Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stress ulcer prophylaxis diminishes but does not eliminate the risk of severe bleeding from this complication. In 70-80% of the cases the source of bleeding is hemorrhagic gastritis. No controlled studies exist which have in particular investigated conservative therapy in patients with stress-induced hemorrhage. Even effective measures to suppress gastric acid secretion or to reduce splanchnic blood flow are ineffective in 10-40% of intensive care unit patients with stress-induced bleeding. In these cases total gastrectomy has so far often been the only therapeutic approach. We report our experience with a new approach in treating severe stress-induced hemorrhagic gastritis after ineffective primary treatment with H2-receptor antagonists, pirenzepine and somatostatin. Continuous gastric lavage with 5-10 l ice-cold Ringer's solution was used until complete cessation of bleeding, as evident from clear lavage. Repeated administration of 12 g sucralfate (60 ml) at 2-h intervals for 24 h through a gastric tube was used to prevent recurrence of bleeding and to promote healing. Sucralfate was reduced on the 2nd and 3rd day to 20 ml 2-hourly and later to 10 ml 4-hourly. In four patients this treatment was used as an ultima ratio when the patients were already scheduled for total gastrectomy. A total of 23 patients were treated during a 7-year period; all of them responded successfully, and no patient required surgery.
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PMID:Conservative treatment of stress ulcer bleeding: a new approach. 141 Dec 92

Practical approaches to the management of acromegaly are discussed. The roles of surgery, radiotherapy, and medical treatment with oral dopamine agonists such as bromocriptine or the long-acting somatostatin analogue octreotide given subcutaneously are reviewed. Most cases need surgery, but cure is rare in patients with macroadenomas, although common with microadenomas. Radiotherapy should be considered in surgical failures, but takes several years to be effective. Medical treatment with octreotide is effective in the majority, for whom it represents a major advance, but it needs to be administered subcutaneously and the development of gallstones and gastritis in long-term treatment are problems. Bromocriptine is usually less effective, but occasionally still plays a role in the therapeutic program. Combinations of the different modalities are usually required in the management of acromegalic patients.
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PMID:Proceedings of the workshop, "Practical approaches to the diagnosis and treatment of acromegaly". 151 40

Gastrointestinal side-effects of prolonged therapy (greater than 2 yr) with the long-acting somatostatin analog octreotide were studied in 10 acromegalic patients. After 2 yr of therapy, 6 of 10 patients had newly developed gallstones, complicated by cholangitis and jaundice in 1. Serum vitamin B-12 concentrations declined in all 10 patients [from 380 +/- 32 to 172 +/- 21 pmol/L (mean +/- SE); P = 0.023] and became abnormally low in 4. Gastric biopsy specimens, obtained during gastroscopy (9 patients), showed moderate to severe active gastritis, with damage to the superficial and deeper layers of the mucosa in 9 of 9 and focal atrophy in 7 of 9 patients. Campylobacter pylori was found in the antral mucosa in 8 of 9 patients. Although information is lacking on similar studies in untreated acromegalic patients, we suggest that patients receiving chronic octreotide therapy be closely monitored for these and possible other side-effects related to gastrointestinal actions of octreotide.
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PMID:Gastrointestinal side-effects of octreotide during long-term treatment of acromegaly. 222 21

Campylobacter pylori (C.p.) infection is often found in patients with antral gastritis and peptic ulcer disease. Pathophysiological links are still unclear, and we therefore tested the hypothesis whether C.p. affects the gastrointestinal peptides and thus influences gastric acid secretion and protective factors. 94 patients were examined by upper GI endoscopy and blood analyzed for gastrin, somatostatin, pancreatic polypeptide and neurotensin. Biopsies of antral mucosa were investigated for C.p. in urease testing, culture and microscopy. C.p. was found in 42 patients (45%). In microscopy all of these patients had chronic gastritis (100%). A significant increase in gastrin uninfluenced by C.p. was found in patients with antral gastritis (normal: 6.4 +/- 0.7, [n = 27]; gastritis without C.p.: 18.4 +/- 5.9 [p less than 0.02], [n = 7]; gastritis with C.p.: 10.7 +/- 2.2, [n = 22]). Somatostatin, pancreatic polypeptide and neurotensin showed no difference.
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PMID:[Campylobacter pylori colonization of the antrum: effect of gastrin, somatostatin, pancreatic polypeptide and neurotensin]. 256 33

The heterogeneity of muscarinic receptors has been well supported by differential characteristics between pirenzepine and atropine both in receptor binding and in whole tissue pharmacology studies. Under these conditions pirenzepine has been classified as a selective receptor antagonist with high affinity for M1 receptors. The antisecretory properties of pirenzepine on gastric acid and pepsin secretion may be attributed to the antagonistic activity of the drug on muscarinic M1 receptors of gastric intramural plexuses, whereas the effect on parietal muscarinic M2 receptors seems of less importance. Additional inhibitory mechanisms on gastric secretion may be represented by pirenzepine-induced increase in somatostatin release from gastrointestinal system. Significant cytoprotective properties of pirenzepine have been observed on a variety of experimentally induced peptic ulcerations. This protective activity may be due to pirenzepine-induced increase in gastric mucosal blood flow as well as to the increase in gastric transmural electric potential difference. In accordance with this pharmacodynamic profile of pirenzepine, numerous clinical studies have revealed its efficacy in the treatment of both duodenal and gastric ulcerations. In addition to this, the clinical usefulness of the drug has been demonstrated in Zollinger-Ellison syndrome, in stress ulceration, in acute gastrointestinal bleeding as well as in gastritis, duodenitis and non-ulcer dyspepsia. In most of the studies pirenzepine has been found to be well tolerated with a low incidence of antimuscarinic effects which may occur at salivary, ocular, cardiac and urinary sites. The clinical use of pirenzepine alone or in association with H2 blockers is recommended in the treatment of peptic ulcer patients, in the case of acute gastrointestinal haemorrhage and in patients non responders to H2 antagonists.
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PMID:[A selective antimuscarinic agent: pirenzepine. Review of its pharmacologic and clinical properties]. 257 37

