Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment with Sandostatin is established in acromegaly, thyroid-stimulating hormone (TSH)-producing pituitary, and endocrine-active gastroenteropancreatic tumors. Potential indications include ectopic hormone syndromes, medullary thyroid carcinomas, pituitary resistance to thyroid hormones, tall stature children, diabetes mellitus and diabetic complications, polycystic ovary syndrome, and Graves' ophthalmopathy. Particularly in the ectopic growth hormone-releasing hormone (GHRH) syndrome, Sandostatin is unequivocally effective and, in the ectopic corticotropin syndrome selected cases can be treated successfully with Sandostatin, leading to marked clinical improvement. In many of the above situations, only subgroups show a response to Sandostatin, which may be identified by scintigraphy with labeled Sandostatin. This pertains also to Graves' ophthalmopathy, for which Sandostatin may be particularly promising and where positive and negative Sandostatin scans have been demonstrated. However, for all these potential indications, larger, well-studied series are needed, before definitive conclusions can be drawn.
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PMID:Potential indications for octreotide in endocrinology. 151 41

In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. The kidney hypertrophy in untreated diabetic animals amounted to 23% four days after streptozotocin injection and followed an increase in kidney somatomedin C content of 60% reaching the maximum after 48 h. In young and old uninephrectomized rats kidney growth was 19% and 16% after four days. In young animals a prompt increase of 50% in kidney somatomedin C was seen as reaching the maximum after 24 h, while the somatomedin C content in kidneys from old animals was maximal after 48 h (increase of 58%) in good accordance with the slightly slower kidney growth. The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. It is noteworthy that Sandostatin administration did not alter the metabolic state in diabetic animals indicating that the inhibition of kidney hypertrophy could not be attributed to improved metabolic control. The results thus support the concept that somatomedin C is involved in initial diabetic and post-nephrectomy renal growth.
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PMID:Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats. 275 63

Natural Somatostatin has a short half-life (3 min), is only active after intravenous administration and causes a rebound hypersecretion of hormones after discontinuation of administration. Recently a long-acting powerful Somatostatin analog was developed (SMS 201-995; Sandostatin) which has a half-life of 113 min after subcutaneous administration. After administration of this analog no rebound hypersecretion of hormones was observed. In the present review the effects of the acute administration and of long-term treatment with SMS 201-995 in acromegalic patients is discussed. In addition the potential role of therapy with Somatostatin analogs and the preliminary effects of Somatostatin and/or SMS 201-995 are discussed in disorders of gastro-intestinal function (haemorrhages, diarrhoea, pancreatitis and endocrine pancreatic tumours), diabetes mellitus, central nervous system disturbances and oncology. Finally, several aspects of the tolerance, tachyphylaxis and side effects of SMS 201-995 are discussed.
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PMID:Non-pituitary actions of somatostatin. A review on the therapeutic role of SMS 201-995 (sandostatin). 287 90

SMS 201-995 (Sandostatin) was studied using low doses (50 to 100 micrograms) administered subcutaneously every 12 hours. A single 50-micrograms dose of SMS 201-995 effectively controlled gastric acid and blood gastrin levels for 12 hours in three patients with benign gastrinomas and was useful in their perioperative management. Higher doses of the agent (500 to 800 micrograms per day) had no effect on metastases in one of two patients with metastatic gastrinoma. In the other patient, one tumor shrank but the other continued to grow after three months of treatment while serum gastrin levels did not change. Cultured metastatic tumor tissue from this patient released different forms of gastrin; growth rates varied, independent of uptake of SMS 201-995, and gastrin release increased. A neonate with nesidioblastosis maintained normal blood glucose levels while receiving SMS 201-995 therapy following a 95 percent pancreatic resection. In two elderly patients with organic hypoglycemia--one with a single benign adenoma and one with multiple adenomatosis--the somatostatin analogue did not prolong the hypoglycemia-free interval. In nine patients with carcinoid syndrome, flushing was uniformly controlled with 50 micrograms of SMS 201-995 administered every eight to 12 hours. One of the nine required exocrine pancreatic replacement. After six months of treatment, three of the nine had no change in tumor size and one had remission of symptoms and stopped treatment. In two patients with vipoma, SMS 201-995 controlled diarrhea and reduced levels of vasoactive intestinal peptide; tumor necrosis occurred in one patient. In a patient with diabetic diarrhea unresponsive to all treatments, SMS 201-995 therapy controlled the diarrhea but did not interfere with control of the diabetes.
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PMID:Somatostatin analogue (SMS 201-995) in the management of gastroenteropancreatic tumors and diarrhea syndromes. 287 47

