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)

An elderly man, not previously known to have chronic pancreatitis, presented with haematemesis and melaena which was endoscopically diagnosed as haemobilia. Retrograde cholangiopancreatography showed blood clot in both the common bile duct and the pancreatic duct and the computed tomographic scan appearances were those of gross calcific chronic pancreatitis. Despite active bleeding, it was not possible to demonstrate its source at angiography, thus precluding therapeutic embolization. Thirty six hours after commencing an infusion of somatostatin, repeat endoscopy showed no evidence of active or recent bleeding. The infusion was continued for 5 days during which time he had no further bleeding.
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PMID:Use of somatostatin in the management of pancreatic haemobilia. 257 52

The most common complication of chronic pancreatitis is pain, which in many cases seems related to pancreatic ductal obstruction with ductal hypertension. Longitudinal pancreaticojejunostomy is indicated in patients with a dilated (larger than 7 mm) duct and pain that requires narcotic analgesics for relief. Chronic pseudocysts may be corrected surgically without the usual 6-week wait, and asymptomatic pseudocysts less than 4 cm in diameter may not require surgery at all. The relative efficacy and risks of percutaneous drainage of pseudocysts versus the standard surgical approaches need to be studied. Pancreatic fistulas may be external or internal, where pancreatic ascites or hydrothorax can be the clinical manifestation. The pharmacologic suppression of pancreatic secretion (e.g., with somatostatin) may be useful in their management, but surgery may be required. Pancreatic resection or internal drainage is usually effective. Persistent jaundice should be relieved surgically by choledochoduodenostomy to avoid the development of secondary biliary cirrhosis. Obstruction at various levels of the gastrointestinal tract (duodenum, small bowel, colon) may require bypass (gastrojejunostomy) or resection. Hemorrhage from major arteries is an infrequent but often lethal complication of chronic pancreatitis, especially associated with pseudocysts. Angiography is invaluable for diagnosis and occasionally for treatment (embolization). Surgery is preferred in good-risk patients, with suture ligation (resection) of the bleeding source. Chronic pancreatitis is the most common cause of splenic vein thrombosis. The resultant hemorrhage from gastric varices is managed effectively by splenectomy.
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PMID:Complications of chronic pancreatitis. 265 60

The present study was designed to examine and compare the peptide composition and relative immunochemical purity of GIH and Boots secretin preparations. Gastrointestinal peptides were measured by radioimmunoassay using antibodies to secretin, gastrin, immunoreactive cholecystokinin, vasoactive intestinal peptide, gastric inhibitory peptide, and somatostatin. Boots secretin was found to contain substantial quantities of gastrin, immunoreactive cholecystokinin, vasoactive intestinal peptide, gastric inhibitory peptide, and somatostatin. In contrast, GIH secretin contained only a very small amount of vasoactive intestinal peptide. GIH also contained approximately three to four times more secretin per unit as did Boots secretin. Intravenous infusion of Boots, but not GIH, secretin in seven healthy volunteers produced significant increases in venous plasma of all peptides. Results of these studies indicate that Boots secretin contains large and variable quantities of gastrointestinal peptides other than secretin and that the contents of both secretin and the other peptides vary among different lots. Because the quantity of these peptides is sufficient to increase significantly their blood levels and consequent biological effects, it is concluded that GIH is preferable to Boots secretin in the clinical evaluation of patients with suspected chronic pancreatitis or gastrinoma.
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PMID:Peptide characterization of secretin preparations. 286 51

