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 alcoholic man presented with bloody ascites, which was confirmed as pancreatic ascites complicating chronic pancreatitis. Endoscopic retrograde pancreatography [ERP] demonstrated a ductal disruption at the head of the pancreas, a fistulous tract, and extravasation to the peritoneal cavity. Furthermore, a computerized tomographic scan subsequent to the endoscopic retrograde pancreatography (ERP-CT scan) gave the three-dimensional anatomy of the fistulous tract by the residual contrast media in the pancreatic duct and the fistulous tract. The pancreatic ascites, which was refractory to conventional medical treatment of a 5-wk duration, was successfully treated by endoscopic placement of a pancreatic stent and administration of a somatostatin analogue.
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PMID:Three-dimensional demonstration and endoscopic treatment of pancreaticoperitoneal fistula. 780 31

From the present review it appears that insulin-dependent diabetes is a common finding in chronic pancreatitis, and impaired secretion of insulin from beta-cells of the pancreatic islets is essential for the development of this form of secondary diabetes. Judged from a positive correlation between insulin secretory capacity and stimulated pancreatic enzyme output, beta-cell function may decrease in parallel with exocrine pancreatic function. However, in patients with insulin-dependent diabetes secondary to chronic pancreatitis beta-cell function was preserved to a greater extent and glucoregulation was better than in comparable Type 1 (insulin-dependent) diabetic patients. Immunological phenomena and associations with certain HLA-alleles characterizing Type 1 diabetes mellitus were not found in insulin-dependent diabetes secondary to chronic pancreatitis. This may contribute to the slower destruction of the beta-cells in chronic pancreatitis than encountered in Type 1 diabetes. The small number of chronic pancreatitis patients who developed totally absence of endogenous insulin production still have some alpha-cell function during i.v. arginine and meal stimulation. However, insulin-induced hypoglycemia and insulin withdrawal did not stimulate glucagon secretion in the secondary diabetic patients in contrast to comparable Type 1 diabetics. Nevertheless, blood glucose counterregulation is intact in the secondary diabetics due to preserved catecholamine secretion. Furthermore, ketonemia develops during dissipation of insulin, in spite of absence of increased glucagon secretion, emphasizing the role of insulin dissipation for the development of ketoacidosis in this form of diabetes. The suggested increased susceptibility to severe hypoglycemia and less tendency to development of ketonemia may further be influenced by altered insulin sensitivity, nutritional factors and concomitant hepatic failure in diabetes secondary to chronic pancreatitis. Pancreatic polypeptide secretion was absent in chronic pancreatitis without endogenous insulin production. Pancreatic polypeptide secreting cells thus seem to be at least as vulnerable as the beta-cells to the destructive processes characterizing chronic pancreatitis, whereas glucagon secreting alpha-cells preserve secretory capacity to a greater extent than PP-cells and beta-cells. No data, however, favour the view that absent pancreatic polypeptide secretion has any major effect on the glucoregulation in diabetes secondary to chronic pancreatitis. Increased plasma concentration of somatostatin was found in patients with insulin-dependent diabetes secondary to chronic pancreatitis. The source of somatostatin in the patients is unknown, but somatostatin may contribute to a reduction in overall blood glucose level in patients without endogenous insulin secretion due to inhibition of glucagon secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diabetes mellitus secondary to chronic pancreatitis. 849 94

Chronic pancreatitis is characterized by the presence of an inflammatory infiltrate, progressive destruction of acinar cells, and fibrosis. The finding that endothelin-1, an endothelium-derived peptide with vasoconstrictive and mitogenic properties, reduces pancreatic blood flow in normal rats suggested that the peptide may be associated with the reduced pancreatic flow seen in animal models of chronic pancreatitis and in the morphological abnormalities of the disease. The aim of this study was to investigate sites of endothelin-1 expression in the pancreas of normal subjects and patients with chronic pancreatitis. The techniques of immunohistochemistry, in situ hybridization, and Northern blotting were used. Endothelin-1-like immunoreactivity was localized predominantly to islet cells both in normal subjects and in patients with chronic pancreatitis. Semi-quantitative analyses of immunostaining showed that endothelin-1-like immunoreactivity in islet cells of patients with chronic pancreatitis was greater than in normal subjects. Co-localization studies with glucagon, insulin, somatostatin, and pancreatic polypeptide showed that endothelin-1-like immunoreactivity co-exists with glucagon and insulin. There was no apparent co-existence of endothelin-1-like immunoreactivity with somatostatin or pancreatic polypeptide. Endothelin-1 mRNA was expressed in sites similar to those of the immunostaining, as well as in vascular endothelial cells. Northern blot analysis showed an increase in the expression of endothelin-1 mRNA in the patient population. There was a significant correlation between intensity of endothelin-1 immunostaining and severity of fibrosis in the patients with chronic pancreatitis. These findings suggest that an elevation in local expression of endothelin-1 may be associated with the morphological and haemodynamic changes of chronic pancreatitis.
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PMID:Expression of endothelin-1 in pancreatic tissue of patients with chronic pancreatitis. 877 21

