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 prostaglandins E2 and 16,16-dimethyl-PGE2 methyl ester were compared with the H2-receptor antagonists burimamide and metiamide for their effects on gastric acid secretion (GAS) and gastric mucosal blood flow (MBF) in rats and dogs, and on ulcer formation in rats. Orally, both 16,16-dimethyl-PGE2 methyl ester (20 microgram/kg) and metiamide (6 mg/kg) were markedly effective inhibitors of GAS stimulated by histamine acid phosphate or pentagastrin in Heidenhain pouch dogs, producing a reduction both in volume of gastric juice and in the concentration of titratable acid. In anaesthetised rats, however, the H2-receptor antagonists, when perfused into the gastric lumen, did not consistently inhibit the increased GAS caused by various secretagogues. In contrast, the prostaglandins, under the same conditions, caused marked inhibition of GAS provoked by all secretagogues. Intravenously, both burimamide and metiamide were effective in inhibiting GAS in rats but were less potent than the prostaglandins. The order of potency was: 16,16-dimethyl-PGE2 methyl ester greater than PGE2 greater than metiamide greater than burimamide. By the oral route, the H2-receptor antagonists were found to be very weak inhibitors of indometacin-induced gastric ulcer in rats, as compared to the prostaglandins. MBF studies in rats and in Heidenhain dogs showed that i.v. or p.o. administration inhibited both GAS and MBF in most cases. The ratio r = [MBF (ml/min)/GAS (mumol H+/min)] was generally increased by both types of compounds, suggesting a preferential effect on GAS.
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PMID:A comparative study of the effects of prostaglandins and H2-receptor antagonists on gastric acid secretion, mucosal blood flow and ulcer formation. 3 81

Gastric juice was neutralized (nGJ) in vivo by 80 ml of a phosphate buffer containing radiolabelled vitamin B12 as dilution indicator. Unprocessed nGJ was analyzed in the double gel diffusion technique for the presence of serum proteins using monospecific antisera. Alpha1-Acid glycoprotein (AGP) was found in a high incidence (36 out of 38 subjects) in nGJ of gastric cancer patients. AGP was also observed less frequently in nGJ of patients with Billroth II resections (6/15), metaplasia (11/52), gastric ulcer (3/24), chronic atrophic gastritis (2/26) and chronic gastritis (3/63). AGP was absent in the control group (0/21), in patients with surface gastritis (0/38) and in subjects with normal acid secretion (0/45). Immunochemical studies demonstrated no identity of AGP with human "gastrointestinal tumor associated antigens." In 7 out of 17 AGP positive samples immunochemical differences between gastric and serum AGP were observed.
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PMID:Alpha 1-acid glycoprotein in gastric cancer juice. 80 43

Uninvolved gastric mucosa from duodenal ulcer, gastric ulcer, and gastric cancer patients was incubated with [1-14C]glucose and [6-14C]glucose in order to assess the relative contributions of the pentose phosphate pathway and Krebs cycle to glucose metabolism. [14C]Glucose counts retained by the tissue, glycolysis, and pyruvate formation were also measured. Tumor tissue from the cancer patients was included in the study. Less than 1.2% of the glucose entering the tissues was metabolized via the pentose phosphate pathway; suggesting that this pathway plays a minor role in energy production from glucose. The major determinant of energy production was the Krebs cycle. Its contribution to glucose metabolism was greatest in the body mucosa of duodenal ulcer patients, less in the uninvolved body mucosa of gastric ulcer patients, and lower still in the corresponding body mucosa of gastric cancer patients. The low levels of Krebs cycle activity seen in the latter tissue resembled those of uninvolved antral mucosa. The smallest Krebs cycle contribution was seen in tumor tissue. [14C]Glucose counts retained by the tissue and glycolysis both tended to vary inversely with Krebs cycle activity among the tissues studied. Thus, both were small in the body mucosa of noncancer patients and somewhat larger in the body mucosa of cancer patients, in uninvolved antral mucosa and in tumor tissue.
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PMID:Krebs cycle, pentose phosphate pathway, and glycolysis in the uninvolved gastric mucosa of peptic ulcer and gastric cancer patients. 91 74

