates gastrin release selectively from the antral mucosa, the response can be used as a marker for antral mucosal atrophy. In this study we have investigated bombesin-stimulated plasma gastrin responses in 21 patients with the intestinal type of gastric cancer and we have compared the results with 12 patients with the diffuse type of gastric cancer, 17 patients with benign gastric ulcer, and 30 dyspeptic patients without endoscopical or histological abnormalities. Gastrin concentrations were also measured in extracts of antral biopsies. Basal plasma gastrin concentrations were not significantly different. In contrast, patients with the intestinal type of gastric cancer had a significantly lower plasma gastrin response to bombesin than did the normal subjects (P less than 0.01) and patients with the diffuse type of gastric cancer (P less than 0.05), but the result was not significantly different from that of the gastric ulcer patients. The antral gastrin content of the patients with the intestinal type of gastric cancer was significantly lower than in controls (P less than 0.005), the patients with the diffuse type of gastric cancer (P less than 0.05), and those with gastric ulcer (P less than 0.05). It is concluded that patients with the intestinal type of gastric cancer have, in contrast to those with the diffuse type of gastric cancer, an abnormally low plasma gastrin response to bombesin. This low response is due to a reduced gastrin content of the antral mucosa.
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PMID:Plasma gastrin responses to bombesin and antral gastrin concentrations in patients with the intestinal type of gastric cancer. 334 93

Only those patients who were examined endoscopically were evaluated. Concomitant examinations, such as biopsy, histologic studies, roentgenograms, scintiscanning, acid secretion, serum gastrin and review of the operative reports, were done. Duodenal ulcers (1,219) and gastric ulcers (421) were examined preoperatively. Of these, selective proximal vagotomy and pyloroplasty and excision of the ulcer were performed for 1,018 duodenal ulcers. Forty-three per cent were examined postoperatively. Selective proximal vagotomy and pyloroplasty and excision of ulcer were performed for 315 gastric ulcers. Thirty-nine per cent were examined postoperatively. Recurrence was calculated in relation with the patients examined postoperatively. Recurrence of duodenal ulcer occurred in 6.3 per cent; of these, 0.9 per cent had duodenal ulcers develop into gastric ulcers. The recurrence rate of gastric ulcer is 8.1 per cent; of these, 0.8 per cent developed into duodenal ulcers, and 0.8 per cent to carcinoma of the stomach. Data of recurrent ulcers were compared with the data for the total number of patients who underwent surgical treatment. The possible causes for a recurrence are demonstrated. In duodenal ulcers, 79 per cent of recurrences are due to technical error (inadequate vagotomy and incomplete drainage); in gastric ulcers, 90 per cent of recurrences are due to technical error. In both duodenal and gastric ulcers, causes are partly based on advanced clinical symptoms. Recurrence rates showed a tendency to increase between 1969 and 1975 and 1976 and 1983. This correlated directly with the deterioration of the clinical signs and symptoms between 1969 and 1983, shown in increased acid secretion, increase and shift of ulcers and stenoses, increase in bleeding and changed epidemiologic findings.
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PMID:Recurrence of peptic ulcer after selective proximal vagotomy and pyloroplasty in relation to changes in clinical signs and symptoms between 1969 and 1983. 342 May

I investigated the significance of bile reflux, when vagotomy was done to stress ulcer, by means of measuring gastric ulcer index, gastric pH and serum gastrin levels of rats. And in order to examine influence of alkali factor of bile, I measured gastric acid output and serum gastrin levels after alkali or acid solution was infused into the untreated rat's stomach. Results were summarized as follows: 1. When I infused alkali solution into the untreated stomach, there was no significant change in serum gastrin level but gastric acid output was significantly accelerated, as compared with infusing acid solution. On the other hand, when I infused alkali solution into the vagotomized stomach, serum gastrin level increased significantly and gastric acid output was significantly accelerated, as compared with infusing acid solution, so, acceleration of acid output observed when I infused alkali solution into the untreated stomach was not suppressed in spite of vagotomy operation. 2. In the vagotomized group, gastric acid output was significantly suppressed and serum gastrin level increased significantly as compared with the untreated group. But, when bile was led into the stomach in the vagotomized group, acid output was accelerated and serum gastrin level also showed a tendency to increase as compared with the group of vagotomy alone. 3. When mild stress was inflicted, stress ulcer formation was significantly prevented in the bile reflux group (vagotomy + pyloroplasty) as well as in the non-bile reflux group (vagotomy + pyloric ligation + gastroileostomy) if vagotomy was done. But, when severe stress was inflicted, stress ulcer formation was significantly prevented in the non-bile reflux group, but not prevented in the bile reflux group. As mentioned above, it was proved that stress ulcer formation was not prevented under a severe stress, if bile reflux existed, even though vagotomy was done. So, if we do vagotomy operation, we need to choose the operation method not to induce bile reflux as much as possible.
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PMID:[An experimental study on the effect of vagotomy on stress ulcer and the influence of bile reflux]. 344

Somatostatin (SS) has been reported to exert potent inhibitory effects on gastric acid, pepsin and gastrin secretion. Although still controversial, the results of several studies have shown a possible influence of a local decrease in gastric somatostatin in the physiopathologic characteristics of peptic ulcer disease. In the present study, immunoreactive SS content (SLI) of antral (SLI-a), corpal (SLI-c) and fundic (SLI-f) mucosal extracts was measured by radioimmunoassay (RIA) in control patients (C) and in those patients with duodenal ulcer (DU) or gastric ulcer (GU) to further study a possible role of SS in peptic ulcer disease. Fifty-five patients (C = 20, DU = 21 and GU = 14) were included in the study. Gastric mucosal samples were obtained either by endoscopic biopsy (4.6 +/- 0.2 milligrams of weight) or operation (52.3 +/- 3.8 milligrams of weight). RIA was performed after a modified Arimura's method and results were expressed as nanograms per milligram of tissue plus or minus standard error of the mean. Chromatographic analysis of gastric mucosal extracts was performed on a Sephadex G-25 fine column. A great interindividual variation in SLI levels was observed (a range of 0.02 to 5.30 nanograms per milligram of weight). The mean SLI concentrations were: C (SLI-a, 2.55 +/- 0.45, SLI-c, 0.99 +/- 0.46 and SLI-f, 1.03 +/- 0.21); DU (SLI-a, 0.48 +/- 0.16, SLI-c, 0.43 +/- 0.13, and SLI-f, 0.58 +/- 0.12), and GU (SLI-a, 1.10 +/- 0.25, SLI-c, 0.40 +/- 0.10, and SLI-f, 0.81 +/- 0.24). Significantly greater amounts of SLI contents were found in the antrum of control patients as compared with those found in the corpus or fundus (p less than 0.05 and p less than 0.01, respectively). SLI-a levels were lower in peptic ulcer patients (DU, p less than 0.001 and GU, p less than 0.05) than in control patients. There was also a significant difference between SLI-a levels in DU versus GU patients (p less than 0.05). No significant differences were found in SLI-c and SLI-f contents in all three groups studied. In conclusion, these results suggest that decreased SS levels in antral gastric mucosa could be the alteration underlying the various physiopathologic mechanisms involved in the development of peptic ulcer disease.
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PMID:Gastric mucosal somatostatin-like immunoreactivity in peptic ulcer. 356 43


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