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)

Glucagon provocation test was performed in the patients with hypergastrinemia and hyperchlorhydria to investigate its diagnostic value. A paradoxical response of plasma gastrin level in the patients with the Zollinger-Ellison syndrome and a marked decrease of plasma gastrin level in the patients with gastric ulcer, duodenal ulcer, excluded gastric antrum, multiple endocrine adenomatosis, pernicious anemia and chronic renal failure were demonstrated by glucagon infusion. Glucagon provocation test, therefore, was considered to be of great value in the diagnosis of the Zollinger-Ellison syndrome, particularly, in the case of an excluded gastric antrum in which secretin provocation test caused the false positive result because of a marked increase of pancreatic secretion. Glucagon provocation test in combination with secretin provocation test, therefore, is at present the most preferable diagnostic procedure for detecting the Zollinger-Ellison syndrome.U
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PMID:Clinical significance of glucagon provocation test in the diagnosis of hypergastrinemia. 611 93

In HGT-1 cells incubated at 20 degrees C for 15 min with 1 mM 3-isobutyl-1-methylxanthine (IBMX), histamine (10(-4)M) increased basal cAMP levels from 2.12 +/- 0.14 to 22.9 +/- 2 pmol per 10(6) cells, with a potency of 6.4 X 10(-6)M. IBMX was added in order to inhibit cAMP degradation by low and high Km cAMP-phosphodiesterases (cAMP-PDE). The use of specific H1, H2 agonists or antagonists indicated that the histamine effect was due to an interaction with typical H2 -receptors that are involved in gastric acid secretion. Cyclic AMP levels were also increased (10-fold) by vasoactive intestinal peptide VIP (3 X 10(-11) - 10(-8)M). Porcine peptide having N-terminal histidine and C-terminal isoleucine amide (PHI) and secretin were respectively 80 and 3600 times less potent than VIP and did not produce additive effect when tested in combinations with VIP. This observation indicates that these two peptides, structurally related to VIP, are acting through the recognition sites for VIP. Combination of VIP and histamine results in additive stimulation on intact cells as well as on membrane-bound adenylate cyclase, suggesting the existence of two cell populations bearing respectively the two sets of receptors. Two other human cancer cell lines originating from nongastric tumors (HT-29 and HL-60) possess only VIP or histamine receptors, respectively, indicating the gastric cellular originality of the HGT-1 cells. It is concluded that HGT-1 cells possess both VIP and histamine H2 receptors with similar pharmacological properties to those characterized in normal human fundic glands (1,2). Therefore, this cell line can be a good model to study drugs used therapeutically during the treatment of patients for gastric ulcer or cancer.
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PMID:Histamine and VIP interactions with receptor-cyclic AMP systems in the human gastric cancer cell line HGT-1. 619 8

In order to explore secretory mechanisms in peptic ulcer, the plasma secretin response to an intraduodenal load of gastric acid stimulated with tetragastrin was studied in 10 patients with duodenal ulcer, nine with gastric ulcer, and five young healthy volunteers. After the injection of tetragastrin plasma secretin level was significantly increased in all subjects. The integrated incremental secretin output significantly correlated with the incremental acid output in the duodenal ulcer group as well as the gastric ulcer group. THere was no significant difference in the integrated incremental secretin output among the three groups. However, the integrated incremental secretin output per unit amount of gastric acid loaded in the duodenum was significantly lower in the duodenal ulcer group than in the other two groups. These results suggest that in patients with duodenal ulcer the secretin release in response to an intraduodenal load of endogenous acid is impaired.
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PMID:Effect of intraduodenal load of endogenous acid on secretin release in patients with peptic ulcer. 709 Nov 36

The effects of various antiulcer drugs and hormones on the cell kinetics of the mouse gastric mucosa were studied using an autoradiographic technique with 3H-thymidine. The drugs or hormones were administered orally or parenterally once or twice a day for 7 consecutive days, and 3H-thymidine was injected after the last administration of the drug. The autoradiograph was prepared and then the labeling index was counted. Cimetidine (100 mg/kg X 2/day, p.o.), geranylgeranylacetone (GGA, 100 mg/kg X 2/day, p.o.) and Cu-chlorophyllin-Na (300 mg/kg X 2/day, p.o.) did not show any effect on the labeling indices in both the tissues of the fundic and pyloric glands, while carbenoxolone (100 mg/kg X 2/day), p.o.) reduced the labeling index in the pyloric glands. Tetragastrin (1 mg/kg X 1/day, i.m.) increased the labeling index in the fundic glands, whereas secretin did not affect it. Hydrocortisone (100 mg/kg X 1/day, S.C.) reduced the labeling index in the fundic glands, and this reducing effect was prevented by combining hydrocortisone with GGA. From these results, it was indicated that the labeling index in the normal mouse gastric generative zone was no influenced by the tested antiulcer drugs, except carbenoxolone; but the index was influenced by tetragastrin and hydrocortisone, especially in the fundic glands. It was also suggested that the changes in the cell kinetics of the gastric mucosa could be related to the etiology of gastric ulcer since there was a possibility that geranylgeranylacetone could control the action of hydrocortisone, an ulcerogenic agent, on the gastric mucosal cell-cycle.
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PMID:[Study on the kinetics of mucus secreting cells in the gastrointestinal tract --effects of various drugs and hormones on the cell kinetics of the generative zone in mouse gastric mucosa]. 712 45

Mucosal secretin content of the duodenum was measured using bioptic specimen in healthy controls and patients of peptic ulcer. Immunoreactive secretin in the duodenal mucosa was found greater in healthy controls (7.73 +/- 2.71 ng/mg dry wt., mean +/- S.D.) than in gastric ulcer patients (5.76 +/- 3.51 ng/mg dry wt.) and duodenal ulcer patients (5.54 +/- 2.48 ng/mg dry wt.), but the difference was not significant. There was no significant relationship between mucosal secretin and acid output in these patients.
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PMID:Mucosal secretion of the duodenum in peptic ulcer disease. 731 82

Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N-nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.
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PMID:The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease. 1704 24


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