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)

Hanisch E, Schwille PO. Effects of various vagotomies and sympathectomies on gastric secretory function in the non-stressed and by immobilization stressed rat. Scand J Gastroenterol 1984, 19, Suppl 89, 99-104 The aim of the present study was to study several gastrointestinal parameters (acid, pepsin secretion, ulcer index, gastrin, somatostatin, glucagon) following various forms of sympathectomies in comparison with vagotomies under two different states of sympatho-adrenal activation in male gastric fistula rats. It is concluded that acid and pepsin appear regulated by the autonomous nervous system, even in the basal state. Gastric ulcer formation/prevention depends on gastric sympathetic innervation and on the state of activation of the adrenal medulla. Basal gastrin, somatostatin, glucagon may be modified by both limbs of the autonomous nervous system.
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PMID:Effects of various vagotomies and sympathectomies on gastric secretory functions in the non-stressed and by immobilization stressed rat. 614 96

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

Seventy-five dialysis patients awaiting renal transplantation were studied. Investigations included single contrast barium meal, serum gastrin assay, gastric acid studies, and fiberoptic gastroduodenoscopy with multiple biopsies. Radiological studies revealed five duodenal ulcers and one gastric ulcer. Endoscopy showed gastroduodenal lesions in 57 patients (49%). Superficial gastritis was present in 50 patients (66.7%), atrophic gastritis in 11 (14.6%), and duodenitis in 30 (40%). Hypergastrinemia was observed in 48 patients (64%). Maximum acid output was markedly elevated in 33 patients. Acid hypersecretion was found to be correlated with the presence of endoscopic lesions and histological evidence of gastritis. Nine of the 11 patients with atrophic gastritis were acid hyposecretors and had low gastrin levels. Pretransplant gastric assessment identified a relevant number of gastroduodenal lesions in these patients. The increased risk of severe posttransplant ulceration justifies thorough gastric assessment and prophylactic antiulcer therapy in all renal transplant candidates.
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PMID:Assessment of the upper gastrointestinal tract in hemodialysis patients awaiting renal transplantation. 634 17

Sulfated gastrins resemble cholecystokinins (CCK) both structurally and functionally. They are less potent than CCK in stimulating gallbladder contraction and pancreatic enzyme secretion, but the plasma concentrations of sulfated gastrin are higher than those of CCK. Therefore, sulfated gastrins may contribute significantly to the endogenous CCK activity. The degree of sulfation of gastrin differs with the localization in the digestive tract. In the antrum and duodenum of normal subjects 45% of the gastrins are sulfated, as in serum. In contrast, the sulfation of gastrin is complete in the jejunum (human) and in the pancreas (rat and cat). Hence, the degree of sulfation of gastrin is similar to that of CCK in the jejunum. The degree of sulfation in antrum, duodenum and serum diminishes with hypergastrinemia, and is thus significantly lower in patients with gastric ulcer or pernicious anemia than in healthy subjects. In the Zollinger-Ellison syndrome, the degree of sulfation of gastrin varies greatly (20-90%) and the distribution between small and large gastrins is equally variable. However, sulfation and proteolytic processing follows a parallel course; complete processing to smaller components is accompanied by complete sulfation of the peptide and vice versa. During ontogenesis sulfated gastrins may be of special importance, since they are the only sulfated members of the gastrin/CCK family of peptides which occur in substantial quantities in the early fetus. Tyrosine-O-sulfation has now been recognized as a widespread modification, and sulfated tyrosyl residues in gastrin, CCK and leu-enkephalin are examples of a derivatization which can govern the biological activity of regulatory peptides.
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PMID:Measurement and occurrence of sulfated gastrins. 638 82

The sensitivity to stimuli of gastric acid and pepsin secretion in duodenal and gastric ulcer was studied using a pentagastrin dose response that was analyzed by an exponential model. By this model, maximum secretory rate (Vmax), the dose of administered pentagastrin giving 50% of Vmax (D50), and the threshold equivalent dose responsible for basal secretory rate are calculated. Using only individual tests in which the data adequately fitted the model, we report on 171 subjects, 120 with duodenal ulcer, 22 with gastric ulcer, and 29 controls. Among the possible influences on secretion, sex and weight were significant, whereas age and activity or duration of ulcer disease were not. Men secreted more acid per kilogram body weight than women in each group, and men with duodenal ulcer secreted more acid and pepsin than normal men or those with gastric ulcer. Because basal secretion in men with duodenal ulcer was a higher proportion of maximum, D50 (the measure of apparent sensitivity) was 25% lower (p less than 0.01) in patients with duodenal ulcer than in controls; when examined by sex, men with duodenal ulcer had a lower D50 than women with duodenal ulcer, men with gastric ulcer, and male controls. D50 in all patients was very much lower for pepsin than for acid. Km, the dose that would be required to stimulate secretion to 50% of maximum if basal = 0 (intrinsic sensitivity), was not different between groups or sexes. Thus the difference in sensitivity between duodenal ulcer patients and controls was seen only in the apparent, and not in the intrinsic sensitivity indices; this was largely a phenomenon of males and could be explained by a higher ratio of basal to maximal secretion. Neither the observed increase of basal nor the maximal rates of acid and pepsin secretion in duodenal ulcer patients could be explained by an increased sensitivity to gastrin.
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PMID:Apparent and intrinsic sensitivity to pentagastrin of acid and pepsin secretion in peptic ulcer. 642 36