Five pancreatic cutaneous fistulas were treated by subcutaneous administration of a long-acting synthetic analog of somatostatin, SMS 201-995. Patients included four men and one woman who ranged in age from 52 to 77 years. The fistulas developed after drainage of a pancreatic abscess, biopsy of a pancreatic mass, splenectomies for idiopathic thrombocytopenic purpura and Felty's syndrome, and operative trauma, respectively. Fistula output consisted of 1,000 ml/day of amylase- and lipase-rich fluid in the patient with a pancreatic biopsy. The other four patients had low-output fistulas (100 to 250 ml/day) that had been draining for 1 to 12 months. Direct communication with the pancreatic duct was demonstrated by endoscopic retrograde cholangiopancreatography, sinography, or both in four of the five patients. Fistula output decreased from 340 +/- 376 ml/day to 63 +/- 36 ml/day on the first day of therapy with two daily doses of 0.05 mg SMS 201-995 (p less than 0.03) and to 13 +/- 19 ml/day on the seventh day of therapy (p less than 0.03). Two patients had prompt closure of their fistulas and one closed in 3 months. One patient with chronic pancreatitis and a duct stricture and one patient with recurring infection did not achieve permanent fistula closure with SMS 201-995. Because of its safety, ease of administration, and efficacy in decreasing fistula output, we believe somatostatin analog therapy is beneficial in hastening closure of pancreatic fistulas.
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PMID:Treatment of pancreatic cutaneous fistulas with a somatostatin analog. 289 56

Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. No significant differences were found between the two diabetic groups regarding glucagon responses to arginine and meal ingestion. In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal. Thus, pancreatic glucagon secretion was preserved in patients with insulin-dependent diabetes secondary to chronic pancreatitis, having no residual beta-cell function. These findings suggest that pancreatic glucagon deficiency is not absolute in insulin-dependent diabetes secondary to chronic pancreatitis. A high level of somatostatin may contribute to a lower blood glucose level in patients with chronic pancreatitis.
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PMID:Pancreatic hormone secretion in chronic pancreatitis without residual beta-cell function. 289 69

Twenty-three patients with recent onset Type 1 (insulin-dependent) diabetes in whom residual insulin secreting B cells were present and 12 patients with disease of more prolonged duration (maximum 9 years), 8 of whom had residual B cells, were studied. Aberrant expression of Class II major histocompatibility complex molecules was demonstrated immunohistochemically on insulin secreting B cells in 21 out of 23 patients with recent onset disease and 6 of the patients with more prolonged disease. No such expression was seen on glucagon secreting A cells or somatostatin secreting D cells. Islets where there was marked hyperexpression of Class I major histocompatibility complex molecules on islet endocrine cells were seen in all cases in which residual B cells were present. Ninety-two per cent of insulin containing islets but only 1% of insulin deficient islets exhibited this phenomenon (p less than 0.001, Chi-squared test). There was evidence to suggest that both these abnormalities of major histocompatibility complex expression preceded insulitis within a given islet. They also appeared to be unique to Type 1 diabetes, being absent in pancreases of patients with Type 2 (non-insulin-dependent) diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to B cells in Type 1 diabetes may be a "multistep" process in which abnormalities of major histocompatibility complex expression on islet endocrine cells are crucial events.
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PMID:Aberrant expression of class II major histocompatibility complex molecules by B cells and hyperexpression of class I major histocompatibility complex molecules by insulin containing islets in type 1 (insulin-dependent) diabetes mellitus. 330 84

Ten patients who had been totally duodeno-pancreatectomized and totally (N = 1) or partially gastrectomized (N = 9) for chronic pancreatitis (N = 9) or pancreatic carcinoma (N = 1) were investigated. None had a measurable basal level of either plasma C-peptide or a C-peptide response to i.v. glucagon. Immunoreactive glucagon (IRG) was present in all patients, and the mean level (69 +/- 8 pg/ml) was not significantly different from the mean observed in normal subjects (81 +/- 16 pg/ml). Plasma IRG was unequivocally stimulated by arginine in 2 of the 10 subjects. The effect of somatostatin on plasma glucose and IRG during an oral glucose tolerance test was studied in 5 of the 10 patients. The effects of somatostatin on spontaneous hyperglycemia, plasma growth hormone, and IRG after withdrawal of insulin treatment was studied in 4 patients. Somatostatin blunted both the hyperglycemic and paradoxical IRG responses to the glucose challenge, and reduced the spontaneous rise of blood glucose that occurred after insulin withdrawal. This latter effect was not related to clear-cut changes in plasma growth hormone or in IRG. These data confirm the existence of circulating IRG in pancreatectomized patients and demonstrate the presence of circulating IRG in a completely gastrectomized and pancreatectomized patient. The somatostatin-induced improvement in glucose tolerance in the oral glucose tolerance test seems to be related to a reduction of the paradoxical IRG response. In contrast, the inhibition by somatostatin of the rise in blood glucose which occurs after insulin withdrawal does not seem to be mediated through IRG or growth hormone.
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PMID:Glucagon immunoreactivity and antidiabetic action of somatostatin in the totally duodeno-pancreatectomized and gastrectomized human. 611 86

