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)

Somatostatin, or SRIF (Somatotropin Release Inhibiting Factor), is a tetradecapeptide of hypothalamic origin, which inhibits the secretion of growth hormone. It has also been recognized in other parts of the central nervous system, in the islets of Langerhans, and the mucosa of the upper digestive tract. Parenteral administration of synthetic SRIF inhibits the release of growth hormone, basal and stimulated by muscular exercise, arginine, L-DOPA, insulin-induced hypoglycemia, and sleeping. It also inhibits insulin and glucagon secretion, basal and stimulated, and several other secretory processes in endocrine and exocrine glands. It may have a depressor effect on some neurons in the central nervous system. Considerable interest has been prompted in the field of diabetology by the demonstration of somatostatin-induced suppression of growth hormone and glucagon : both hormones are over-secreted in many diabetic patients, and both may be noxious for small blood vessels in the diabetic. The eventual therapeutic use of somatostatin in humans is restricted, for the moment, by the unavaibility of long-acting SRIF preparations and the possibility of some adverse effects mainly affecting hemostasis. Evaluation of the physiological role (s) for this newcomer, and of the eventual pathophysiology of endogenous somatostatin, represent an unexpected and exciting field of neuro-endocrinology.
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PMID:[Somatostatin, a new hormone? (author's transl)]. 79 89

The incorporation of somatostatin into parenteral nutritional units has considerable advantages in the treatment of patients subjected to this combined therapy with respect to a reduction in the cost of the therapy and an increase in its effectiveness. This study evaluates the stability of somatostatin in "all-in-one" parenteral nutritional units formulated with or without lipids and preserved at 5 or 25 degrees C for a study period of 7 days. The concentration of somatostatin was determined by high resolution liquid chromatography. All the parenteral nutritional units tested remained stable with regard to content in somatostatin for at least 7 days. The t90 values were around 13.3 days for nutritional mixtures without lipids preserved at 5 degrees C, manifesting the positive influence of refrigeration and lipid emulsion on the stability of somatostatin. None of the PNV showed modifications in pH, colour, precipitation or breakage of lipid emulsion during the study period. The above means that somatostatin can be prepared and administered together with Total Parenteral Nutrition in parenteral nutritional units formulated in the same container.
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PMID:[Somatostatin stability in parenteral nutrition units]. 167 15

61 patients with postoperative enterocutaneous fistulas of the small intestine, were admitted to the Intensive Care Unit from 1983 to 1989 and divided in two groups. Group A (n = 46) was treated with Total Parenteral Nutrition (TPN), while B (n = 15) received a combination of TPN and Somatostatin. The reduction of fistula output was significantly greater in group B. Spontaneous closure was observed in 30.4% of the cases in group A and in 53.3% in group B. A significant difference in the time taken to close the fistula between group A and B (29.7 +/- 18 versus 11.1 +/- 1.6 days) was observed.
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PMID:[Somatostatin and/or total parenteral nutrition for the treatment of intestinal fistulas]. 198 16

The authors present the case of an extremely premature baby affected by severe Necrotizing Enterocolitis (NEC) needing intestinal resection and ileostomy. An enteric fistula developed 3 days after ostomy closure. The baby was started on Total Parenteral Nutrition (TPN), and 7 days later the fistula output remained constant. Somatostatin (SM) was then given intravenously (3.0 micrograms/Kg/hr) and the fistula closed on the 3rd day of treatment. Since SM was introduced in 1986 as an adjunct treatment to TPN in enteric fistulas, the authors believe that theirs is the first report of a successful SM treatment in a premature.
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PMID:Treatment of an enteric fistula with somatostatin in a premature. 256 61

The aim of the study was to evaluate and control the therapeutic validity of Somatostatin administration and the clinical benefits of parenteral nutrition during acute pancreatitis. We selected 31 patients with 1st and 2nd degree pancreatitis according to Ranson's classification. Diagnosis was based on clinical and humoral data and confirmed by echography and CT examinations. The most common etiological cause was biliary++ lithiasis (74.2%). All the patients in the study were split into two groups and received conventional treatment. The therapeutic schedule administered to group 1 included somatostatin (250 micrograms/h for 72-96 h), while group 2 received total parenteral nutrition with 2,000-2,500 Kal/day trough a central vein. The data obtained from our study demonstrated that both somatostatin and parenteral nutrition are valid tools during the acute phase of the disease. It must be pointed out that the former significantly influences the clinical course and allows a precise control of the painful symptomatology, the objective picture and the curve of the main hematochemical parameters. Parenteral nutrition betters the anabolic response of the organism during the acute phase and carries out an indirect antienzymatic response, so favouring a quicker recovery than observed in the group treated with somatostatin.
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PMID:[Role of somatostatin and parenteral nutrition in the treatment of acute pancreatitis. Personal experience]. 256 58

