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 and its long-acting analogue SMS 201-995 (Sandostatin) have been suspected of causing steatorrhoea. The aim of this study was to examine the effect of SMS 201-995 on fat assimilation in healthy subjects, using 14C-triolein and 3H-oleic acid as tracers of dietary triglycerides and free fatty acids, respectively, and 51CrCl3 as non-absorbable marker. Six healthy male volunteers participated in the double-blinded, randomized, crossover study. In each test period either 1 ml of SMS 201-995, containing 200 micrograms, or 1 ml of isotone saline was given subcutaneously three times within 16 h. Faeces were collected for 3 days, every stool separately. The faecal 14C-triolein and 3H-oleic acid excretion was calculated from two aliquots of faeces. In addition, the mean daily faecal fat excretion was estimated. When placebo was given, the median 14C-triolein excretion was 1% (range, 0.9-1.6%), the median 3H-oleic acid excretion was 5% (range, 3-10%), and the daily faecal fat excretion was 4 g/day (range, 1-6 g/day), all within normal limits. When SMS 201-995 was given, the faecal 14C-triolein excretion increased to a median of 75% (range, 43-119%), the 3H-oleic acid excretion increased to a median of 82% (range, 46-126%), and the faecal fat excretion increased to a median of 22 g/day (range, 4-34 g/day), all clearly above normal. The faecal 14C-triolein/3H-oleic acid test showed triglycerides and free fatty acids to be equally malassimilated, which indicates malabsorption.
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PMID:The long-acting somatostatin analogue SMS 201-995 causes malabsorption. 269 Mar 16

We have reviewed data pertinent to three tumor syndromes that derive from overproduction of three GEP peptide hormones. The clinical syndrome of somatostatin excess remains well defined with diabetes, diarrhea, steatorrhea being predominant features. With the availability of assays and increasing awareness, more cases are being diagnosed in the intestine and these differ somewhat in their presentation with cholecystitis, GI bleeding, or a mass as the cardinal features. An unusual association with MEN II pheochromacytoma and neurofibromatosis is emerging. PPomas remain enigmatic. Although diarrhea is a feature, these tumors are usually silent and present with hypatomegally, abdominal pain, and jaundice because of the large size and malignant nature. Neurotensinomas remain rare and truly difficult to separate from the symptom complex produced by VIP excess. Edema, hypotension, cyanosis and flushing should alert one to the possibility of a neurotensin-secreting tumor.
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PMID:Somatostatinomas, PPomas, neurotensinomas. 282 62

Amelioration or cure of hypertension, hypercortisolism, diarrhea with steatorrhea, and massive proteinuria resulted from excision of a pheochromocytoma that contained immunoreactive ACTH, VIP, and somatostatin. Ectopic ACTH production by the tumor was clearly the cause of the hypercortisolism, and the possible involvement of VIP and somatostatin in the diarrhea and steatorrhea was considered. The response to tumor removal suggested that the mesangioproliferative glomerulonephritis shown on renal biopsy was also a paraneoplastic phenomenon.
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PMID:Hypercortisolism, diarrhea with steatorrhea, and massive proteinuria due to pheochromocytoma. 286 63

A case of endocrine pancreatic tumour secreting the 2 antagonistic peptides that regulate growth hormone, somatostatin and somatocrinin, is reported. Such tumours are extremely rare and only one other case has been published so far, although pancreatic malignant tumours frequently secrete several hormones. In our patient, the association of diabetes with steatorrhoea, hypochlorhydria, anaemia and biliary lithiasis suggested hypersecretion of somatostatin. Acromegaly, suggested by clinical signs, was confirmed by an excess of growth hormone and somatomedin, and pre-operative somatrocrinin assay confirmed its extra-pituitary origin. Finally, the presence of hyperparathyroidism due to parathyroid gland hyperplasia and of a Recklinghausen disease constituted a multiple endocrine neoplasia syndrome. The significance and implications of this double secretion in vivo are discussed.
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PMID:[Endocrine pancreatic tumor secreting somatostatin and somatocrinin]. 286 53

