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)

SMS 201-995 (Sandostatin) was studied using low doses (50 to 100 micrograms) administered subcutaneously every 12 hours. A single 50-micrograms dose of SMS 201-995 effectively controlled gastric acid and blood gastrin levels for 12 hours in three patients with benign gastrinomas and was useful in their perioperative management. Higher doses of the agent (500 to 800 micrograms per day) had no effect on metastases in one of two patients with metastatic gastrinoma. In the other patient, one tumor shrank but the other continued to grow after three months of treatment while serum gastrin levels did not change. Cultured metastatic tumor tissue from this patient released different forms of gastrin; growth rates varied, independent of uptake of SMS 201-995, and gastrin release increased. A neonate with nesidioblastosis maintained normal blood glucose levels while receiving SMS 201-995 therapy following a 95 percent pancreatic resection. In two elderly patients with organic hypoglycemia--one with a single benign adenoma and one with multiple adenomatosis--the somatostatin analogue did not prolong the hypoglycemia-free interval. In nine patients with carcinoid syndrome, flushing was uniformly controlled with 50 micrograms of SMS 201-995 administered every eight to 12 hours. One of the nine required exocrine pancreatic replacement. After six months of treatment, three of the nine had no change in tumor size and one had remission of symptoms and stopped treatment. In two patients with vipoma, SMS 201-995 controlled diarrhea and reduced levels of vasoactive intestinal peptide; tumor necrosis occurred in one patient. In a patient with diabetic diarrhea unresponsive to all treatments, SMS 201-995 therapy controlled the diarrhea but did not interfere with control of the diabetes.
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PMID:Somatostatin analogue (SMS 201-995) in the management of gastroenteropancreatic tumors and diarrhea syndromes. 287 47

Long-acting somatostatin analogues such as SMS 201-995 (Sandoz) are being evaluated in a wide range of clinical indications, including gut neuroendocrine tumours and acrogemaly. Long-term continuous SMS 201-995 treatment has achieved useful symptomatic improvement in diarrhoea in 4 patients with metastatic VIPomas who had relapsed following previous treatment. Clinical improvement has outlasted suppression of VIP secretion (suggesting an additional direct antisecretory action of SMS 201-995) and has occurred despite expansion of hepatic metastases. In 6 patients with tumours secreting gastrin and/or glucagon, secretion of these peptides was acutely inhibited by SMS 201-995. However, endocrine and clinical responses to chronic treatment have been less consistent. SMS 201-995 is active orally at doses of 4-8 mg and when given thrice-daily to 6 patients with active acromegaly, suppressed mean 24-h growth hormone levels by 51-88%. Despite significantly reduced plasma insulin concentrations, glucose tolerance did not deteriorate. SMS 201-995 was also effective in suppressing thyroid-stimulating hormone (TSH) and thyroid hormone secretion in a patient with mild thyrotoxicosis due to non-tumoural inappropriate TSH hypersecretion. In all cases SMS 201-995 treatment has been well tolerated and has few side-effects.
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PMID:Clinical evaluation of SMS 201-995. Long-term treatment in gut neuroendocrine tumours, efficacy of oral administration, and possible use in non-tumoural inappropriate TSH hypersecretion. 289 35

The case history of a patient with an islet cell carcinoma, which produced both gastrin and vasoactive intestinal polypeptide (VIP), is presented. Although several examples have been observed of the combined production of these hormones by pancreatic endocrine tumors, few reports have related the clinical details of such cases. Resolution of diarrhea occurred in our patient after institution of nasogastric suction and cimetidine therapy, suggesting that gastric hypersecretion, rather than VIP activity, accounted for this problem. Chemotherapy with streptozotocin and 5-fluorouracil was highly effective in ameliorating clinical symptoms, diminishing serum levels of gastrin and VIP, and greatly reducing the bulk of metastatic disease in this case.
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PMID:Pancreatic islet cell carcinoma with gastrin and vasoactive intestinal polypeptide production. 299 97