Plasma immunoreactive glucagon, C-peptide and substrates (glucose, lactate, and alanine) were measured in 21 pancreatectomized patients and 28 patients with chronic calcifying pancreatitis during arginine infusion. Results were compared with those obtained in control and in insulin-dependent diabetic subjects, and in pancreatectomized subjects receiving a combined infusion of glucagon and arginine or somatostatin and arginine. Plasma immunoreactive glucagon in the pancreatectomized patients was 230 +/- 26 pg/ml (control subjects 100 +/- 13 pg/ml, p less than 0.001), but was unchanged following arginine or somatostatin. Following ethanol extraction of plasma it became undetectable. Similar results were obtained in patients with chronic pancreatitis. In contrast to the insulin-dependent diabetic subjects, no changes in blood glucose, lactate, and alanine concentrations were found during arginine infusion in the pancreatectomized or pancreatitis patients. Addition of glucagon restored the metabolic response to arginine in the pancreatectomized patients. Our results confirm previous smaller studies that in pancreatectomized patients, A cell function is absent or insignificant.
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PMID:Absence of islet alpha cell function in pancreatectomized patients. 612 Aug 75

The injection of neoprene into the pancreatic ducts of dogs has been used to destroy exocrine function prior to pancreatic transplantation. The subsequent histological changes and the evolution of lesions over a period of 3-36 months are described. Animals were sacrificed or biopsied at various intervals (3, 15 and 36 months) and the pancreases showed the disappearance of exocrine acini and changes of chronic pancreatitis. An immunoperoxidase procedure with insulin, glucagon, somatostatin and pancreatic polypeptide antisera was used to show the persistence of pancreatic endocrine cells. After the injections, sclerosis progressively increased and secondary lesions of the islets were seen, although functional islets persisted. This technique was then applied to pancreas transplantation in man. Eight transplants from seven diabetic patients were available for examination. In four cases, there were early technical failures, but four pancreatic transplants continued to function for 28-889 days until suppuration destroyed one of the grafts and the three other patients died. The persistence of endocrine cells in sclerotic tissue was observed in histological and immunopathological examinations.
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PMID:Pathology of the pancreas after intraductal neoprene injection in dogs and diabetic patients treated by pancreatic transplantation. 635 16

The present investigation defined the pattern of pancreatic, pituitary and adrenal responses after insulin-induced hypoglycemia in chronic calcific pancreatitis (CCP) related to alcohol abuse, and assessed the role of some of these hormones in the counterregulation of blood glucose. We studied 6 Black men with recently diagnosed CCP, all showing radiological evidence of pancreatic calcification and normal glucose tolerance, as well as 7 matched nonobese male controls. After a standard iv insulin tolerance test inducing marked hypoglycemia, patients with CCP showed significantly impaired mean plasma pancreatic glucagon and pancreatic polypeptide responses compared to the controls. Mean basal plasma somatostatin levels tended to be higher in chronic pancreatitis and remained so throughout the test without altering consistently; in the controls somatostatin peaked significantly at 30 min. Concerning extrapancreatic hormonal changes, plasma growth hormone, prolactin and total catecholamines responded normally in CCP, but plasma cortisol rose to significantly higher levels than controls at 60 and 120 min after the injection of insulin. This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. We conclude that patients with CCP show impaired pancreatic hormone release after insulin hypoglycemia with the exception of somatostatin; there is also an excessive rise in plasma cortisol, possibly related to the long standing abuse of alcohol in the past.
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PMID:Hormonal profile after insulin-induced hypoglycemia in chronic calcific pancreatitis. Pancreatic, pituitary and adrenal responses. 639 52


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