The beneficial effect of the long-acting analogue of somatostatin SMS 201-995 in the treatment of acromegaly is described in three cases, and current published experience is reviewed. A total of 64 patients from 10 series have received the drug from one to 25 months, usually in doses of 50-150 micrograms every eight hours by subcutaneous injection. Clinical and chemical improvement was observed in the majority of subjects but normal 24-hour serum growth hormone levels were achieved in no more than 35 percent of this group and possibly less. We have found that higher doses, up to 1,500 micrograms per day, which have generally been free of side effects, are sometimes required to normalize growth hormone secretion. A reduction of up to 33 percent in pituitary tumor size has been reported in more than half of the 27 cases studied from four groups. Clinically important side effects are infrequent, but diarrhea, usually transient, occurred in about 13 percent, with frank steatorrhea in 2 to 6 percent of cases. Alteration in carbohydrate metabolism, such as transient glucose intolerance at the start of therapy in non-diabetic acromegalic patients, and increased sensitivity to insulin or oral hypoglycemic agents in diabetic acromegalic patients, is common. Overall, SMS 201-995 appears to be a valuable new agent for the treatment of acromegaly, but long-term safety needs to be established.
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PMID:Role of a long-acting somatostatin analogue (SMS 201-995) in the treatment of acromegaly. 287 53

We used an octapeptide analogue of somatostatin, SMS 201-995, in dosages ranging from 150 to 450 micrograms/d administered subcutaneously in three daily doses for 1 to 16 months, to treat 22 patients with advanced malignant islet cell carcinomas. Of the 22 patients, there were 9 with gastrinomas; 3 with glucagonomas; 4 with insulinomas; 1 with ectopic production of parathyroid hormone; and 3 with mixed syndromes. The only biochemical marker in 1 patient was pancreatic polypeptide, and 1 patient had no demonstrable peptide production from the tumor. In 14 patients, dramatic decreases in the levels of circulating peptides (insulin, vasoactive intestinal polypeptide, gastrin, and glucagon) have been accompanied by major alleviations of symptoms. Steatorrhea appears to be the most significant toxicity. This analogue of somatostatin may be appropriate for use as early therapy in patients who have symptoms from syndromes related to islet cell carcinomas but in whom there is no immediate threat from tumor progression.
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PMID:Treatment of metastatic islet cell carcinoma with a somatostatin analogue (SMS 201-995). 288 85

Ten acromegalic patients, four previously untreated, were studied before and at regular intervals during treatment with the long-acting somatostatin analog SMS 201-995 (200-300 micrograms daily for 2 or 3 sc injections for 16-108 weeks). All patients had rapid clinical improvement, with disappearance of excessive perspiration, paresthesias, and headache within the first 6 weeks of therapy. The mean 24-h serum GH concentrations fell from 44.0 +/- 7.8 (+/-SE) micrograms/L before to 5.9 +/- 1.0 microgram/L at the end of therapy. The GH levels from 2-6 h after the acute administration of 50 micrograms SMS 201-995 before the start of therapy correlated significantly with the mean 24-h GH concentrations after 16-108 weeks of treatment (P less than 0.05). The initially increased serum somatomedin-C (Sm-C) levels normalized in 5 of these 10 patients; the mean values were 7.3 +/- 0.9 U/mL before and 2.9 +/- 0.7 U/mL at the end of therapy. The Sm-C and mean GH levels continuously decreased during long term therapy; the concentrations after 1.5-2 yr of therapy were significantly lower than those after 6-12 months of therapy (P less than 0.01 and P less than 0.01, respectively). A slight decrease in the size of the pituitary tumor was noted by computed tomography in three of six patients. Transient clinically detectable steatorrhea occurred in two patients. Postprandial hyperglycemia occurred during therapy in eight patients, while in two patients with type 2 diabetes mellitus carbohydrate tolerance improved in one and deteriorated in the other. SMS 201-995 is a highly effective medical treatment for acromegaly. Clinically improvement occurs rapidly, and the inhibition of serum GH and Sm-C levels persisted even after more than 1 yr of therapy. No important subjective side-effects were noted. SMS 201-995 is an excellent drug in patients in whom acromegaly persists after surgery and for interim treatment to shorten the period of clinical activity after irradiation.
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PMID:SMS 201-995 induces a continuous decline in circulating growth hormone and somatomedin-C levels during therapy of acromegalic patients for over two years. 288 85

