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)

The stimulating effect of AOC-tetragastrin, caerulein, Histalog and secretin on human gastric acid and pepsin secretion was studied in gastric ulcer patients. The pattern of gastric acid and pepsin secretion after the administration of caerulein was closely resembled to that of gastrin. Slight increase of pepsin secretion after gastrin or caerulein could be based on "wash-out" action caused by the increase of acid secretion after the stimulants. Stimulating effect on gastric pepsin secretion of histalog and secretin would be independent of gastric acid secretion.
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PMID:Clinical study on gastric secretion with special reference to pepsin secretion. 34 50

A rare case of the Zollinger-Ellison syndrome associated with hyperparathyroidism and ectopic gastric tissue in the lower esophageal mucosa is reported. Preoperatively the patient, a 53-year-old woman, had hyperchlorhydria and her fasting serum gastrin concentration was mildly elevated. There was a considerable increase in the gastric acid output and concentration of serum calcium after secretin infusion. At operation the patient had a gastric ulcer 10 cm in diameter, an islet cell tumour of the pancreas 14 cm in diameter, and ectopic gastric mucosa in the distal third of the esophagus. A gastrectomy was perfomed, the pancreatic tumour excised and part of the distal esophagus removed through a left thoracotomy. Four months after the operation the gastrin concentration had returned to low normal, but the serum calcium values remained high. One month later two parathyroid adenomas were removed which effectively cured the hypercalcemia.
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PMID:Zollinger-Ellison syndrome associated with parathyroid adenomas and ectopic gastric tissue in the lower esophageal mucosa. 44 42

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

Biopsy specimens of the duodenal mucosa were assayed to determine their secretin-like activity in 9 controls, 9 patients with gastric ulcer, 19 patients with duodenal ulcer, 4 patients with gastric and duodenal ulcer, and 13 patients with chronic pancreatitis. The bioassay of secretin was done on the pancreatic secretion in anesthetized rats. The sensitivity was in the orcer of 0.0625 CHR unit/rat (4 ng/rat). In the range between 0.0625 and 0.5 CHR units a satisfactory dose dependency was recognized. The following results were obtained. 1) The level of duodenal mucosal secretin-like activity in patients with gastric ulcer was the same as that in the controls, but was elevated in 32% of the patients with duodenal ulcer, 50% of those with gastric and duodenal ulcer, and 8% of those with chronic pancreatitis. 2) The high level of secretin-like activity noted in patients with duodenal ulcer was suspected to be related to the hypersecretion of gastric acid which is characteristic of this disease, but there was no correlation between gastric acid secretion and secretin-like activity in the duodenal mucosa.
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PMID:Secretin-like bioactivity in the duodenal mucosa in patients with peptic ulcer and chronic pancreatitis. 70 76

The patient with gastric ulcer (GU) has abnormal reflux of bile-containing duodenal contents into the stomach. Antral gastritis is prominently associated with GU and is more extensive with severe reflux and with ulcer chronicity and probably when bile salts are accompanied by other constituents of duodenal fluids. Smoking is significantly associated with GU, and it produces reflux in normal subjects and in patients with duodenal ulcer, which in turn is commonly associated with GU. Reflux has not been shown to precede either the gastritis or the gastric ulcer and probably persists despite ulcer healing. The pyloric spincter in the patient with GU probably contracts subnormally to endogenous or exogenous secretin or CCK. This can be explained by associated hypergastrinemia since antral acidification improves the response. Because the pylorus may be usually open, abnormal reflux may be related as much or more to disturbances of other gastroduodenal functions known to control the movement of chyme through what may be a relatively passive pyloric zone. Speculation from animal models implicates bile reflux in aspirin-induced and shock-related gastric ulceration and assigns to bile a possible explanation, in part at least, for the apparent therapeutic efficacy of a carbenoxalone derivative and an antipepsin agent. Similar speculation warrants a search in the patient with GU for abnormalities of gastroduodenal peristalsis-related electric activity and for impaired release of secretin, possibly from antral cells of production. Possible abnormal purinergic inhibition of the gastric fundus and pylorus also warrants further study.
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PMID:The incompetent pyloric sphincter. Bile and mucosal ulceration. 77 71

