Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent clinical experiences with 34 Z-E patients indicates that the clinical features and course of the syndrome is less dramatic than described originally. Eighty-five per cent of the patients presented stories of abdominal complaints lasting more than five years and resembling the complaints presented by duodenal ulcer patients (DU). Ulcers were present in 91 per cent of the patients. Fifty-one per cent had either ectopic or multiple ulcers. One third had a single duodenal ulcer resembling an ordinary ulcer. No patients died from complications to the ulcer diathesis. Marked hypersecretion of acid and gastrin was present in the ZE group (BAO:33.7 +/- 7.4; PAO:62.8 +/- 6.1 meq H+/h; gastrin: 5094 pmol/l), but because of great individual variation in the ZE, some overlapping with the acid and gastrin measurements of the DU was seen. The diagnostic value of provocative tests using secretin, calcium, glucagon and food stimulations demonstrated a considerable overlapping between the two groups, indicating that these tests are of little clinical value. Tumours were found in half the patients, revealing malignancy in ten. The ZE can be diagnosed in most cases by combining symptomatology, with measurements of acid and gastrin.
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PMID:The clinical diagnosis of the Zollinger-Ellison syndrome. 29 36

The results from a short-term (28 days) treatment of patients with duodenal ulcer are reported. The average surface of the ulcers from 40.4 mm2 (initial average value) diminished to 7.3 mm2 by the 14 th day of the treatment. The graphic study of the kinetics of healing of the ulcer process revealed that in a treatment with 0.8--1.0 g Simetidin, a diminution of the ulcer by half (t/2) could be expected by the seventh day. In 16, out of the 21 treated, the ulcer epithelized by the 14th day of the treatment. In one patient a prolonged treatment of 42 days proved to be necessary to guarantee the epithelization of the ulcer. In 2/3 of treated patients, the pain complaints, the sensation of warmth and acidity disappeared by the end of the first week of the treatment. The average values of the basic and peak acid output (BAO and PAO), the N-acetyl neuramine acid output, the gastrin basic level, GOT, GPT and creatinine in serum do not change after the treatment. A significant reduction of hemoglobin concentration in the gastric juice is established after the treatment with Simetidin.
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PMID:[Results of the short-term (28 days) cimetidine treatment of duodenal ulcer]. 38 Jan 69

A total of 16 healthy subjects had gastric secretory studies where acid was either measured by the conventional aspiration technique (AT) or by intragastric titration at a pH of 5.0 (IT). In a first study food- and pentagastrin-stimulated PAO levels, both measured by IT, were within similar ranges. However, as compared to the respective AT data of the same subjects, the mean IT results were 35% higher, although both values were well correlated. In a second study a similar difference was observed between IT and AT data throughout the whole range of the pentagastrin dose-response curve. Both curves followed Michaelis-Menten kinetics and had similar Km values, while Vmax values were significantly higher at IT. This constellation excludes an increase of the gastrin sensitivity of the parietal cells as a cause for the higher IT data. It is, however, in keeping with the hypothesis that the distension stimulus present at IT potentiates the pentagastrin-stimulated acid secretion. It is likely that methodological problems such as overtitration of acid at IT and transpyloric loss of acid at AT additively contribute to the relatively large difference between AT and IT values. It is therefore not possible to fully interchange AT and IT data, despite their good correlation.
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PMID:A comparison between intragastric titration and aspiration technique under basal conditions and after food or pentagastrin stimulation. 68 41

Fortyseven uremic patients on RDT underwent a gastric secretion study and a contemporary evaluation of serum levels of Calcium (Ca), Phosphate (iP), Magnesium (Mg), Alkaline Phosphatase (AP), immunoreactive gastrin (Gas), parathyroid hormone (PTH), calcitonin (CT). Secretory test (pentagastrin 6 microgram/kg) was performed in the morning, after 12 hours of fasting, in the interdialytic interval. Female patients, male patients on RDT from less 1 year and hyposecretor patients were excluded from the study. On the basis of these criteria 25 normal or hypersecretor males between 20 and 55 years old were selected. A significant positive correlation was found between PTH and CT, while a negative significant correlation was found between CT and BAO and CT and PAO. Similarly, a significant negative correlation was found between PTH and BAO and PTH and PAO. Multiple regression study showed that the negative influence of CT on BAO and PAO is more relevant than the positive influence of PTH. These data suggest that PTH and CT are involved in gastric acid secretion in uremia. Since the inhibitory effect of CT is prevailing on the stimulating effect of PTH, patients with higher levels of PTH and CT have a lower gastric acid secretion. CT might therefore be considered as a protective factor against hypersecretion in uremia.
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PMID:Gastric acid secretion, calcitonin and secondary hyperparathyroidism in uremic patients undergoing regular dialysis therapy (RDT). 73 94

A method for measurement of gastrin in gastric mucosa has been developed, and distribution of gastrin in the stomach of pig, dog, cat, rabbit, and man was examined. Measurable amounts of gastrin were found in corpus of all species, but the content in the antrum was considerably higher. The highest concentration of gastrin was seen in man. The borderline between corpus and antrum was abrupt, and in both parts of the stomach gastrin was evenly distributed. In 44 patients with duodenal ulcer the antral gastrin concentration was 21.3 mug eqv. per g mucosa, in 15 patients with prepyloric ulcer 23.0, in 10 patients with gastric ulcer 5.9, and in 16 patients with gastric carcinoma 7.9. The control group consisted of 10 healthy volunteers and 12 patients with minor abdominal complaints. Mean antral gastrin concentrations were 28.1 and 20.7 respectively. No significant relationship was observed between PAO and gastrin content of antral mucosa in any group.
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PMID:Measurement of immunoreactive gastrin in gastric mucosa. 115 37