Activity of the main enzymes of pentose phosphate pathway of carbohydrate metabolism was studied in human mucosa of the stomach. In the mucosa glucose-6-phosphate dehydrogenase in gastric ulcer and 6-phosphogluconate dehydrogenase in normal stomach were shown to be less active as compared with these enzymatic activities in duodenal ulcer. A distinct decrease in the activity of glucose-6-phosphate dehydrogenase was observed in the ulcerous region, independently of the ulcer localization either in corpus ventriculi or in duodenum, as compared with the parts of the mucosa away from the impairment; the lowest enzymatic activity was estimated in the gastric ulcer zone. Activities of 6-phosphogluconate dehydrogenase and transketolase were the same in the ulcerous and normal mucosa and did not depend on the localization of the impairment. Contents of lactic and pyruvic acids were similar in mucosa of the stomach both in gastric and duodenal ulcer.
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PMID:[Characteristics of the pentose phosphate pathway of carbohydrate metabolism in the gastric mucosa of persons with peptic ulcer]. 91 74

26 years after a partial gastric resection (Billroth II) for recurrent gastric ulcer a 62-year-old man developed severe intestinal osteopathy. For three years he had increasing pain in the lower back and hip with a noticeable waddling gait. Serum concentration of calcium (2.0 mmol/l) and 25-hydroxy-vitamin D3 (38 mmol/l) were reduced, those of alkaline phosphatase (572 U/l) and parathormone (532 pg/ml) increased. Radiology demonstrated Looser's zones in the ribs and iliac crest. Osteodensitometry showed obviously diminished bone density. Iliac crest biopsy revealed signs of osteomalacia and secondary hyperparathyroidism. Within three months of starting oral vitamin D3 and calcium the symptoms had definitely receded and serum concentrations of calcium and alkaline phosphatase had become normal (2.4 mmol/l and 156 U/l, respectively). Osteopathic symptoms are often the expression of an abnormal calcium/phosphate metabolism. The cause often lies in the gastrointestinal tract; not rarely it is a late complication of a gastrojejunostomy.
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PMID:[Intestinal osteopathy following partial gastric resection]. 131 Apr 61

Studies of basal and histamine-stimulated gastric acid secretion were performed in 42 controls, in 133 patients with duodenal ulceration, in 57 patients with gastric ulceration, in 13 patients with both duodenal and gastric ulceration, and in 20 patients with gastric carcinoma. All these subjects were Chinese. Statistical analysis of the results showed that all clinical groups differed from the controls in both basal and stimulated secretion. The mean basal acid output of Chinese controls and of patients with duodenal ulcer in most cases did not differ statistically when compared with western series. The basal secretion of Chinese patients with gastric ulceration, however, was statistically higher than in most of the western series. The histamine-stimulated response of Chinese controls and patients with duodenal ulcer was statistically much lower than in all western series with which they were compared. For Chinese patients with gastric ulcer, the stimulated responses were in some instances lower than and in others similar to results obtained in some western series. In contrast to most western reports, the basal and histamine-stimulated secretion in Chinese patients with gastric ulcer was significantly higher than in controls. In the Chinese controls and Chinese patients with peptic ulcers the response after histamine was generally lower than western reports. This was due to the inadequacy of the standard dose of histamine acid phosphate of 0.04 mg/kg body weight in Chinese subjects. A dose of 0.06 mg/kg body weight produced a significantly higher acid output. In the comparatively leaner Chinese subjects, therefore, a dose of histamine acid phosphate of 0.06 mg/kg is required for maximal stimulation of gastric acid secretion. This agrees well with the results of a similar study in Indian subjects.
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PMID:Gastric acid secretion in Chinese with particular reference to the dose of histamine required for maximal stimulation. 549 52