Parenteral somatostatin has been used to suppress growth hormone secretion in acromegalic patients, but long-term treatment is hampered by its short half-life of a few minutes in the circulation. An octapeptide analogue of somatostatin (SMS 201-995) has recently been developed that has greater potency and selectivity in suppressing growth hormone than the native hormone. In this study somatostatin and somatostatin octapeptide infusions were compared in 13 patients with active acromegaly. The octapeptide had a longer duration of action in the suppression of growth hormone than native somatostatin. A twice daily dose of 100 micrograms significantly suppressed growth hormone during the day. Prolactin was not suppressed, even in hyperprolactinaemic patients, and suppression of insulin was of short duration. Two patients had diarrhoea, but this disappeared when treatment with the octapeptide was stopped. Somatostatin is known to suppress pancreatic exocrine function, and it is therefore important to look for evidence of malabsorption during long-term treatment with the octapeptide. Somatostatin octapeptide is therefore useful in the treatment of acromegaly, but evidence of malabsorption should be watched for; nonparenteral routes of administration need to be assessed.
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PMID:Somatostatin octapeptide (SMS 201-995) in the medical treatment of acromegaly. 287 97

A woman presented with persistent ileostomy diarrhoea unresponsive to conventional drug treatment and necessitating parenteral nutrition. Output was four to six litres of watery fluid per 24 hours while she was receiving oral nutrition and two to three litres when she was starved. Treatment with a long acting analogue of somatostatin (50 micrograms subcutaneously every 12 hours) reduced the ileostomy output to 2.0-2.5 litres/24 hours with an oral diet and the effluent became semiformed. Parenteral fluids could be stopped. Somatostatin may have a role in the treatment of secretory diarrhoea, but prospective controlled trials are necessary.
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PMID:Use of a long acting somatostatin analogue in controlling life threatening ileostomy diarrhoea. 614 92

The authors, on the basis of their experience concerning the observation and treatment of 50 patients sucering from "pure" pancreatic fistula, appraise the results of the therapy adopted. From their experience it results the Total Parenteral Nutrition (TPN) is the choice protection in such patients. They report some encouraging preliminary results through the use of Somatostatin.
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PMID:[Pancreatic fistulas: evaluation of medical treatment in 50 observed cases]. 615 77

A shortened small intestine may end at a stoma or be anastomosed to the colon. Patients with a jejunostomy, but not those with a colon, lose large amounts of sodium. The intake and absorption of sodium can be increased by sipping a sodium-glucose solution; stomal loss can be reduced by restricting water or low-sodium drinks. If a stoma is situated less than 100 cm along the jejunum, a constant negative sodium balance may necessitate parenteral saline supplements. Gastric anti-secretory drugs or a somatostatin analogue reduce jejunostomy losses in such patients but do not restore a positive sodium balance. Loperamide or codeine phosphate benefit some patients. Magnesium deficiency can usually be corrected by oral magnesium oxide supplements. An elemental or hydrolysed diet is not beneficial. Patients with a jejunostomy can maintain a normal diet without fat reduction. When the colon is present, unabsorbed carbohydrate is fermented to absorbable short chain fatty acids. Unabsorbed long chain fatty acids and bile salts cause watery diarrhoea and increased colonic oxalate absorption with hyperoxaluria. Such patients benefit from a high carbohydrate, low-fat and low-oxalate diet. Parenteral nutrition is needed only by the few patients unable to maintain health or avoid socially disabling diarrhoea despite these measures.
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PMID:Review article: practical management of the short bowel. 769 44

Variceal esophageal bleeding is a frequent and severe complication of portal hypertension. Balloon compression was the standard therapy for many years. Currently, endoscopic hemostasis with sclerosis or ligation appears to be more effective but requires an experienced operator who is not always present at emergency situations. Parenteral administration of vasoactive agents is one therapeutic option offering new perspectives for the future. Data in the literature suggest that terlipressin or somatostatin would be the preferential choice because of the adverse effects of vasopressin. Data is insufficient concerning sandostatin. Currently, the trend is to administer vasoactive agents as soon as possible, prior to hospitalization and, perhaps, in association with endoscopic hemostasis. Treatment should be maintained for several days although the cost/benefit ratio remains a question of debate.
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PMID:[What vasoactive agent should be chosen in rupture of esophageal varices in cirrhosis?]. 925 45


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