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)

The Zollinger-Ellison syndrome (ZES) is caused by mainly pancreatic, gastrin-producing tumours, which show a high rate of malignancy. The clinical picture is dominated by gastric hypersecretion, which results in the development of peptic ulcerations of the stomach and duodenum, reflux esophagitis, or diarrhea. The differentiation from other types of hypergastrinemia is done by provocative tests, mainly the secretin-test. Because of the high malignancy rate, therapeutically, a symptomatic treatment of gastric hypersecretion by H2-receptor antagonists or in cases of ineffective conservative treatment total gastrectomy is performed. In patients with duodenal gastrinomas or in the rare cases with benign pancreatic tumours resection of the tumours is the therapy of choice.
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PMID:[Zollinger-Ellison syndrome]. 632 97

A case of Zollinger-Ellison syndrome with some peculiar aspects is described. The disease started with painless dyspepsia, watery diarrhea, relevant loss of body weight and absence of peptic ulcer. After a steroid treatment performed at home without any rationale, diarrhea stopped totally for 18 months and body weight returned to normal. Subsequently, the disease recurred with more typical clinical characters: juxtapyloric ulcer, increase in serum gastrin levels and positive secretin test, presence of gastrinomas at angiography. The monitoring of gastric pH showed a persistent hyperacidity during medical treatment with H2 and muscarinic antagonists. The localization of gastrinomas was extrapancreatic, at the root of jejunal mesentery. Excellent results were obtained by surgical treatment which consisted in resection of the principal neoplastic masses with total gastrectomy. The patient's general conditions after two years are good.
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PMID:[Description of a case of Zollinger-Ellison syndrome]. 632 67

The gut hormone response to a breakfast meal was studied in 12 subjects hospitalised for an episode of acute diarrhoea (presumed infective) who were otherwise well and in 13 healthy control subjects. Fasting blood glucose concentrations were low but basal insulin concentrations were raised. Basal concentrations of pancreatic polypeptide and both basal and postprandial responses of motilin, enteroglucagon, and vasoactive intestinal polypeptide (VIP) were also significantly greater than controls. No abnormalities in plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP) or pancreatic glucagon were found. The suggested physiological actions of the raised hormones may be relevant to the pathophysiology of diarrhoea.
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PMID:Gut hormones in acute diarrhoea. 634 84

In 12 patients treated 2 to 58 months previously for medullary carcinoma of the thyroid, basal serum concentrations of calcitonin, gastrin, vasoactive intestinal polypeptide, glucagon, insulin, and pancreatic polypeptide were measured in search of any correlation between these and the clinical course of the disease. All patients had elevated serum calcitonin levels indicating present disease. One patient had increased serum concentrations of several hormones. Another had achlorhydria and high serum gastrin levels. No relationship between calcitonin and gastro-intestinal polypeptides was found in 11 patients. No correlations were found between serum levels of polypeptides and the occurrence of diarrhoea in 5 patients. It is concluded that gastro-intestinal polypeptides, which are produced by other apudomas, are not secreted in more than normal concentrations under basal conditions, by the majority of patients previously treated for medullary carcinoma of the thyroid.
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PMID:Gastro-intestinal polypeptides in patients treated for medullary carcinoma of the thyroid. 637 28

Subtotal pancreatectomy specimens from two adults with hyperinsulinemic hypoglycemia and one adult with watery diarrhea syndrome were investigated. All three specimens were originally diagnosed as "nesidioblastosis"; none had a neoplasm, and all patients were cured of their endocrine dysfunction by the surgical procedure. Tissue samples were studied by light microscopy and light microscopic immunohistochemistry for serotonin, ACTH, bombesin, calcitonin, gastrin, glucagon, insulin, HPP, somatostatin, and VIP. The results were compared with those obtained from the parallel study of ten adult pancreata obtained at autopsy from patients without pancreatic disease or endocrine dysfunction. The total endocrine cell mass was not notably greater in the pancreata from patients with endocrine dysfunction than in the controls. Both groups had an estimated 95% of the endocrine cell population organized in islets while the remaining 5% was irregularly dispersed amidst the exocrine ducts and acini. Findings more conspicuous in patients with endocrine dysfunction but not absent in the controls included: large islets, islets with irregular contours and ragged edges, and large individual islet cells with abundant cytoplasm and bizarre nuclei. Immunoreactivity for insulin, glucagon, and somatostatin was demonstrated in all cases; the ratio among these hormones in the patients with endocrine dysfunction and in the controls was similar. In the patients with hyperinsulinemic hypoglycemia, step sections sequentially stained for insulin and somatostatin showed a close topographic relationship between these cell types. In the patient with the watery diarrhea syndrome, VIP immunoreactive cells were easily identified admixed with exocrine components; they were only rarely seen within islets. We suggest that the hyperinsulinemic hypoglycemia in these adults was not due to simple quantitative abnormalities in total endocrine cell mass nor to its maldistribution nor to lack of topographic proximity between insulin and somatostatin cells. We speculate that the syndrome may be based on still unknown derangements of insulin secretion, release, and/or its degradation. In the case of the watery diarrhea syndrome, the readily identifiable VIP immunoreactive cells represent the emergence of a functional expression regarded as ectopic for the endocrine cells of the pancreas. We conclude that nesidioblastosis per se cannot be viewed as the structural basis of these endocrine dysfunctions since many of its features were present in control pancreata lacking any such association.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adult nesidiodysplasia. 640 Jun 29