Using vitamin B12 labelled with Co58 as an exogenous marker, and bilirubin as an endogenous marker, the duodeno-gastric reflux was determined quantitatively in 13 gastric ulcer patients under basal conditions and under stimulation (1 CU secretin/kg body weight + 1 CU pancreozymin/kg body weight) of the exocrine pancreas; in addition, a histological examination of the gastric mucosa was carried out by taking multiple biopsies from along the greater and lesser curvatures of the stomach. Altogether, a more marked mean duodeno-gastric reflux was found in the ulcer patients than in the 14 control subjects. If, however, the ulcer patients are differentiated in accordance with the results of the histological findings in the biopsy material, it is seen that an increased reflux is found only in those ulcer patients presenting with an intestinal metaplasia in the antrum. Statistically, no increase in the duodeno-gastric reflux can be verified under secretin/pancreozymin stimulation of the pancreas.
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PMID:Duodeno-gastric reflux in gastric ulcer patients in relation to intestinal metaplasia of the gastric mucosa. 98 64

The secretin-like activity contained in bioptic specimens of duodenal mucosa was measured by means of bioassay in healthy controls and patients of peptic ulcer. It was found that the activity tended to be increased in duodenal ulcer in comparison with gastric ulcer which did not differ from healthy controls. Possibilities of impaired release and/or increased production of secretin-like substance in duodenal ulcer were discussed.
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PMID:Secretin-like activity in duodenal mucosa and peptic ulcer. 123 93

This clinical study was based on 307 peptic ulcer patients treated with gastrectomy over a 15-year period in our department. Numbers of surgical cases for peptic ulcer remarkably decreased after the introduction of cimetidine in 1980. A median age of gastric ulcer patients was in sixth decades, whereas duodenal ulcer in fifth decades. Surgical indications were 60 percent in intractable ulcer, 30 percent in complication as bleeding, stenosis and perforation, and 10 percent in suspicious malignancy. After cimetidine introduction intractable cases decreased from 63 percent to 44 percent. There was no remarkable difference in the fasting and peak plasma secretin concentrations in postprandial period between peptic ulcer patients and normal controls, however, in gastrectomized patients the plasma secretin response decreased in postprandial state. Follow up study was made on a point of postoperative recurrence and postgastrectomy syndrome. Small stomach syndromes such as insufficient food intake and body weight loss were observed in 10 and 30 percent in the gastrectomized patients, but 86 percent of the patients were satisfied with the results of operation. We concluded that gastrectomy for peptic ulcer was treatment of choice from the point of low recurrence rate and no severe postgastrectomy disorders.
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PMID:[Results of long follow-up study for peptic ulcer patients treated with gastrectomy]. 320 48

Campylobacter pylori may cause gastritis and has been proposed as an etiologic factor in the development of peptic ulcer. However, it may be an acid-sensitive microbe and before it can be implicated in the pathogenesis of peptic ulcer, it should be consistently found in ulcer patients with normal acid secretion. Thirty-six patients with C. pylori by Warthin-Starry stain underwent gastric analysis; 25 were normochlorhydric and 11 hypochlorhydric. Ulcers were present in 19 normochlorhydric patients (10, gastric; 9, duodenal) and 2 hypochlorhydric patients (gastric). Median basal acid output was higher for those with duodenal ulcer (38 mmol/h) than gastric ulcer (28 mmol/h) or miscellaneous endoscopic features (33 mmol/h). The hypergastrinemia seen in 12 patients with negative secretin provocation tests was believed to be due to various nongastrinoma conditions. Campylobacter pylori was found in 6 normogastrinemic patients with elevated acid output and in 1 gastrinoma patient with marked acid hypersecretion. Histologic chronic gastritis was present in all subjects and 29 had active chronic gastritis. Twenty-three patients were taking H2-receptor antagonists at the time of diagnosis which did not seem to interfere with culture results. Using standard acid secretory tests, we conclude that C. pylori can survive in a wide range of acid conditions.
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PMID:Acid secretion and serum gastrin levels in individuals with Campylobacter pylori. 334 93

Duodeno-gastric reflux has been studied in normal subjects and patients with duodenal and gastric ulceration during the responses to parenteral secretin and cholecystokinin-pancreozymin and to acidification of the small intestine. Reflux was absent or slight in normal subjects and most patients with duodenal ulcer but was appreciable in most patients with gastric ulcer. Duodeno-gastric regurgitation may occasionally resultin a misleading assessment of pancreatic exocrine secretory capacity.
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PMID:Aspects of duodeno-gastric reflux in man. 503 39


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