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

A 54-year-old man presented with unrelenting abdominal pain. An upper gastrointestinal x-ray showed a gastric ulcer. The duodenum showed minimal cap deformity suggestive of antecedent ulcer disease. The upper small intestine was within normal limits. Gastroduodenoscopy revealed a duodenal polyp. Biopsy of the polyp identified the presence of a gastrinoma. Serum gastrin level before endoscopic polypectomy was 489 pg/ml. Endoscopic polypectomy was performed and electron micrographs of the tissue revealed endosecretory granules of the gastrinoma. Complete removal of the gastrinoma was suggested by comparative gastric analyses, by serum gastrin levels of 93, 180, and 167 pg/ml, and by the clinical course.
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PMID:Endoscopic diagnosis and removal of a duodenal wall gastrinoma. 647 95

The results of a 5-year follow-up of 289 consecutive, peptic ulcer patients treated by antrectomy and gastroduodenostomy, with or without vagotomy, are presented. Patients with a preoperative gastric acid secretory capacity (PAO) below 40 mmol/h were treated by antrectomy alone, while subjects with a higher PAO had a vagotomy in addition. The antrectomy was defined by lithmus indication of the corpus-antrum border and by histologic verification, including gastrin cell counting. The over all incidence of gastroscopically verified recurrent ulceration was 8.5%. In patients with ulcer location in the bulb or the pyloric/prepyloric region (juxtapyloric ulcer) and treated by antrectomy alone, the recurrence rate was 18% (n = 102), and in gastric ulcer patients it was 4% (n = 47). Altogether 14 patients with recurrent ulcer were subsequently reoperated on by vagotomy showing no further recurrence. Antrectomy combined with vagotomy was primarily performed almost exclusively in patients with juxtapyloric ulceration, in whom the recurrence rate was 2% (n = 106). According to a postoperative insulin test, the patients with recurrence after antrectomy and vagotomy were incompletely vagotomized. In patients who remained free of symptoms or signs of recurrent disease, the median reduction in gastric acid secretory capacity was about 60% after antrectomy alone and 80% after antrectomy and vagotomy. In juxtapyloric ulcer patients with recurrence after antrectomy alone there was a small median reduction in PAO one month after operation (26%) and then an increase close to the preoperative level (6% reduction). In patients with a postoperative reduction in PAO of less than 35%, there was a high probability of recurrent ulcer, about 70%. In spite of selection of patients with a comparatively low preoperative PAO (less than 40 mmol/h) for antrectomy alone, the recurrence rate was 18% in patients with juxtapyloric ulcer location. In this selected group of patients the preoperative PAO was not higher in patients with ulcer recurrence than in patients who were asymptomatic after the operation. Selecting patients with juxtapyloric ulcer for antrectomy, with or without vagotomy, on the basis of gastric acid secretory capacity therefore seems unjustified. When vagotomy was added to antrectomy and gastroduodenostomy it seemed to increase the risk of developing serious (Visick 3u and 4) postgastrectomy syndromes; 12% after antrectomy and vagotomy versus 3% after antrectomy alone. Vagotomy appeared to be associated with an increased risk of bile reflux gastritis, gastric mycosis, and milk intolerance. Dumping and diarrhoea after vagotomy often coincided with milk intolerance. Antrectomy, with or without vagotomy, did not markedly impair recorded nutritional parameters.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antrectomy and gastroduodenostomy with or without vagotomy in peptic ulcer disease. A prospective study with a 5-year follow-up. 657 6

Two hundred millilitres of an isotonic solution of CaCl2 (0,118 M) were injected and left 15 min in the stomach of normal subjects (SN1; n = 21), of patients with gastric ulcer (UG; n = 16), patients with duodenal ulcer (UD; n = 40), patients with normochlorhydric gastritis (G1; n = 13) and patients with hypo- or achlorhydric gastritis (G2; n = 7). Gastric acid secretion and gastrinemia were measured during 90 min. After intragastric calcium injection, the acid secretion was increased during 60 min in almost all subjects (87 to 100 p. 100 of subjects in the various groups) whereas gastrin release was increased in the majority (57 to 84 p. 100) of cases. The possible dissociation between the acid and gastrinic responses implies that the calcium-induced acid response is independent of the calcium-induced gastrin release. During control experiments in normal individuals, continuous intragastric perfusion (300 ml/h) of NaCl 0.15 M failed to alter gastric acid secretion or gastrin release, whereas continuous intragastric perfusion of CaCl2 0,118 M enhanced gastric acid secretion and gastrin release. The action of CaCl2 0,118 M is therefore not attributable to gastric distension but directly to calcium itself. The stimulation of acid secretion by intragastric calcium was more conspicuous in patients with gastric or duodenal ulcer than in normal subjects. The release of gastrin was higher in gastritis and duodenal ulcer than in the normal group. It is hypothesized that intragastric calcium increases the cholinergic tone of the parietal cell.
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PMID:[Effects of intragastric calcium on gastric acid secretion and release of gastrin in normal man and in various pathological cases]. 661 72

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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