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)

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.
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PMID:Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels. 93 Sep

To find out whether non-steroidial anti-inflammatory drugs (NSAIDs) inhibit the proliferation of mucosal cells that normally leads to healing of gastric ulcers a microdissection technique was used to quantify mitosis in gastric glands at the ulcer edge in relation to that in the adjacent mucosa. The regeneration index thus obtained of the ulcer edge was greater in the 9 subjects with gastric ulcers not taking NSAIDs (mean index 3.1 [SEM 0.61]) than that in the 8 patients taking NSAIDs (index 1.49 [0.16]). In rats in which gastric ulcers were produced with a cryoprobe, the ulcers were larger and slower to heal in those receiving indomethacin than in controls; also, immunohistochemical staining indicated significantly fewer mitotic cells in glands adjacent to the ulcer in indomethacin-treated rats (8 mitoses [SEM 3]) than in control animals (25 [5]). The prostaglandin E1 analogue misoprostol reversed the inhibition of healing and substantially restored the proliferative rate in the animals. Inhibition of epithelial cell division normally involved in gastric ulcer healing would contribute to the high prevalence of gastric ulcer during NSAID therapy.
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PMID:Inhibitory effect of non-steroidal anti-inflammatory drugs on mucosal cell proliferation associated with gastric ulcer healing. 197 50

Single biopsies of human gastric mucosa from controls and different groups of patients were used for enzymatic cell isolation by pronase and collagenase and subsequent count of parietal and nonparietal cells. This procedure was tested in regard to its validity and delivered the following cell numbers. Total gastric cells/mg wet weight gastric mucosa: normal gastric mucosa [controls (C), n = 95] 31,500 +/- (SEM) 1,490, chronic superficial gastritis (GI; n = 49) 36,300 +/- 2,770, chronic gastritis with beginning atrophy (GII; n = 36) 44,100 +/- 3,050 (p less than 0.025), chronic atrophic gastritis (GIII; n = 12) 40,100 +/- 5,760, duodenal ulcer (DU; n = 26) 29,340 +/- 2,280, gastric ulcer (GU; n = 23) 37,090 +/- 3,000, gastric resection according to Billroth I (BI; n = 7) 57,480 +/- 12,360 (p less than 0.005) and Billroth II (BII; n = 12) 52,560 +/- 6,730 (p less than 0.005). Parietal cells/mg wet weight gastric mucosa: 1,910 +/- 490 (C), 1,980 +/- 140 (GI), 1,700 +/- 200 (GII), 1,170 +/- 220 (GIII, p less than 0.025), 2,580 +/- 240 (DU, p less than 0.05), 1,690 +/- 150 (GU), 1,500 +/- 250 (BI), 1,360 +/- 320 (BII). Parietal cell concentration (density) did not differ in males and females and did not change with age. The method delivers relevant cell numbers, is suitable to detect qualitative differences and can be used for the interpretation of biochemical studies.
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PMID:Morphologically different biopsy specimens of the human gastric mucosa. I. The use of enzymatic cell isolation for quantitative determination of parietal cells. 301 1

Gastric stasis and duodenogastric reflux have each been implicated in the pathogenesis of various upper gastrointestinal disorders. However, the relationship between intragastric bile and gastric emptying has not been explored. In each of nine healthy volunteers (seven men and two women, ages 22-47 years), gastric emptying of 300 ml 10% dextrose labeled with [99mTc]DTPA was measured twice using gamma camera imaging. During one study, 20 min after ingestion of the test meal, 525 mg of freeze-dried, sterilized human T-tube bile dissolved in 20 ml water was introduced into the stomach via a previously sited fine-bore nasogastric tube. Intragastric bile salt concentrations were calculated to be within the range 1.7-2.9 mM. In control studies, 20 ml of water alone was similarly introduced. Emptying at 20 min was comparable for both groups of studies (38 +/- 3% vs 39 +/- 4%; mean values +/- SEM). For each individual study, emptying from 20 to 60 min was well represented by a single exponential function (r = 0.81-0.99). Half-emptying times for curves fitted over this period were similar in the two groups (bile: T1/2 = 18.8 +/- 2.6 min; control T1/2 = 18.8 +/- 1.9 min). These results indicate that intragastric bile, in concentrations similar to those found in patients with gastric ulcer, has no effect on gastric emptying of dextrose in normal subjects.
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PMID:Intragastric bile does not perturb gastric emptying of liquids in humans. 334 20

