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)

To determine its efficacy and safety in treating obesity, a silicone-rubber balloon was passed into the stomach of 10 nondieting, obese subjects. In a counterbalanced sequence, the balloon was inflated with 400 mL for 1 mo and deflated for 1 mo. Lower intakes of solid and liquid test meals (NS), significantly slower gastric emptying, and concomitant changes in glucose, insulin, glucagon, and cholecystokinin concentrations consistent with slower emptying resulted during balloon inflation. After balloon inflation, one small gastric ulcer developed, which subsequently healed. Significant weight loss occurred during the second and third week of the inflation period (F[1,9] = 5.0, p less than 0.05). However, the weight loss was small and the significant effect did not continue through the fourth week.
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PMID:Gastric balloon to treat obesity: a double-blind study in nondieting subjects. 218 57

In a double-blind placebo-controlled study, the effect of calcitonin on gastric emptying and on serum concentrations of gastrin, insulin, glucose, calcium and phosphorus after a mixed solid-liquid meal was examined in six patients with type I gastric ulcer. Synthetic salmon calcitonin 415 pmol i.v. was given as a bolus followed by a 90-min infusion to reach an overall dose of 62.25 pmol.kg-1. Gastric emptying of a radiolabelled meal was measured with a gamma camera. Calcitonin suppressed gastric emptying in all patients examined. The mean gastric transit time, MTT90, increased from 38.1 +/- 0.4 min after placebo to 43.1 +/- 0.6 min after calcitonin (P less than 0.001). Calcitonin significantly blunted the postprandial gastrin release: AUC0-90 10,398 +/- 2886 ng. l-1 min (placebo) and 8238 +/- 2573 ng. l-1 min (calcitonin), P less than 0.05, and abolished the postprandial insulin release--AUC0-90 2244 +/- 230 mU.l-1 min (placebo) vs. 638 +/- 198 mU.l-1 min (calcitonin), P less than 0.01. A steady increase in the serum glucose during calcitonin infusion, reaching up to 5.6 +/- 0.31 mmol.l-1 at the end of the infusion, was observed. Calcitonin did not significantly affect serum calcium or phosphorus concentrations. The authors conclude that a delayed gastric emptying is to be expected in patients undergoing calcitonin treatment.
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PMID:Effect of calcitonin on gastric emptying and on postprandial gastrin and insulin release in patients with type I gastric ulcer. 221 26

A total of 42 patients with gastric ulcer and ulcer of the duodenal bulb were investigated. A decrease in the blood concentration of STH and cortisol, high indices of gastric acidifying function in the 2nd hour after insulin administration were noted in the patients with gastric ulcer indicating a decrease in the trophic influence of the hormones of the hypophysis-adrenal system on the GI tract, on the one hand, and raised sensitivity of parietal cells to the effects of this system, on the other hand. In the patients with duodenal ulcer the blood levels of STH and cortisol did not change, indices of gastric acidifying function within the 1st hour after insulin administration were higher than during the 2nd hour indicating an important role of the vagus nerve hypertonicity in the pathogenesis of this disease.
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PMID:[Secretion of cortisol and growth hormone in patients with peptic ulcers of the stomach and the duodenal bulb]. 328 3