A case of a 58-year-old woman with an unusual variant of malignant islet-cell tumor showing oncocytic features is described. Using the light microscopy technique, the tumor appeared comprised of solid nests of uniform cells with abundant, eosinophilic cytoplasm and round nuclei with granular chromatin. Ultrastructurally, the cells contained numerous abnormal mitochondria, dilated rough endoplasmic reticulum, and scattered dense-core neurosecretory granules, often associated with cytoplasmic filaments. Tumor cells were focally immunoreactive for insulin, glucagon, and somatostatin and diffusely immunoreactive for alpha 1-antitrypsin as assayed by the avidin--biotin technique. The tumor was immunonegative for human chorionic gonadotropin, gastrin, adrenocorticotropic hormone, and serotonin. The patient exhibited some of the clinical features associated with glucagonoma syndrome, including diabetes mellitus and chronic diarrhea. The tumor behaved in a malignant fashion, with widespread lymphatic involvement and bony metastases at the time of presentation. This report of an oncocytic islet-cell carcinoma supports the concept of oncocytic differentiation in islet-cell tumors in a fashion analagous to oncocytic carcinoids.
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PMID:Functioning oncocytic islet-cell carcinoma. Report of a case with electron-microscopic and immunohistochemical confirmation. 300 44

A 44-year-old woman with hepatocellular carcinoma presented with intractable watery diarrhea and her condition was evaluated angiographically. Surgical ablation of the tumor resulted in complete resolution of the diarrhea. The tumor cells of the hepatocellular carcinoma were found to contain vasoactive intestinal polypeptide, gastrin, and prostaglandinlike immunoactivity. To our knowledge, this is the first report of such an association.
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PMID:Hepatocellular carcinoma presenting with intractable diarrhea. A radiologic-pathologic correlation. 301 24

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85

Enprostil is a synthetic prostaglandin E2 analogue with gastric anti-secretory, cytoprotective, and gastrin lowering properties. The current multi-center, double-blind, placebo-controlled study was undertaken to evaluate the efficacy and safety of enprostil (35 micrograms twice daily) for the treatment of duodenal ulcers. The study enrolled 87 patients between the ages of 18 and 85 with an endoscopically proved duodenal ulcer between 0.5 and 3.0 cm in its longest dimension and with no other serious medical conditions or abnormal laboratory tests results. Treatment groups were comparable in age, sex, smoking status, ulcer history, and baseline ulcer size. The results indicated that the healing rate for enprostil at two weeks was 38 percent, compared with a placebo rate of 23 percent (p = 0.151). At four weeks, 70 percent of the enprostil-treated patients had healed ulcers, compared with 49 percent of the placebo-treated patients, a statistically significant difference (p = 0.048). Although within the enprostil group the healing rate was higher in nonsmokers (86 percent) than in smokers (58 percent), this difference did not reach statistical significance. Side effects included diarrhea (14 percent) and headache (7 percent). These results indicate that 35 micrograms of enprostil twice daily provides effective and safe therapy for patients with duodenal ulcer.
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PMID:Treatment of duodenal ulcer with enprostil, a prostaglandin E2 analogue. 309 58