Cimetidine, N"-cyano-N-methyl-N'-[2[[(5-methyl-1H-imidazol-4-yl) methyl]-thio]ethyl]guanidine, is a specific histamine H2-receptor antagonist drug that is widely used in medicine to treat gastric ulcer disease and other pathological hypersecretory states. To study the bioavailability of cimetidine, it was necessary to develop a rapid and reliable high-performance liquid chromatography procedure for quantitating the drug in body fluids. In this new procedure, cimetidine is adsorbed directly from urine or plasma, without prior clean-up, on to a mini-column prepacked with C18 material (Sep-Pak C18 cartridge). Acetonitrile is used to elute the drug, and the eluate is analyzed by high-performance reversed-phase liquid chromatography on a Partisil 10 ODS column, with an aqueous phosphate-methanol mixture as the mobile phase and UV detection at 228 nm. This method for analyzing cimetidine in body fluids is rapid, accurate and precise and differs from previously reported methods in that it eliminates the need for performing bothersome single or multiple, dualphase solvent extractions. Moreover, slight modifications in the composition of the mobile phase permit the simultaneous determination of cimetidine metabolites.
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PMID:Bioanalysis of cimetidine by high-performance liquid chromatography. 686 23

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.
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PMID:Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients. 844 8

The production of superoxide radicals as a result of decreased Cu,Zn-superoxide dismutase activity is considered to be the most important factor in the pathogenesis of diethyldithiocarbamate (DDC)-induced gastric antral ulcers in rats. The aim of the present study was to identify possible sources of superoxide radicals and the role of platelet-activating factor (PAF) in DDC-induced ulcer formation. Groups of rats were pretreated with a drug or antiserum before DDC (800 mg/kg) administration. The size of the DDC-induced gastric antral ulcers was measured. Pretreatment with anti-rat polymorphonuclear leukocyte serum or CV-3988 (a specific antagonist of PAF) 20 mg/kg significantly reduced the size of DDC-induced gastric antral ulcers. The results confirmed that superoxide radicals play an important role in the pathogenesis of DDC-induced gastric ulcer in rats and suggested that NADPH (reduced nicotinamide-adenine dinucleotide phosphate) oxidase in PAF-activated polymorphonuclear leukocytes may be involved in the generation of these radicals.
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PMID:Sources of superoxide radicals involved in the pathogenesis of diethyldithiocarbamate-induced gastric antral ulcer in rats. 950 50

C-X-C Chemokines play an important role for neutrophil extravasation through microvessels. Although the level of interleukin (IL)-8 is known to increase in the Helicobacter pylori-infected gastric mucosa, another C-X-C chemokine, GROalpha, has not been evaluated in the H. pylori-associated gastric mucosal injury. The present study was designed to investigate gastric contents of GROalpha in relation to those of IL-8 in the gastric mucosa of H. pylori-infected peptic ulcer patients. Thirty-eight patients with gastric ulcer and 41 with gastritis underwent endoscopy with informed consent and 49 were found to be H. pylori positive and 30 H. pylori negative. Biopsies from the gastric corpus were performed in each patient to examine the H. pylori colonization by bacterial culture, the rapid urease test and histological specimens as well as measurement of the contents of human GROalpha and IL-8. Helicobacter pylori infection was eradicated in 21 patients by triple therapy (lansoprazole 30 mg, amoxycillin 2.0 g, clarithromycin 600 mg; 2 weeks). The samples for GROalpha and IL-8 assay were homogenized in 0.02% aprotinin containing phosphate-buffered solution and the mucosal contents of GROalpha and IL-8 in the supernatants were quantified by sandwich enzyme immunoassay methods. The levels of GROalpha and IL-8 in H. pylori-positive gastric mucosa were significantly higher than those in the H. pylori-negative mucosa. There was a significant linear correlation between the levels of GROalpha and IL-8 (r = 0.798, P < 0.01). After the eradication of H. pylori by the triple therapy, the levels of GROalpha and IL-8 were significantly decreased. The GROalpha showed an increase in the H. pylori-positive gastric mucosa in a similar fashion as IL-8 contents, suggesting a pathogenetic role for GROalpha in H. pylori-associated gastric mucosal injury.
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PMID:Enhanced levels of C-X-C chemokine, human GROalpha, in Helicobacter pylori-associated gastric disease. 964 51


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