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

The dose response curves for acid and pepsin output to increasing intravenous doses of pentagastrin (0.01, 0.02, 2, 8, and 16 micrograms/kg per hour) were determined in six male patients with duodenal ulcer and six with type 1 corporeal gastric ulcer before and 3 to 6 months after selective proximal vagotomy and excision of the gastric ulcer. The maximal secretory capacity (maximal response) of acid and pepsin was greater in the duodenal ulcer patients than in the corporeal gastric ulcer patients, but the sensitivity of the oxyntic and peptic cells to pentagastrin (the dose required for half the maximal response) was equal for the two ulcer groups. Selective proximal vagotomy reduced the acid response to insulin by 96 to 100 percent. The acid secretory capacity and the sensitivity of the oxyntic cells to pentagastrin was reduced by selective proximal vagotomy to the same extent in the duodenal ulcer patients and the corporeal gastric ulcer patients. Selective proximal vagotomy reduced the pepsin secretory capacity in the duodenal ulcer patients but did not reduce the already low capacity in the corporeal gastric ulcer patients. Selective proximal vagotomy decreased the sensitivity of the peptic cells in both ulcer groups. Similar results were obtained when the dose response curves were analyzed according to Michaelis-Menten kinetics. Our results justify clinical trials of selective proximal vagotomy with complete ulcer excision for treatment of type 1 corporeal gastric ulcer.
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PMID:Acid and pepsin responses to graded doses of pentagastrin in duodenal and corporeal gastric ulcer patients before and after selective proximal vagotomy. 393 70

A study was made of changes of the content of hormones (gastrin, insulin, glucagon, triodonthyronine, thyroxine, thyrotrophin, somatotrophin, adrenocorticotrophin and hydrocortisone) under the influence of standard food load in 166 patients with GIT diseases (gastric ulcer, duodenal ulcer, chronic anacid gastritis and chronic enteritis). Forty-three healthy persons entered the control group. Hormones were determined in the peripheral blood by radioimmunoassay. Taking food in healthy persons was shown to cause the stimulation of the secretion of most hormones. To elucidate the mechanisms of hormonal shifts after food load, hormones were also studied after per os intake of solutions with different pH. Disorders of postprandial reactions of the endocrine system which were specific for these nosological forms, were revealed in GIT diseases. The results of the study are of interest in view of new approaches to functional interrelationships of the GIT with endocrine glands.
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PMID:[New approaches to studying the functional relations of the gastrointestinal tract with the endocrine glands]. 408 61

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

A questionnaire was used to study the choice and use of gastric function tests by members of the British Society of Gastroenterology.Pentagastrin has largely replaced older drugs as the stimulant of choice for evoking maximal acid secretion. Insulin tests are being used in situations where they are unlikely to provide useful clinical information. Fewer physicians than surgeons measure gastric secretion, and they use tests less often. The reluctance of physicians to test patients with uninvestigated dyspepsia or gastric ulcer seems justified, but in patients having dyspepsia with negative x-ray films, or after gastrectomy or vagotomy, the greater investigative keenness of surgeons seems commendable. Only half the surgeons ever try to assess the completeness of their vagotomies, and in only one-third of this half is it their usual practice. Criticism is made of the practice of routine measurement of acid in patients with duodenal ulcer, and of the use of acid measurements to decide whether a patient should have surgery or which type of operation should be performed.
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PMID:Use of gastric function tests by British gastroenterologists. 554 Dec 30

A case of metastatic islet cell carcinoma of the pancreas associated with the production of multiple polypeptide hormones (insulin, glucagon, and gastrin) is described. Three years prior to the histologic diagnosis the patient presented with a gastric ulcer and an androgen responsive pancytopenia with hypoplastic bone marrow. Discontinuation of androgen therapy resulted in relapse of pancytopenia. After the diagnosis of islet cell carcinoma of the pancreas was established, the patient was treated with 5-fluorouracil (5-FU) and streptozotocin and subsequently elevated serum polypeptide hormones returned toward normal levels. Concurrent with the normalization of peptide hormones another complete hematologic remission was achieved without use of androgens. Injection of the patient's serum into female rats produced a significant fall in leukocyte (P less than 0.02) and platelet counts (P less than 0.005), but no significant decrease in hematocrit. The clinical course and laboratory findings in this case suggest the presence of a previously undescribed serum factor released by an islet cell tumor capable of suppressing hematopoiesis.
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PMID:Pancreatic islet cell carcinoma associated with multiple hormone secretion and pancytopenia. Evidence of a serum factor suppressing hematopoiesis. 629 5


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