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 gastrointestinal tract is the largest endocrine organ in the body. However, gastrointestinal hormones are not confined to the gut and many of them are delivered to their target tissue by neural and paracrine routes as well as the circulation. Regulatory peptide is therefore a more appropriate term than gastrointestinal hormone. The functions of these regulatory peptides include effects on intake, digestion and absorption of food, and changes in gut secretions, motility and growth. Since these peptides do not act alone but in concert it has been difficult to ascribe particular functions to individual peptides. However, the recent and on-going development of specific regulatory peptide agonists and antagonists has resulted in major advances in our understanding of the physiology of these peptides. In turn these findings are creating new therapeutic avenues providing some return from all the research on these gastrointestinal regulatory peptides. The somatostatin derivative (octreotide or sandostatin) is the most obvious example. Although only approved in Australia for treatment of carcinoids and VIPomas, the prospects include treatment of other gastroenteropancreatic tumours, acromegaly, idiopathic diarrhoea, fistula closure, dumping, and ERCP or post-operative pancreatitis. A new gastrokinetic agent, that acts via the motilin receptor, is undergoing trials for the treatment of impaired gastric emptying. The trophic effect of gastrointestinal peptides has clinical significance. For instance, gastrin antagonists inhibit cell proliferation of colon carcinoma cell lines. Furthermore the trophic effect of gastrin must be considered when potent gastric acid inhibitors, which cause a reflex increase in gastrin, are used. The outlook is for more mammalian regulatory peptides to be discovered adding further to the complexity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastrointestinal hormones: from basic science to a clinical perspective. 220 81

Chronic diarrhoea occurs in several endocrine gland disorders, largely in gut neuro-endocrine tumours, due to the release of various agents into circulation, which affect gastrointestinal function (Table I). In the strict physiological sense, these agents may be hormones (such as gastrin), paracrine substance (somatostatin), neurotransmitters or neuro modulators (vasoactive intestinal polypeptide; VIP) or unknown agent(s) yet to be identified. For each of these syndromes or diseases (Table I), this review considers the characteristics of diarrhoea, its pathogenesis and the therapeutic aspects. The approach to the diagnosis of these syndromes, including localization of tumour tissue and the selection of appropriate anti-tumor treatment are also outlined.
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PMID:Endocrine diarrhoeas: current concepts. 221 45

A patient with pernicious anemia developed severe intractable diarrhea night and day. Investigation revealed chronic atrophic gastritis and a markedly elevated level of serum gastrin. No obvious explantation for the diarrhea was found, but after antrectomy, the gastrin level returned to normal and the diarrhea subsided. Possible mechanisms for an association between diarrhea and hypergastrinemia include colonic hypermotility secondary to release of acetylcholine and inhibition of fluid and electrolyte reabsorption within the small bowel.
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PMID:Hypergastrinemia, gastric endocrine cell hyperplasia, and intractable diarrhea. 226 46

7 gastrinomes and 1 gastrin-producer complex carcinoma-carcinoid tumor were examined by light and electron microscopical-method and by immunohistochemical method. In six cases, the tumor was in the pancreas or in the wall of duodenum; in two cases its localisation was of extra-gastroenteropancreatic (liver, lymph node). All patients developed Zollinger-Ellison syndrome, three patients bled and one had diarrhea. One patient had other tumors, besides gastrinome, which were characteristic of MEN-I syndrome. By immunohistochemical methods all tumors proved to be gastrin and neuron-specific-enolase positive. In four cases somatostatin positivity, in some cases glucagon, pancreatic polypeptide, S-100 protein, keratin and carcinoembryonal antigen positivity were detected. Relation could not be detected between other polypeptide hormones, produced besides gastrin, and biological behaviour of tumor and clinical symptoms.
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PMID:[Gastrinoma and carcinoma-carcinoid tumor causing Zollinger-Ellison syndrome]. 238 29

There have been new developments in the diagnosis and therapy of Zollinger-Ellison syndrome. The main symptoms of the syndrome are ulcers at atypical sites and nocturnal hypersecretion. Diarrhea and steathorrhea are equally common and may be misinterpreted. Diagnosis is established by the paradoxical rise in plasma gastrin after intravenous secretin provocation. Fasting plasma gastrin levels alone may be misleading and suffer from both false positive and false negative results. Previously, total gastrectomy was necessary to prevent complications. Today the symptoms can be controlled by adequate H2-receptor blocker treatment, if necessary combined with an antimuscarinic drug such as pirenzepine. Exploratory surgical attempts to remove the tumor have a success rate of only 20% and only half of those may be cured. However, the new technique of transhepatic pancreatic vein catheterization, supplemented by determination of local hormone gradients, allows preoperative localization of even small tumors. In the last two years the author has had experience of 5 patients with endocrine tumors of the pancreas (1 insulinoma, 4 gastrinoma) who underwent this procedure. In every case the tumor was localized, removed by surgery and the patients subsequently cured of the syndrome, even including 2 patients with multiple endocrine neoplasia (MEN 1). It is concluded that this chance of cure should be offered to every patient with this syndrome.
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PMID:[Diagnosis and curative therapy in Zollinger-Ellison syndrome]. 240 28