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxta-pyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9 +/- 1.2 ng/mg (mean +/- 1 SEM) in control patients. Duodenal gastrin concentration was similar to control values in patients with duodenal ulcer, pyloric channel ulcer, vagotomy and pyloroplasty, and gastric atrophy and hypergastrinemia. In gastric ulcer patients, duodenal gastrin concentration, 2.8 +/- 0.6 ng/mg, was significantly less than the control value (P less than 0.05). Duodenal gastrin concentration was approximately one third of antral gastrin concentration in control, duodenal ulcer, and gastric ulcer patients and was approximately one fifth of antral gastrin concentration in vagotomy and pyloroplasty patients and gastric atrophy patients. Duodenal and antral gastrin concentrations were significantly correlated in normal controls and in gastric ulcer patients. The finding of normal duodenal gastrin concentration in patients with vagotomy and pyloroplasty and patients with gastric atrophy suggests that, unlike antral gastrin concentration, duodenal gastrin concentration is unaffected by a decrease in acid secretion rate. The low duodenal gastrin concentration in gastric ulcer patients indicates that the duodenum may be involved in the pathophysiology of gastric ulcer disease.
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PMID:Duodenal gastrin concentration in upper gastrointestinal disorders. 376 3

The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-34 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 +/- 1.3%, mean +/- SEM) compared with 48.0 +/- 2.1% in normo-gastrinemic patients (p less than 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 +/- 0.7%) in hypergastrinemic compared with 4.9 +/- 0.3% in normogastrinemic patients (p less than 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 +/- 4.5%) but decreased in gastric ulcer (36.7 +/- 1.6%, p less than 0.01) and pernicious anemia (31.3 +/- 1.9%, p less than 0.001) compared with 48.2 +/- 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 +/- 0.9%) compared with 4.8 +/- 0.4% in control patients (p less than 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.
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PMID:Decreased sulfation of serum and tissue gastrin in hypergastrinemia of antral origin. 397 77

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

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

The concentrations of gastrins containing the active C-terminal tetrapeptide amide (mainly gastrin-34 and gastrin-17) and the N-terminal tridecapeptide fragment of gastrin-17 were measured in antral and duodenal biopsy specimens. The antral concentration of the N-terminal gastrin fragment was much higher in patients with active duodenal ulcer (33.4 +/- 6.8 nmol g-1, mean +/- SEM, n = 15) than in controls (5.6 +/- 2.9 nmol g-1, n = 10), patients with gastric ulcer (5.6 +/- 1.8 nmol g-1, n = 10) or patients with pernicious anaemia (7.7 +/- 2.5 nmol g-1, n = 6). No differences were found between the groups regarding gastrin-34 and gastrin-17 concentrations. In duodenal extracts, the N- and C-terminal gastrin concentrations were similar in all groups of patients. These data suggest that the posttranslational processing of antral gastrin is abnormal in patients with active duodenal ulcer disease.
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PMID:Abnormal processing of antral gastrin in active duodenal ulcer disease. 643 50

The basal concentrations of sulfated and non-sulfated gastrins in serum were measured radioimmunochemically in healthy subjects and in normo- and hyper-gastrinemic diseases. The degree of sulfation in patients with duodenal and gastric ulcer, chronic pancreatitis, gallstone disease, and chronic renal failure were similar to that of healthy controls, in whom 37.7 +/- 1.9% (mean +/- SEM) of serum gastrins were sulfated. In eight patients with the Zollinger-Ellison syndrome 57 +/- 5.4% of the gastrins were sulfated (p less than 0.005, compared with controls). In patients with pernicious anemia (no. = 20) only 24.4 +/- 2.0% of the gastrins were sulfated (p less than 0.005, compared with controls). An inverse correlation (r = -0.63, p less than 0.01) was found between the degree of sulfation and the total gastrin concentration in pernicious anemia but not in gastrinoma patients. The results indicate that diseases with increased synthesis of gastrin are accompanied by an abnormal degree of sulfation.
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PMID:Variations in the sulfation of circulating gastrins in gastrointestinal diseases. 666 33


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