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)

There is still much to learn about the cause of postgastrectomy syndromes. Fortunately, most patients can be managed by conservative measures unless a mechanical cause, amenable to operative correction, is found. Thus, it is important to determine the type of postgastrectomy problem that is affecting the patient. In carefully selected patients, remedial operations may ameliorate the patient's symptoms and permit him or her to return to a normal lifestyle. Humoral factors have attracted increasing attention, especially in patients with the dumping syndrome. The somatostatin analogue octreotide has provided relief from the vasomotor and gastrointestinal symptoms of severe dumping but must be given three to four times a day by injection.
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PMID:Management of postgastrectomy syndromes. 229 3

Octreotide is an analogue of somatostatin. Like endogenous somatostatin, it exerts a potent inhibitory effect on the release of anterior pituitary growth hormone and thyroid-stimulating hormone, and peptides of the gastroenteropancreatic endocrine system, while overcoming some of the shortcomings of exogenously administered somatostatin, namely a short duration of action, a need for intravenous administration and postinfusion rebound hypersecretion of hormone. Clinical studies have shown that octreotide is effective in the treatment of acromegaly and thyrotrophinomas. In comparative trials octreotide was significantly superior to bromocriptine in patients with acromegaly. Octreotide also appears to provide a significant advantage over existing therapies in the management of the carcinoid syndrome and offers considerable therapeutic potential in reversing carcinoid crises which may be life-threatening. Trials in patients with tumours producing vasoactive intestinal peptide demonstrated that octreotide may be an effective first-line choice for this condition, which has usually metastasised and become refractory to traditional symptomatic therapy. In limited studies in patients with high-output secretory diarrhoea, including cryptosporidium-related diarrhoea associated with AIDS and in patients with small bowel fistulas, octreotide has been shown to be effective in reducing stool/fistula output. However, well-designed clinical trials are still required to confirm its long term usefulness in these disorders. Similarly, although the use of octreotide in other conditions such as neonatal hypoglycaemia caused by nesidioblastosis, reactive pancreatitis, insulin-dependent diabetes mellitus, postprandial hypotension and the dumping syndrome has provided encouraging preliminary results, more studies are needed to clarify the place of octreotide in their treatment. Overall, octreotide appears to be well tolerated with the most frequently reported reactions being pain at the site of injection and gastrointestinal symptoms such as abdominal cramps, nausea, bloating, flatulence, diarrhoea and steatorrhoea. These adverse effects usually abate with time. Additionally, octreotide, like endogenous somatostatin, may also result in cholelithiasis, presumably by altering fat absorption and possibly by decreasing motility of the gallbladder. Thus, octreotide represents a new departure from traditional therapies in the treatment of various pathophysiological states associated with excessive peptide production and secretion. It offers a significant advantage over existing therapies in the medical management of patients with acromegaly, thyrotrophinomas, the carcinoid syndrome, tumours producing vasoactive intestinal peptide and severe secretory diarrhoea in whom conventional management options have either become exhausted or have provided suboptimal symptomatic relief.
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PMID:Octreotide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in conditions associated with excessive peptide secretion. 268 36

The effect of long acting somatostatin analogue, SMS 201-995, on postprandial dumping syndrome was studied in eight patients with Billroth II gastric resection. Each patient was subjected to two oral glucose challenges with 75 g glucose. One challenge was premedicated with 50 micrograms SMS 201-995 subcutaneously 15 min before the oral intake of glucose, the other with placebo. With placebo all patients experienced the subjective symptoms of the early dumping syndrome with significant (P less than 0.001) increases (mean (s.d.)) in pulse rate (from 66 (8) to 102 (10) beats/min), in packed cell volume (from 0.36 (0.05) to 0.43 (0.1) l/l) and in the plasma levels of vasoactive intestinal polypeptide (from 3.0 (0.5) to 10.2 (1.8) pmol/l). During the somatostatin study the subjective symptoms and the changes in the various parameters were not detected. In the control study seven patients showed postprandial hypoglycemia. In these patients significant elevations (P less than 0.001) in the insulin level (from 10 (0.9) to 40 (9.1) microE/ml) and gastric inhibitory peptide (GIP) concentration (from 100 (13) to 220 (41) ng/l) were seen, compared with the initial values. During the application of SMS 201-995 hypoglycaemia did not develop and plasma insulin and GIP concentrations remained unchanged. These results indicate that the long acting somatostatin analogue alleviates the symptoms of early and late postprandial dumping syndromes.
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PMID:Long acting somatostatin analogue in dumping syndrome. 269 Oct 13