A 60 year old man developed steatorrhoea, weight loss, mild diabetes mellitus, labile hypertension and limb cramps. Raised plasma concentrations of catecholamines, particularly noradrenaline and a computed tomography-scan showing an adrenal tumour strongly suggested a pheochromocytoma. Adrenoreceptor blockade reversed the symptoms, decreased faecal fat, and increased duodenal trypsin to normal concentrations. After adrenalectomy the patient was asymptomatic and there was no steatorrhoea. The blood glucose concentrations became normal. Immunocytochemistry revealed the tumour cells to store large amounts of enkephalin and somatostatin reactive material and moderate amounts of immunoreactive beta-endorphin and dynorphin.
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PMID:A mixed endocrine adrenal tumour causing steatorrhoea. 289 May 60

Four patients with advanced endocrine malignancies were treated with a somatostatin analogue (SMS 201-995) for palliation of hormone-induced symptoms during 3-6 months. Two had the carcinoid syndrome (one midgut and one foregut), one had medullary thyroid carcinoma and an ectopic ACTH syndrome, and one patient had a metastatic gastrinoma. The carcinoid patients had excellent symptomatic relief with a low dose of the drug, 50 micrograms subcutaneously twice daily, in one case despite progression of tumour disease and biochemical tumour markers. These findings indicate an action of the drug not only on hormonal release but also at peripheral sites. The patient with medullary thyroid carcinoma had relief of gastrointestinal symptoms when the drug dose was increased (100 micrograms twice daily). The levels of ACTH in peripheral blood were reduced, but not the calcitonin levels. The gastrinoma patient had undergone a major pancreatic resection (Whipple procedure) and was treated with omeprazole. SMS 201-995 reduced the peripheral gastrin levels acutely, but during the treatment fasting gastrin values increased, and the tumour growth progressed. Treatment was stopped owing to elevated fasting glucose level, increased steatorrhoea, and clinical attacks of cholangitis. Special attention is advocated for patients with major pancreatic resection and biliary reconstruction, who may be susceptible to physiological effects of somatostatin (or its analogues)--that is, impaired insulin release and decreased motility.
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PMID:The use of a long-acting somatostatin analogue in the treatment of advanced endocrine malignancies with gastrointestinal symptoms. 289 Nov 86

We describe a patient with a small somatostatinoma of the papilla of Vater without clinical evidence for diabetes mellitus, diarrhea, steatorrhea, or cholelithiasis, showing normal plasma basal levels for somatostatinlike immunoreactivity. The diagnosis was based on histologic and immunohistochemical analysis of tumor tissue and hypersomatostatinemia induced by the calcium-pentagastrin test. Before removal of the tumor both diagnostic tests recommended for the detection of a somatostatinoma, a tolbutamide test and a calcium-pentagastrin test, were performed. Whereas the calcium-pentagastrin test provoked a markedly elevated plasma somatostatin level in association with a depressed plasma neurotensin level, the tolbutamide test surprisingly did not. After removal of the tumor the calcium-pentagastrin test no longer induced hypersomatostatinemia. Further studies are needed to determine whether the calcium-pentagastrin test is a more reliable diagnostic test than the tolbutamide test in somatostatinomas with normal plasma basal levels.
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PMID:Comparative diagnostic value of the calcium-pentagastrin test versus the tolbutamide test in a patient with a somatostatinoma. 302 98


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