Major pancreatic resection is still accompanied by considerable morbidity (35%) and mortality (10%). Typical complications, such as pancreatic fistula and abscess, are chiefly associated with exocrine pancreatic secretion. The hormone somatostatin and its analogue octreotide are well known as potent inhibitors of exocrine pancreatic secretion. In two randomised, double-blind, placebo-controlled, multicentre trials we assessed the prophylactic effect of the perioperative inhibition of exocrine pancreatic secretion by octreotide to prevent postoperative complications. Each patient received 3 X 100 micrograms/day octreotide or placebo subcutaneously. A significant reduction in fistula, abscess, fluid collection, sepsis and postoperative pancreatitis occurred with patients undergoing pancreatic resection for cancer. Results were similar in a second study, using the same protocol but recruiting only patients with chronic pancreatitis. A new randomised, controlled multicentre trial is also described, in which 300 patients with severe acute pancreatitis are being treated with or without octreotide in double-blind fashion. The results will clarify the influence of inhibition of exocrine pancreatic secretion by octreotide on the course of acute pancreatitis, and hence its potential, through inhibition of digestive enzyme secretion, as a treatment for acute pancreatitis.
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PMID:Efficacy of somatostatin and its analogues in pancreatic surgery and pancreatic disorders. 881 84

The aims of medical therapy in chronic pancreatitis are mainly to relieve the recurrent pain and to correct any malabsorption secondary to digestive insufficiency resulting from deficient exocrine pancreatic function. The treatment of the pain initially involves the use of dietary measures and analgesic drugs. The results of the use of pancreatic extracts and somatostatin reported in the literature are controversial, as are those of coeliac plexus block. Of unquestionable efficacy, at least in the short to medium term, are surgical decompression interventions in patients, with pain refractory to these measures and who present significant dilation of Wirsung's duct at ERCP. Endoscopic decompression constitutes an alternative to surgical decompression. In view of the transitory results of endoscopic decompression, which, in any event, should be implemented only by endoscopists possessing the necessary experience and expertise, the use of this technique may perhaps be targeted at carefully selected patients to be submitted to surgical decompression. As far as maldigestion is concerned, which occurs only when the pancreatic functional deficit reaches 90% or more, replacement therapy with pancreatic extracts must be resorted to. Multi-Unit Dose preparations are to be preferred, consisting in gastro-protected microspheres measuring not more than 2 mm in diameter and containing high doses of lipase, since at least 30,000 I.U. of lipase are required in the post-prandial phase for reasonably satisfactory correction of the steatorrhoea. Should this fail to prove effective, it is good policy to add antisecretory drugs (H2-antagonists, proton-pump inhibitors).
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PMID:[The medical therapy of chronic pancreatitis. Problems, progress and outlook]. 902 57

Under physiological conditions, the pancreas scarcely influences the function of the cardiovascular system, although the hormones produced in the healthy pancreas (insulin, glucagon and somatostatin) affect the myocardial contractility in pharmacological doses. Among the diseases of the pancreas, the pancreatic tumours (insulinoma, glucagonoma and vipoma), furthermore the acute and chronic pancreatitis involve cardiovascular complications, which influence the outcome of the disease. Although the clinical picture is dominated by the metabolic changes of the excessively produced hormones in pancreatic tumours, the cardiac and vascular effects of the hormones may be considerable. In acute necrotizing pancreatitis, enzymes released from the pancreas and inflammatory mediators transform acute necrotizing pancreatitis into "multiple organ disease"; one of the important forms of this disease is the cardiovascular shock syndrome. One of the best-known complications of chronic pancreatitis is the pancreoprive diabetes mellitus, and beside that other, nonspecific cardiac alterations (e.g. ECG-changes) may occur.
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PMID:[Cardiovascular complications of pancreatis diseases]. 928 88