Administration of 2-DG accompanied by simultaneous neutralization of gastric contents with sodium bicarbonate resulted in a rise in serum gastrin in 4 patients without gastric disease, 4 with duodenal ulcer and 4 with gastric ulcer. The rise in gastrin equals that observed on stimulation with meat extract. Patients with gastric ulcers display a low PAO and a small rise in gastrin compared with normals and patients with duodenal ulcers. This finding correlates well with the chronic atrophic changes of the antral mucosa in patients with gastric ulcer.
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PMID:[Behavior of serum gastrin under vagus stimulation with 2-deoxy-D-glucose with special reference to acid secretion and the mucosal histology]. 125 25

The aim of this study was to evaluate changes in peptic acid secretion, and in fasting and meal-stimulated plasma gastrin levels after a 7-day course of omeprazole 30 mg/day or ranitidine 300 mg/day, administered in accordance with a randomized, double-blind, double-dummy protocol. Ten duodenal ulcer patients were studied. Their acid and pepsin output was determined prior to and after treatment. Plasma gastrin levels were also determined under basal conditions on day 7 of treatment, and 24 hours after the last administration of the drug. With regard to acid output, omeprazole resulted in a 98% reduction in BAO and an 80% reduction in PAO, both significantly greater than those achieved with ranitidine (BAO 50%, PAO 25%). No significant changes in pepsin secretion were observed. The increase in fasting plasma gastrin observed after ranitidine and omeprazole was 86% and 242%, respectively, on day 7, and 13% and 103% twenty-four hours after final dose. Increases in meal-stimulated plasma gastrin were, respectively, 126% and 125% on day 7 and 8 after omeprazole, whereas the increase with ranitidine was 62% only on day 7 of treatment, with subsequent normalization. In addition to confirming the well-known effect of omeprazole on the physiology of gastric secretion, our data show that administration of therapeutic doses of traditional H2-antagonists is accompanied by a secondary hypergastrinemia, which is rapidly reversible after discontinuation of therapy.
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PMID:Gastric acid secretion and plasma gastrin during short-term treatment with omeprazole and ranitidine in duodenal ulcer patients. 142 86

The results of gastric secretory studies in 192 cases of recurrent ulcer after surgery for duodenal ulcer were analyzed and compared with the secretory data collected in a control group of 74 duodenal ulcer patients who had undergone various forms of gastric surgery, but who did not develop a recurrent ulcer (controls). The patients studied comprised 46 cases of recurrent ulcer after partial gastrectomy, 10 cases of recurrent ulcer after partial gastrectomy and bilateral truncal vagotomy, 56 cases of recurrent ulcer after truncal vagotomy and drainage, 52 cases of recurrent ulcer after highly selective vagotomy, and finally 28 cases in which the recurrent ulcer led to the diagnosis of the Zollinger-Ellison syndrome. The entire study was based upon an analysis of the basal acid output, the response to maximal stimulation by pentagastrin or by histalog and by insulin in the case of previous vagotomy, and finally on an assessment of basal serum gastrin. The analysis has suggested minimal secretory levels with discriminative values useful for the postoperative diagnosis of recurrent ulcer and for an assessment of the completeness of vagotomy (ratio PAO Insulin/PAO pentagastrin or histalog). Moreover, an analysis of various elements of the sequential basal pentagastrin-insulin test permitted us to approach the pathophysiological mechanism responsible for ulcer recurrence, and to identify suitable criteria for selection of the best treatment.
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PMID:Gastric secretory investigation of recurrent ulcer after surgery for duodenal ulcer. 177 83

The effect of omeprazole on acid secretion and gastrin levels has been investigated in 10 elderly duodenal ulcer patients in remission. Doses of 5, 10, 20 and 40 mg omeprazole were given once daily for 7 consecutive days and the basal (BAO) and peak (PAO) acid output and fasting plasma gastrin concentration were measured 24 h after the seventh dose. Omeprazole suppressed PAO significantly and dose-dependently after doses of 10, 20 and 40 mg, the suppression being 42%, 75% and 85%, respectively. No patient showed complete inhibition of PAO and at least 20 mg had to be given to obtain a marked inhibitory effect in all patients. Increasing the dose to 40 mg had only a slight additional effect compared to 20 mg. There was a relationship between degree of acid inhibition and the increase in fasting plasma gastrin. PAO had to be suppressed by more than 80% before a moderate increase in fasting plasma gastrin was observed. The optimal once-daily oral dose of omeprazole for inhibition of acid secretion in elderly patients appears to be 20 mg. Omeprazole 20-40 mg may cause a moderate increase in fasting plasma gastrin.
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PMID:Omeprazole in elderly duodenal ulcer patients: relationship between reduction in gastric acid secretion and fasting plasma gastrin. 188 35

Basal and pentagastrin-stimulated gastric acid secretion and basal serum gastrin level were investigated in 55 active duodenal ulcer patients with antral colonization with Helicobacter pylori (HP) and 17 patients without. Our study shows that basal (BAO) and pentagastrin-stimulated gastric acid secretion (MAO and PAO) were significantly higher in HP positive than in HP negative patients with duodenal ulcer disease. There were also a tendency to increase in basal serum gastrin concentration in HP positive patients. We suggest that antral HP increases antral gastrin release and gastric secretion. Increased acid secretion then causes duodenal ulcers by producing a low intraduodenal pH.
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PMID:[Duodenal ulcer disease: Helicobacter pylori and hyperchlorhydria]. 191 66


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