A patient with intractable diarrhea was found to have hyperchlorhydria, hypergastrinemia, and an increase in serum gastrin in response to secretin. At surgery the pancreas was completely normal, and an 8-cm adrenal adenoma was removed. Postoperatively the diarrhea ceased, and serum gastrin and gastric acid levels returned to normal. Tissue gastrin levels in the adrenal tumor were 1,000 times the expected values. Circumstantial evidence suggests that this tumor may have been secreting gastrin.
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PMID:A gastrin-producing adrenal tumor? 652 6

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

During a 3-year period proximal gastric vagotomy without drainage and selective gastric vagotomy with drainage were performed in 61 patients with duodenal ulcer. Of these, 57 patients were followed for 3-6 years. 77% were symptom-free (Visick I); 8,3% were improved but still have periods of dyspepsia (Visick II) and 14% were failures because of recurrent ulcer (Visick III). There were seven duodenal recurrences in the bulb, and one prepyloric recurrence. There were no operative deaths or major complications. The side effects, like diarrhoea and dumping, after proximal gastric vagotomy and selective vagotomy were mild and rare. The majority of our patients gained their ideal body weight within the first six months from surgery. Blood chemistry did not show any deficiency in haemoglobin secondary to vagotomy, but plasma basal level of gastrin was constantly higher after surgery. It is concluded that 3-6 years after proximal gastric vagotomy and selective gastric vagotomy for duodenal ulcer there was a 14% recurrence rate, but the absence of mortality, severe complications or significant side effects seems to be at least as important as the high recurrence rate.
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PMID:Proximal gastric vagotomy without drainage and selective gastric vagotomy with drainage for surgical therapy of duodenal ulcer: a retrospective study. 660 44

Eleven adult Basenji dogs with immunoproliferative small intestinal disease (IPSID) were studied. Two items of history related to the digestive tract were characteristic: (i) chronic intractable diarrhea in most dogs, and (ii) progressive emaciation. Anorexia was intermittent in only a few dogs. In addition, skin lesions of various degrees of severity were observed, including alopecia of pinnae and ventrum, hyperpigmentation and hyperkeratosis of pinnae, and necrosis and ulcerations of margins of pinnae. The cause of the skin lesions was not determined; however, hypothyroidism did not appear to contribute to the skin changes. Standard hematologic and serum chemical values were not consistently abnormal. However, a poorly regenerative anemia, mild neutrophilia, and increased aspartate aminotransferase and alanine aminotransferase activities were generally observed in severely affected dogs. The Pelger-Huet anomaly was identified in dog 3. Maldigestion and malabsorption as determined by the N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test was documented to varying degrees in dogs with IPSID. Maldigestion was correlated with functional pancreatic exocrine insufficiency. Severe malabsorption was documented in only 3 dogs. Serum gastrin values were evaluated in these dogs because of a prior observation of parietal cell hyperplasia and gastric ulceration. Hypergastrinemia was documented in 3 dogs. Additional studies will be necessary to determine whether an acid hypersecretory state contributes to the pathogenesis of IPSID in Basenjis.
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PMID:Clinical and laboratory characterization of Basenjis with immunoproliferative small intestinal disease. 660 87

Cholecystokinin (CCK) is structurally similar to gastrin and is known to competitively inhibit the action of gastrin on the parietal cell, but little information has been accumulated about circulating levels of CCK in patients with duodenal ulcer (DU). In a group of 18 healthy volunteers (controls) and 22 DU patients (13 with active DU, nine with inactive DU), we stimulated endogenous release of CCK with oral administration of Lipomul corn oil. Plasma concentrations of CCK were measured by radioimmunoassay; ultrasonographic measurements of gallbladder volume were used as a biologic correlate for CCK in control patients and in patients with active DU. No significant difference was found in fasting plasma concentrations of CCK between controls (107 +/- 8 pg/ml) and DU patients (123 +/- 15 pg/ml), or in their total integrated release of CCK during the first hour after Lipomul ingestion (3.7 +/- 0.7 ng-min/ml in controls, 2.8 +/- 0.4 ng-min/ml in DU patients). Furthermore, no significant difference was found in integrated release of CCK between patients with active DU (2.9 +/- 0.6 ng-min/ml) and those with inactive DU (2.8 +/- 0.6 ng-min/ml). Gallbladder volume was highly correlated with plasma concentrations of CCK in controls (r = -0.91) and in active DU patients (r = -0.98). Patients with active DU had significantly smaller volumes of their resting gallbladders, they emptied less of their resting gallbladder contents in response to fat, and they showed diminished sensitivity to endogenously released CCK compared to controls. In six patients with active DU who underwent truncal vagotomy and drainage, integrated release of CCK increased significantly, from 1.9 +/- 0.6 ng-min/ml before vagotomy to 9.3 +/- 3.0 ng-min/ml after vagotomy. We found no evidence to suggest that abnormalities in release of CCK contributes to the development of duodenal ulcers. We speculate, however, that the increased release of endogenous CCK after truncal vagotomy may possibly play an etiologic role in the syndrome of postvagotomy diarrhea.
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PMID:Plasma concentrations of cholecystokinin in patients with duodenal ulcer disease. 669 Nov 83


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