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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Suppression of gastric acid forms the basis of treatment of duodenal and gastric ulcer, but the precise relationship between suppression of acidity and healing rates has not been defined. We examined the results of controlled trials and clinical pharmacological studies of 24-h intragastric acidity involving antisecretory agents. Data on 24-h and nocturnal hydrogen ion activity and nocturnal acid output were obtained, and the healing rates in duodenal ulcer were calculated. Duodenal ulcer healing rates after 4 weeks showed a significant correlation with suppression of 24-hour hydrogen ion activity (r = 0.63; P less than 0.05), and a highly significant correlation between healing and the suppression of nocturnal hydrogen ion activity (r = 0.93; P less than 0.0001). Nocturnal acid output was not significantly correlated. For gastric ulcer, no such association was seen for suppression of either 24-hour or nocturnal hydrogen ion activity. Duodenal ulcer is regarded as an acid-related disorder, but in gastric ulcer other factors may be more important in pathogenesis and treatment.
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PMID:The correlation between acid suppression and peptic ulcer healing. 346 40

To evaluate the relationship between the onset of peptic ulcer and gastric emptying, some factors which were thought to regulate gastric emptying, i.e. the stage of the ulcer, the location of the ulcer and gastric acidity were studied in cases of gastric ulcer with deformed stomach and were proven to have little influence on gastric emptying. Further, the main cause of delayed gastric emptying was revealed to be the deformity itself, because the shortening of the distance from the gastric angle to the pyloric ring at the lesser curvature (sac-shaped stomach) and the indentation of the corpus ventriculi (hourglass-shaped stomach) significantly delayed gastric emptying. Moreover, it was found that the healing of gastric ulcer was delayed in cases of deformed stomach with delayed gastric emptying when the ulcer was at an active stage. Therefore the improvement of gastric emptying by some methods was thought to be necessary to promote ulcer healing and prevent ulcer recurrence in gastric ulcer patients who had a deformed stomach.
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PMID:Gastric emptying in deformed stomach. 356 51

Investigations were carried out on duodeno- and jejunogastric reflux, gastric juice acidity, microbial population and the concentration of nitrites in 199 subjects. In gastric cancer patients or those with gastric ulcer, chronic atrophic gastritis, stomach resection or more seldom with removal of the gallbladder, a significant increase over normal values of the pH, duodenogastric reflux, microbial flora contamination (especially intestinal) and nitrite concentration was found. In smokers the salivary nitrite concentration was greater than in non-smokers and in direct relationship to gastric concentrations. The parallelism of these alterations suggests a causative relation between them and their presence in diseases or conditions of notorious increased incidence in gastric cancer highlights the direction to be followed in the primary prophylaxis of this disease.
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PMID:Contributions to the study of gastric carcinogenesis. 358 44

Gastric ulcerations induced in rats by a combination of indomethacin and cold-stress (5 +/- 1 degrees C) for 6 hr were more severe than those induced by indomethacin or cold-stress alone. The acidity of gastric juice was increased in rats treated with indomethacin plus cold-stressed. Histamine H2 receptor antagonists, (H+-K+) ATPase inhibitors and prostaglandins inhibited gastric ulcer formation in indomethacin plus cold-stress treated rats, whereas anticholinergics aggravated the ulceration. The indomethacin plus cold-stress induced acid secretion was inhibited by cimetidine and omeprazole in pylorus-ligated rats. Atropine had less effect on the increase in acidity than cimetidine and omeprazole. These findings indicate that the ulcer formation in indomethacin plus cold-stress treated rats is related the increased in acidity of gastric juice. This gastric ulcer model may be useful for evaluating antiulcer agents.
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PMID:Effects of indomethacin and cold-stress on gastric acid secretion and ulceration. The effects of anti-acid secretory agents in rats. 367 83

Gastric acid secretion, incidence of gastric mucosal lesion, and gut hormone responses were studied in 24 patients with liver cirrhosis. Gastric acid output in these subjects showed normal acidity and was nearly similar to that in patients with gastric ulcer. The incidence of gastric mucosal lesion was high, especially in patients whose plasma disappearance rate of indocyanine green was low. Plasma levels of both gastrin and gastric inhibitory polypeptide were higher in cirrhotic patients than in control subjects both in the fasting state and after the ingestion of a test meal. Gel chromatography of the postprandial plasma of cirrhotics showed a higher immunoreactivity at the second peak than in controls. This is because cirrhotics have a higher percentage of authentic gastric inhibitory polypeptide, although the elution patterns were similar in both groups. It is suggested that impairment of extraction of some molecular components of both gastrin and gastric inhibitory polypeptide may occur in the cirrhotic liver.
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PMID:Gastric acid secretion and gastrin and gastric inhibitory polypeptide release in cirrhotic patients. 388 51