A somatostatin analog (SMS 201-995) was used to treat symptomatic patients with a residual tumor burden of gastrinoma or medullary thyroid carcinoma and pathologic elevations of circulating marker peptides associated with these neuroendocrine tumors. Possible inhibitory effects of the analog on marker peptides, patients' symptoms, or tumor progression were studied in a dose-response protocol and during several months of self-injection of SMS 201-995. Both patients reported remarkable relief of secretory diarrhea and other symptoms, and serum gastrin was successfully suppressed by increasing doses of the analog. However, no effect was seen in reduction of hypercalcitoninemia. Morphologic imaging of residual tumor showed no progression of medullary thyroid carcinoma during treatment and, in the case of hepatic gastrinoma metastases, remarkable tumor regression was confirmed. No toxicity or glucose intolerance was experienced. Somatostatin analog shows promise for palliative management of endocrinologic symptoms due to neuroendocrine tumors, and an inhibitory effect can be measured in some but not all peptide markers. Further evidence of its negative trophic effect on tumor blood flow may suggest an antineoplastic potential, as well as palliative use of this new treatment.
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PMID:Somatostatin analog: effects on hypergastrinemia and hypercalcitoninemia. 243 92

Nine patients with pancreatic apudomas (seven gastrinomas, one glucagonoma, one tumor secreting a substance P-like component) and nine with metastasized carcinoid tumors were treated with a somatostatin analogue (SMS 201-995), administered subcutaneously twice daily for 3 days. Treatment was pursued for 2 to 12 months in nine patients in whom SMS was clinically and/or biologically beneficial. In gastrinomas, SMS decreased plasma gastrin in all but one patient, inhibited the residual gastric acid secretion under H2-blockers and improved diarrhea; in the glucagonoma patient, glucagonemia decreased and skin lesions disappeared. In carcinoid syndrome, clinical efficacy was partial and inconstant; daily 5-hydroxyindole acetic acid (5-HIAA) output was slightly decreased. Plasma substance P levels decreased in six patients with initially high concentrations. No antitumoral activity or side effects have been so far evidenced. SMS 201-995 is a useful, well-tolerated agent in secreting pancreatic apudomas and to a lesser extent in carcinoid syndrome, where high-dosage regimens may be required.
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PMID:Clinical and hormonal effects of a long-acting somatostatin analogue in pancreatic endocrine tumors and in carcinoid syndrome. 243 3

Endocrine pancreatic tumors are slowly growing neuroendocrine neoplasms with a malignant potential which may cause symptoms such as hypoglycemia, multiple ulcers, diarrhea, flush, hyperglycemia and skin rash. A prospective study was performed on 84 patients with endocrine pancreatic tumors. In 59 patients (70%) the tumors were malignant. Of the 84 patients, 23 had insulinomas, 25 gastrinomas, 20 nonfunctioning tumors, 14 the WDHA syndrome, 1 somatostatinoma and 1 glucagonoma. The median age at diagnosis was 53 years and the median delay from first symptom to diagnosis was 2 years. The most common site of the pancreatic primary tumor was the tail (41%), and metastases were most frequently located in the liver (60%) and lymph nodes (44%). Plasma chromogranin A + B was elevated in 94%, serum pancreatic polypeptide (PP) in 74%, plasma neurotensin in 67% and serum gastrin in 62%. Serum HCG-alpha and -beta subunits were elevated in 41 and 30% respectively, all except 3 having a verified malignant tumor. The median survival from first symptom and diagnosis was 14.2 and 8.7 years respectively. Patients with MEN-1 had a significantly better survival from diagnosis than sporadic cases (median 15.1 versus 5.8 years). Patients who received interferon after failing chemotherapy had a significantly better survival than those given chemotherapy alone (5-year survival 65 and 50% respectively).
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PMID:Neuroendocrine pancreatic tumors. Clinical findings in a prospective study of 84 patients. 247 25

The clinical, microscopic, immunohistochemical and ultrastructural features of 7 gastrinomas and 1 combined carcinoma-carcinoid tumor were evaluated. The tumors were located in the pancreas or duodenal wall in 6 cases, and on extragastro-enteropancreatic sites in 2 (liver or peripancreatic lymph node). All patients had the Zollinger-Ellison syndrome, 3 of them with additional bleeding and 1 with diarrhea. One patient with gastrinoma had additional tumors characteristic of the MEN-I syndrome. Immunohistochemistry showed gastrin and neuron-specific enolase-positivity in all of the tumors. Somatostatin was found in 4 cases, and single cell glucagon, pancreatic polypeptide. S-100 protein, keratin as well as carcino-embryonic antigen positivity in another few. Additional hormone production did not appear to be connected with biological behaviour of the tumors or with the clinical symptoms.
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PMID:Studies into gastrinomas and combined carcinomatous carcinoid tumors. Optical light- and electron microscopy and immunohistochemistry. 248 34

Enprostil, a synthetic PGE2, has been shown to have an inhibitory effect on gastric acid secretion, a mucoprotective effect and a postprandial lowering effect on gastrin. A double blind randomized study was performed in 80 patients, in order to evaluate the efficacy and safety enprostil (35 mu b.i.d) as compared to cimetidine (400 mg b.i.d) in duodenal ulcer. Healing rates after two, four and six weeks of treatment, as based on endoscopic evaluation, were 35, 72 and 83 p. 100 for enprostil and 45, 73 and 83 p. 100 for cimetidine, respectively. There were no significant differences between treatment groups. The time to relief of nighttime and daytime ulcer pain and antacid consumption were similar in the two groups. The patient's overall subjective assessment was better in the cimetidine group, but this was not confirmed by physicians' opinions. Diarrhea was observed in 7 p. 100 of patients treated by enprostil compared with 5 p. 100 for patients treated by cimetidine. One enprostil treated patient withdrew from the trial prematurely because of abdominal pain. This study demonstrates the efficacy and safety of enprostil in the treatment of active duodenal ulcer at the dosage of 35 micrograms twice daily.
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PMID:[Efficacy and tolerability of enprostil in the treatment of duodenal ulcer. Comparison with cimetidine]. 249


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