The dumping syndrome, which may follow partial gastrectomy or truncal vagotomy and drainage, may be refractory to treatment. The aim of this study was to determine the effect of the somatostatin analogue, SMS 201-995 (octreotide), on dumping provoked by hypertonic glucose. Ten patients with symptoms and signs of dumping were studied. After a dumping provocation test with placebo, all patients developed severe symptoms: seven patients had early dumping, two had both early and late dumping and one had late dumping alone. With either 50 or 100 micrograms SMS 201-995, the symptoms of early dumping were much reduced in all patients, and those of late dumping were completely abolished. The packed cell volume, pulse and systolic blood pressure changes of early dumping were significantly reduced by SMS 201-995 and the fall in blood glucose in patients with late dumping was abolished. SMS 201-995 may be a useful treatment for early and late dumping.
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PMID:Somatostatin analogue SMS 201-995 (octreotide) as a possible solution to the dumping syndrome after gastrectomy or vagotomy. 270 45

Somatostatin has been shown to be effective in the management of the dumping syndrome and there have been reports of the effective use of long acting somatostatin analogue in the management of this condition. However, there have been few reports of the prolonged use of a somatostatin analogue in the late dumping syndrome. We describe a patient in whom this management provided good long term symptomatic relief which was confirmed biochemically.
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PMID:Long-term symptomatic relief of postprandial hypoglycaemia following gastric surgery with a somatostatin analogue. 278 Apr 62

Infusion of somatostatin reduced the symptoms of the early dumping syndrome after oral glucose was given and also reduced the associated tachycardia and rise in packed cell volume. It inhibited the secretion of enteroglucagon, neurotensin, and vasoactive intestinal polypeptide, which are raised in patients with the dumping syndrome and may have an aetiological role. It also prevented the reactive hypoglycaemia of late dumping by inhibiting the release of gastric inhibitory polypeptide and insulin. Somatostatin, possibly through its inhibitory effects on hormonal secretion, may have a role in the management of patients with the early and late dumping syndrome.
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PMID:Somatostatin and the dumping syndrome. 285 44

The newly isolated hormonal peptide PYY is mainly localized to endocrine cells of the lower intestinal mucosa. The release of PYY by oral glucose was studied in six patients with the dumping syndrome to ascertain the effect of this condition on PYY release. Plasma PYY concentrations were greatly increased following oral glucose in patients with the dumping syndrome compared with healthy controls. In a separate series of experiments, the effect of somatostatin infusion on the PYY release by glucose in these patients was investigated. The release of PYY was completely blocked by infusion of somatostatin, and its release from the bowel in normal subjects may therefore be modulated by local somatostatin in the gut. PYY has been shown to inhibit gastric acid secretion and emptying, at plasma concentrations similar to those seen after glucose, in patients with the dumping syndrome. PYY may therefore be a factor involved in the pathophysiological changes associated with this condition.
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PMID:Plasma peptide YY (PYY) in dumping syndrome. 286 74