Although increased gastric acidity may be important in the pathogenesis of duodenal ulcer, it has a less well-defined role in the formation of gastric ulcers. The present study was undertaken to determine (1) the 24-hour intragastric pH and serum gastrin profiles of 31 patients with duodenal ulcers, eight patients with gastric ulcers, and seven healthy volunteers and (2) the effect of 600 mg of cimetidine BID on these measurements. There was considerable overlap of basal acid output values in the three groups, and mean values did not differ significantly. In response to pentagastrin, the peak acid output was significantly higher in the duodenal ulcer group than in the gastric ulcer or healthy group. There were no intergroup differences in intragastric hydrogen ion (H+) activity after meals, overnight, and over 24 hours, when all subjects received placebo. However, the pH values remained at or above 4.0 for a longer period during the night in the gastric ulcer patients than in the duodenal ulcer patients or healthy subjects. There were no intergroup differences in basal gastrin concentration, but the postprandial gastrin response after each meal was higher in the gastric ulcer group than in the other two groups. In the gastric ulcer group, cimetidine suppressed H+ activity at all times; in the duodenal ulcer and healthy groups, cimetidine suppressed H+ activity only after breakfast, overnight, and over 24 hours. Cimetidine enhanced the serum gastrin response to food to a greater extent in the ulcer patients than in the healthy subjects. In the healthy subjects, the ratio of H+ to gastrin (H+:G) was higher than in the duodenal or gastric ulcer patients but was suppressed only minimally by cimetidine, whereas cimetidine markedly suppressed the H+:G ratio in both groups of ulcer patients. Patients with a history of duodenal or gastric ulcers differed from healthy volunteers in their food-stimulated gastrin response and in their H+:G ratio when treated with cimetidine. Intergroup differences in gastrin response to food, but not in intragastric pH in response to food, suggests that defective control of or response to gastrin may be important in the pathogenesis of acid-peptic disease. Cimetidine, which was effective in H+ suppression in all subject groups, may alter the sensitivity of the parietal cells to gastrin in patients with duodenal or gastric ulcers.
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PMID:Interrelationship between gastric acidity and gastrin concentration in patients with duodenal or gastric ulcer and in healthy subjects. 401 26

Basal serum gastrin in 40 patients with benign gastric ulcer was 103 +/- 10.7 pg/ml, a level significantly higher than corresponding estimations in normal subjects and patients with duodenal ulcer. Following stimulation by a protein meal, a mean rise of 124 pg/ml was achieved at 75 minutes and prior atropinization induced a rise of 208 pg/ml at 90 minutes. Insulin hypoglycaemia produced a rise of 63 pg/ml which was not significantly changed with concomitant neutralization of gastric contents. These results suggest that patients with gastric ulcer have higher basal gastrin levels than normal and this is probably related to the lowered antral acidity. In addition, the protein meal and insulin hypoglycaemia responses suggest an increased antral G cell mass and the possibility of additional gastrin release from sites outside the antrum. It is doubtful whether the relative hypergastrinaemia has an aetiological role in gastric ulcer but it may have a role in the maintenance of gastric ulcer.
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PMID:Gastrin studies in gastric ulcer. 502 20

Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (+/- SEM) gastrin levels were 15.7 +/- 1.5 pg/ml in the duodenal ulcer group, 32.1 +/- 4.3 pg/ml in normals, 118 +/- 18.1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease.The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.
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PMID:Serum gastrin in duodenal ulcer. I. Basal levels and effect of food and atropine. 513 20

Peptic ulcer should no longer be regarded as a single disease entity but as a group of heterogeneous conditions, as evident epidemiologically, genetically, clinically and pathophysiologically. In duodenal ulceration, "hyperacidity" must be the major culprit since specific therapeutic reduction of gastric acidity results in ulcer healing in about 70% of patients. However when the physiologic abnormalities leading to hyperacidity are analysed, it is obvious that each abnormality occurs usually in about a third of the patients only. Each of these abnormalities, however, can theoretically lead to an abnormal postprandial acid output or abnormal nocturnal acid output, and may explain why the majority of patients appear to have "hyperacidity". Indeed, controlling the meal-stimulated acid secretion alone and controlling the nocturnal acid secretion alone have been shown to heal duodenal ulcer. Corpus gastric ulcers, prepyloric ulcers, and gastric ulcers associated with duodenal ulcers appear physiologically distinct, and often behave differently on clinical grounds. This may explain why therapeutic reduction of acid secretion is less successful in healing gastric ulcer than duodenal ulcer.
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PMID:Aetiology of peptic ulcer. 637 55

The influence of oral carbenoxolone sodium (50 mg X 3 daily) on prostaglandin E2 release into gastric juice has been examined in nine peptic ulcer patients (duodenal ulcer, n = 6; prepyloric ulcer, n = 1; gastric ulcer, n = 2) during modified sham feeding and following bolus stimulation of acid secretion by pentagastrin (6 micrograms/kg). Carbenoxolone increased the overall mean of prostaglandin E2 concentrations in gastric juice following modified sham feeding by 32 +/- 9% (mean +/- SEM; P less than 0.02) and decreased the acidity slightly but significantly (P less than 0.05). A marked rise in prostaglandin E2 levels (46 +/- 11%; n = 5; P less than 0.02) was observed in for duodenal ulcer patients and the patient with a prepyloric ulcer responding to therapy (i.e., pain relief and ulcer healing within 4 weeks of treatment). A significant peak (P less than 0.05) related to modified sham feeding was observed only during medication, while a late gradual increase in prostaglandin E2 levels--not associated with vagal stimulation--occurred both in control and carbenoxolone experiments. No significant differences were observed following pentagastrin stimulation. The initial peak in prostaglandin E2 levels observed during medication favours the notion that the mechanism of drug action relies on inhibition of enzymatic degradation while the late increase in prostaglandin E2 levels may be explained by artificial prostaglandin formation during the aspiration procedure.
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PMID:Effect of carbenoxolone on gastric prostaglandin E2 levels in patients with peptic ulcer disease following vagal and pentagastrin stimulation. 641 22


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