The efficacy of medications to treat pancreatic diseases, even when proven effective by experimental studies, are difficult to prove by controlled clinical trials. In the treatment of acute pancreatitis, prophylactic antibiotics, somatostatin, protease inhibitors, and cholecystokinin (CCK)-receptor antagonists are advocated for use in the early stages of acute pancreatitis, but the data are insufficient to mandate prophylaxis use or recommend their use as a standard of care. In the treatment of chronic pancreatitis, digestive enzymes, oral active protease inhibitors, CCK-receptor antagonists, or somatostatin are administered for pain relief. Extracorporeal shock-wave lithotripsy and oral dissolution therapy with trimethadione are used to treat pancreatic stones. The goals of treatment of acute pancreatitis should be to ameliorate the severity of pancreatic inflammation or to prevent its complications. Although several treatments seem to be promising from the studies reviewed, these medications require prospective comparison with the standard procedures and long-term evaluation.
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PMID:Pharmaceutical development for treating pancreatic diseases. 954 90

A series of 34 patients with pancreatic resections was evaluated with respect to the occurrence of local and general complications. Two groups were compared, depending on whether or not treatment with somatostatin was instituted. Postoperative morbidity and mortality were less frequent when somatostatin was given (resp. 50.0 and 5.5%) than when it was omitted (resp. 68.7 and 31.2%). Less complications were observed after resections performed for chronic pancreatitis than for pancreatic cancer in the non somatostatin-treated group. It is concluded that somatostatin treatment may be beneficial in preventing complications after elective pancreatic surgery.
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PMID:The influence of somatostatin on postoperative outcome after elective pancreatic surgery. 961 59

The aims of this study were (1) to assess possible variations in the serum levels of epidermal growth factor (EGF), insulin-like growth factor I (IGF I) and somatostatin in patients with pancreatic cancer as compared to other pancreatic or extrapancreatic diseases and (2) to ascertain the role of these substances in tumour growth and spread. 35 patients with pancreatic cancer were compared to 15 patients with chronic pancreatitis, 15 with benign hepatobiliary diseases, 23 with benign or malignant gastro-intestinal diseases and 22 control subjects. Increased EGF and IGF I serum levels were found in 10% of patients with pancreatic cancer. Somatostatin levels were increased in 8/16 (50%) patients with pancreatic cancer. No correlation was found between EGF, IGF I or somatostatin and tumour size or stage. In pancreatic cancer somatostatin serum levels were correlated with total bilirubin (p < 0.04), while EGF and IGF I were inversely correlated with fasting serum glucose levels (p < 0.05). In conclusion, (1) the serum levels of EGF, IGF I and somatostatin were not related to tumour size and clinical stage of pancreatic cancer, (2) the serum levels EGF and IGF I may be related to altered glucose metabolism, and (3) liver impairment can influence somatostatin serum levels.
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PMID:Serum growth factors in patients with pancreatic cancer. 1005 Jan 5

Acute pancreatitis may follow a mild or a severe course. Whereas mild or edematous pancreatitis is a self-limiting disease with a low complication rate and low death rate, morbidity and mortality in severe or necrotizing pancreatitis are still unacceptably high. The major problem is the lack of a specific drug, especially in the early phase of the disease, to interfere with the systemic inflammatory response syndrome and to limit or prevent complications of the disease. Although the initiating pathophysiological process is not known, the destruction of the gland ('autodigestion') by digestive enzymes may be responsible for disease progression. Inhibition of pancreatic activity, which reduces exocrine secretion and further prevents the release and activation of enzymes, was therefore suggested as a specific treatment concept. The results of clinical investigations using somatostatin or its analogue are controversial, since all these trials had low statistical power. In a recent multicenter randomized controlled study with a large number of patients (n = 302) (and an adequate level of disease severity), no benefit of octreotide on progression or outcome was found. Chronic pancreatitis is characterized by an irreversible destruction of the exocrine and endocrine pancreatic parenchyma leading to maldigestion and diabetes. Pain, which may be caused by increased ductal pressure, is one of the most dominant symptoms in chronic pancreatitis. However, no beneficial effects on pain with pancreatic exocrine secretion-inhibiting drugs have been demonstrated. Treatment of other complications of the disease (pseudocyst formation, fistula and pancreatic ascites), with somatostatin or octreotide has given conflicting results. However, in a prophylactic clinical setting (e.g. elective pancreatic surgery) the inhibition of exocrine pancreatic secretion reduces complications.
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PMID:The role of octreotide and somatostatin in acute and chronic pancreatitis. 1020 28


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