Hypochlorhydria induced by potent antisecretory drugs is followed by a marked elevation of serum gastrin levels which leads to changes in ECL cell density in rats. "Soft" antiulcer drugs like prostaglandins do not increase gastrin levels. Their use in peptic ulcer disease seems to be mainly limited by a relatively high incidence of diarrhea and abdominal cramps. Rioprostil is a new prostaglandin E1 analogue. We compared the potency and duration of action of rioprosil 600 micrograms nocte with 300 micrograms bid on human gastric secretion in a placebo-controlled double-blind study. We further evaluated the clinical effectiveness of rioprostil 600 micrograms nocte in the acute treatment of duodenal ulcer. Nocturnal gastric acidity (24:00 to 08:00) was inhibited from 54.5 +/- 1.7 mmol H+/L (placebo experiments; n =9) to 26.7 +/- 3.5 mmol H+/L (52%) by rioprostil 300 micrograms bid (p less than 0.05) and to 14.4 +/- 3.8 mmol H+/L (74%) by rioprostil 600 micrograms nocte (p less than 0.05). During the daytime (09:00 to 18:00), H+ activity was reduced by 33% and 15% respectively (n.s.). Two hundred and three patients with endoscopically proven duodenal ulcers were randomly allocated to treatment with either rioprostil 600 micrograms nocte or ranitidine 300 mg nocte for 4 weeks in a prospective double-blind study. The two groups were similar. After 2 and 4 weeks treatment respectively, about 55% and 85% of patients healed on rioprostil 600 micrograms nocte and 55% and 90% on ranitidine 300 mg nocte. There were no differences between the treatment groups in ulcer pain relief.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandins and peptic ulcer disease: nocturnal administration of rioprostil vs ranitidine in duodenal ulcer healing. 310 57

Enprostil, a synthetic analogue of prostaglandin E2, is effective in the treatment of patients with duodenal or gastric ulcers. As demonstrated in pharmacological studies in healthy volunteers and in patients with inactive ulcer disease, gastric acid secretion is suppressed by up to 80% for almost 12 hours after single doses of enprostil. The drug also reduces the secretion of pepsin, another 'aggressive' factor in peptic ulcer disease. Interestingly, in contrast to the H2-receptor antagonists, which either increase or have no effect on serum gastrin concentrations, enprostil inhibits basal and postprandial gastrin release. Although the possible effects of enprostil on 'defensive' factors in peptic ulcer disease-which are thought to protect the mucosa-require much further clarification, some evidence obtained in man indicates that bicarbonate secretion is enhanced by enprostil. Further, data from animal studies suggest that microvascular integrity may be preserved by a direct action of enprostil on the gastric mucosa. In healthy volunteers, the administration of enprostil in antisecretory doses protects the gastric mucosa against of enprostil in antisecretory doses protects the gastric mucosa against aspirin-induced injury. Cumulative rates of ulcer healing observed in patients with duodenal ulcers after 4 weeks' treatment with enprostil 35 micrograms twice daily were about 50 to 80%, which were similar to those seen in comparative trials with usual therapeutic doses of cimetidine or pirenzepine, but less than occurred with ranitidine. Moreover, enprostil has been shown to relieve daytime pain in a similar percentage of patients as do these H2-receptor antagonists, but night-time pain appears to respond less well to therapy with the prostaglandin. As evidenced by a few controlled trials in patients with gastric ulcers, treatment with enprostil 35 micrograms twice daily for 6 weeks provides ulcer healing in parallel with pain relief as effectively as cimetidine and ranitidine in a high percentage of patients (about 80% after 6 weeks). Prophylactic treatment with enprostil after initial ulcer healing has reduced the rate of duodenal ulcer relapse in patients 'at risk', but to a lesser extent than has ranitidine. Gastrointestinal symptoms-abdominal cramping and pain, flatulence, nausea and notably, diarrhoea-are the most frequently reported side effects during therapy with enprostil. Diarrhoea occurs in about 10% of patients, but is rarely of a severity necessitating treatment discontinuation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enprostil. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of peptic ulcer disease. 312 Dec 76

Zollinger-Ellison Syndrome in a 12-year old castrated male European Shorthair cat is described. The clinical symptoms were vomiting, weight loss, listlessness and alternating diarrhoea and obstipation. An endocrine tumour near the pancreatic duct had metastasised to the liver. Many duodenal ulcers were present. Immunohistochemistry revealed cells positive for gastrin and neuron-specific enolase (NSE) scattered throughout the tumour.
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PMID:Zollinger-Ellison syndrome in a cat. 317 93


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