Many of the features of the dumping syndrome may be manifestations of hypovolemia and mechanical distension of the gut, resulting from abnormal fluid secretion in the upper gastrointestinal tract. The object of the present study was to assess the effect of somatostatin, an inhibitor of upper gastrointestinal secretions, on the response to a dumping provocation test, using a double-blind, placebo-controlled method. Four patients were studied; two had undergone total gastrectomy for gastric carcinoma and two had undergone gastric bypass for morbid obesity. Each subject received, on two separate occasions, a challenge of 200 ml of 50% glucose administered orally after an overnight fast. Somatostatin in 150 mm of NaCl (250 micrograms bolus followed by 300 micrograms/hr infusion) was given intravenously during one dumping provocation test and placebo (150 mm of NaCl) during the other according to a Latin square design. When the subjects received the placebo there were significant increases in pulse rate and packed cell volume after oral glucose (p less than 0.05, paired t test), which did not occur when they received somatostatin. The glucose challenge also produced a more rapid increase in serum osmolality and blood glucose during administration of placebo than when somatostatin was given. Marked diarrhea developed in all placebo-treated subjects but in none when they received somatostatin; however, three of the subjects developed marked abdominal pain during dumping provocation tests when treated with somatostatin, which did not occur when placebo was given. Although somatostatin appears to suppress some of the objective responses to a dumping provocation test, it may not prove particularly useful in the treatment of dumping symptoms.
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PMID:The effect of somatostatin on dumping after gastric surgery: a preliminary report. 286 91

Somatostatin is present in the gastrointestinal tract in appreciable amounts. The highest concentrations of the polypeptide are found in the stomach, the upper small intestine, and the pancreas. Within the gastrointestinal tract, somatostatin inhibits various functions, including endocrine and exocrine secretion, motility, blood flow, absorption, and growth. The polypeptide regulates these functions by endocrine, paracrine, neurocrine or luminal mechanisms. Abnormalities of endogenous somatostatin have been implicated in several gastrointestinal disorders, including the somatostatinoma syndrome, antroduodenal D-cell hyperplasia, peptic ulcer, obesity, and liver cirrhosis. Because of its potent inhibitory effects, somatostatin or somatostatin-analogues have been used as therapeutic agents in various clinical conditions, such as upper gastrointestinal haemorrhage, endocrine pancreatic tumours, gastrointestinal and pancreatic fistulas, pancreatitis, secretory diarrhoea, and dumping syndrome. The recent availability of the synthetic long-acting somatostatin-analogue SMS 201-995 (Sandostatin) has greatly facilitated the therapeutical application of somatostatin-polypeptides.
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PMID:Clinical and pathophysiological aspects of somatostatin and the gastrointestinal tract. 289 34

In six patients suffering from severe early dumping and six patients with late dumping after peptic ulcer surgery, the effect of the somatostatin analogue SMS 201-995 was compared with placebo. In early dumpers subcutaneous administration of 50 micrograms SMS 201-995 prior to meal ingestion induced a strong improvement of dumping symptoms as reflected by a decrease of the Sigstad dumping score from 12 +/- 2 during placebo to 5 +/- 2 (p less than 0.05). Furthermore, the postprandial increase of pulse rate was abolished; maximum pulse rate decreased from 85 +/- 7 beats/min to 67 +/- 7 beats/min (p less than 0.05). SMS 201-995 did not significantly affect postprandial changes in packed cell volume. In late dumpers 50 micrograms SMS 201-995 reduced peak plasma insulin after oral glucose from 173 +/- 16 mU/L during placebo to 35 +/- 9 mU/L during SMS 201-995 (p less than 0.05) and increased individual plasma glucose nadirs from 1.9 +/- 0.3 mmol/L to 7.5 +/- 3.3 mmol/L (p less than 0.01). Both in early and late dumpers SMS 201-995 improved postprandial expiratory breath hydrogen excretion indicating slowing of gastrointestinal hurry. SMS 201-995 is a powerful therapeutic agent for the management of patients suffering from the dumping syndrome after gastric surgery.
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PMID:Treatment of the dumping syndrome with the somatostatin analogue SMS 201-995. 289 92


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