The effects of Somatostatin and Ranitidine were studied in 46 patients with acute hemorrhages of the upper digestive tract, 23 were medicated with Somatostatin, 12 with acute gastric hemorrhages of medicamental etiology and 11 with ulcers. The doses was 500 micrograms bolus and than infusion of 250 micrograms/h. 23 patients were treated with 300 mg/day I.V. of Ranitidine, 12 had acute gastric hemorrhages also of medicamental etiology and 11 with ulcers. Somatostatin stopped the bleeding in 100% of the patients with hemorrhagic gastritis, meanwhile Ranitidine only in 76%. This is statistically significative (p less than 0.04648). Hemorrhages in patients with ulcers were stopped by Somatostatin in 73% and by Ranitidine in 64%. This is not statistically significative (p = 0.4995). No collateral effects were observed in both groups of patients.
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PMID:[Effect of somatostatin and ranitidine in acute hemorrhage of the upper digestive tract]. 257 30

Fifty-eight subjects including controls, patients with duodenal ulcer, non-operated or treated with a superselective vagotomy underwent endoscopic fundic and antral biopsies. Histologic classification of the two mucosae was performed. We examined the relationship between the histologic grade of gastritis in the two mucosae, then between the histologic aspect of the antral mucosa and antral gastrin-and somatostatin-cell densities, the basal intraluminal secretion of gastrin and somatostatin. There was a significant correlation between the histologic aspect of fundic or antral mucosa and the age of patients, except in the case of vagotomized patients. Fundic and antral histologic patterns were also correlated in each patient, except for vagotomized. Gastrin and somatostatin cell densities showed no variation in function of the degree of inflammation of non atrophic gastritis. These cell densities showed a tendency to decrease in atrophic gastritis, especially when intestinal metaplasia was present. Intraluminal gastrin secretion was increased in patients with mild atrophic gastritis (p less than 0.05 to p less than 0.02) in comparison with those whose histology was roughly normal. It was also increased in severe atrophic gastritis. The highest intraluminal secretion of somatostatin was observed in patients with mild atrophic gastritis while this secretion fell noticeably in those showing severe atrophic gastritis, as compared to the other groups. This work seems to suggest a relationship between intraluminal peptides and the evolution of gastritis. While results are still preliminary, they do not indicate that these peptides, thus released, play any pathophysiologic role.
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PMID:[Histologic aspect of the human gastric mucosa: relation to gastrin and somatostatin cells and the intraluminal secretion of these peptides]. 287 63

The increased duodeno-gastric reflux often associated with gastric or duodenal ulcer disease causes hypersecretion of acid in response to pentagastrin and hypergastrinaemia in response to meal. It is proposed that these functional changes are mediated by an alteration in somatostatin activity that is produced by the alkaline nature or pancreatic component of the reflux. When duodenal reflux is confined to the antrum, an increased acid output from normal secretory mucosa is delivered to the duodenum where ulceration may occur. When alkaline reflux affects the body of the stomach, gastritis is produced, with local fundic hypersecretion, which may lead to ulceration of the damaged gastric mucosa. Duodenal reflux may therefore be a common factor in the pathogenesis of gastric and duodenal ulcer, and it probably acts by producing a hormonal defect.
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PMID:Duodeno-gastric reflux--a common factor in pathogenesis of gastric and duodenal ulcer. 610 72

As an attempt to approach the pathogenesis of peptic ulcer disease, antral gastrin and somatostatin concentrations were studied in normal subjects, patients with duodenal ulcer and gastric ulcer. In the patients with peptic ulcer, antral somatostatin concentrations were significantly lower than those in normal subjects. In non-ulcer subjects, including normal subjects and patients with atrophic gastritis, antral somatostatin concentrations were correlated inversely with the degree of antral gastritis, while in the patients with peptic ulcer, especially in duodenal ulcer, they were low, irrespective of histological picture of antral mucosa. In the patients with duodenal ulcer, low antral somatostatin concentrations with high antral gastrin/somatostatin ratio may cause increased serum gastrin levels and increased gastric acid secretion. From the above findings, it has been concluded that low antral somatostatin levels may be related to the pathogenesis of duodenal ulcer disease.
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PMID:Antral gastrin and somatostatin concentrations in peptic ulcer patients. 612 90

In this study we have investigated the mucin profile and the endocrine cell population in gastric endoscopic biopsies from 22 patients affected by chronic gastritis and intestinal metaplasia and in five surgical specimens of stomachs removed because of intestinal-type carcinoma (4) or peptic ulcer (1). High iron diamine-Alcian blue (HID-Ab) staining and peptide immunocytochemistry (peroxidase anti-peroxidase technique) were used. Forty-one foci of intestinal metaplasia were detected, 15 produced sulphomucins and 26 sialomucins. Of the endocrine cells investigated, gastrin and somatostatin cells were the most frequently observed, while cholecystokinin, glucose-dependent insulinotropic peptide-, secretin- and enteroglucagon-containing cells were also found in the metaplastic areas, but less frequently. No significant correlation was found between the type of mucin and the types of endocrine cells present, the latter usually resembling those normally found in the small intestine. On the basis of these results we conclude that intestinal metaplasia involves mucin- and peptide-producing cells of the stomach in a variable manner, with no correlation between the two.
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PMID:Endocrine cells in intestinal metaplasia of the stomach. 615 74


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