Ten diabetic teenagers were admitted into our hospital for two nights, separated by one week. In a double-blind cross-over randomized study they received either 50 micrograms of the new long-acting somatostatin analogue Sandostatin sc or placebo. All patients were between 12 and 16 years of age, C-peptide negative with a duration of diabetes of at least four years. They had either conventional therapy or insulin pump therapy. Insulin doses and diets were kept unchanged. Blood samples were taken half hourly from 17.00 h until 09.30 h the next morning from an indwelling venous catheter. Hormonal and metabolic profiles on the two nights were evaluated by means of a distribution free time sequential co-movement analysis and by the paired Wilcoxon's signed rank test. After Sandostatin was given at 22.00 h, GH levels were significantly suppressed during 4 h. During that period blood glucose was slightly but significantly lower than after placebo. The free-insulin profiles from both nights were very comparable. Co-movement analysis showed a significant correlation between glucose and free insulin variations with a 30-min backward shift of the glucose curve. However, after Sandostatin administration this relation was lost in the period between 22.00 and 07.00 h, indicating a different effect of insulin on glucose levels during the nights Sandostatin was given. Early morning glucose rises were associated with free insulin levels below 20 mU/l. This association was not altered during the Sandostatin nights. Glucagon was not suppressed by Sandostatin except at 120 min after injection, and remained unchanged during the rest of the observation period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-acting somatostatin analogue (Sandostatin) reduces late night insulinopenic ketogenesis in diabetic teenagers. 289 37

SMS 201-995 (Sandostatin) is an octapeptide which differs in its action from native somatostatin in four ways: 1) it inhibits GH hormone secretion in preference to insulin secretion; 2) it can be administered subcutaneously or even orally; 3) it is long-acting (t1/2 after sc administration 113 min), and 4) there is no rebound hypersecretion of hormones when the effect of the analogue lingers off. In this paper a guide is offered for the use of Sandostatin in the treatment of acromegaly (after unsuccessful operation and/or radiotherapy) and of metastatic endocrine pancreatic tumours and carcinoids. A dose regimen for these two types of patients is suggested and the adverse reactions which can be expected are summarized. In addition, preliminary data are shown and the limitations are discussed of possible future indications of the analogue in the treatment of cancer, diabetes mellitus and gastrointestinal diseases.
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PMID:A guide to the clinical use of the somatostatin analogue SMS 201-995 (Sandostatin). 289 38

The infusion of natural somatostatin (SRIF) has been able to partially correct postprandial hyperglycemic reactions in insulin-dependent diabetes mellitus (IDDM). SMS 201-995 (Sandostatin) is a long-acting derivative with a growth hormone-suppressive effect 10-60 times more potent than the native peptide. The effect of SMS 201-995 (50 micrograms s.c.) on glucose control by exogenous insulin has been documented in a series of type I diabetics after stabilization of blood sugar by an artificial pancreas. Inhibition of counterregulatory mechanisms significantly diminished the postprandial hyperglycemia, and insulin requirements, both total and 2 h after meals, were markedly decreased. Also the effect of a single s.c. injection of 100 micrograms SMS 201-995 on the dawn phenomenon in a patient with poorly adjustable diabetes was investigated. The glucose escape observed during the control night was blocked by SMS 201-995. Thus, the stabilizing action of this peptide on postprandial and nocturnal hyperglycemia in unstable diabetes warrants further studies.
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PMID:Effect of a long-acting somatostatin derivative SMS 201-995 (sandostatin) on glucose homeostasis in type I diabetes mellitus. 290 Feb 5

Somatostatin (SRIF) is effective in the nonoperative management of a variety endocrine tumors. A potential role of SRIF for treatment of patients with primary hyperparathyroidism (pHPT) has been suggested. In a controlled, prospective, triple-blinded, randomized clinical trial, the somatostatin analogue octreotide (SMS 201-995, Sandostatin) was evaluated in 40 patients with well documented pHPT. Amongst other biochemical parameters, serum calcium and-phosphate and levels of parathyroid hormone, calcitonin, and osteocalcin as well as octreotide were assessed before and for 4 hours after a single iv. application of 200 micrograms ocreotide or placebo. SRIF-receptor autoradiography was performed in parathyroid tissue samples. Baseline values revealed a constellation of biochemical parameters typically found in pHPT. Following 200 micrograms octreotide, no significant changes in any of the biochemical parameters investigated for were observed. Multivariate analysis was performed to identify patient subpopulations in which any given combination of laboratory parameters changed in response to either drug or placebo. However, no 'responders' to octreotide were identified. 45% of patients receiving octreotide, reported side effects. Parathyroid tissue samples were negative for SRIF-receptor expression. It is concluded that a single dose iv. application of octreotide does not result in appreciable changes of biochemical parameters relevant in pHPT and carries a high rate of side effects. Furthermore, absence of SRIF-receptors in parathyroid tissue from patients with pHPT, together with lack of octreotide effects, suggests that somatostatin-analogues may not be effective in the non-operative therapy of pHPT.
Exp Clin Endocrinol Diabetes 1995
PMID:Influence of somatostatin to biochemical parameters in patients with primary hyperparathyroidism. 878 13

Disease activity in acromegaly is accurately reflected by growth hormone (GH) concentration during oral glucose tolerance test (OGTT) and insulin-like growth factor-I (IGF-I) levels, representing an integrated index of GH activity. This prospective study was performed to evaluate whether plasma IGF binding protein 3 (IGFBP-3) might also reflect the hormonal disease activity in pituitary acromegaly after operative treatment during early and late follow-up. Twenty-two acromegalic patients were studied. Data were obtained pre-, intra- and post-operatively in 13 cases. In 9 patients the acromegalic activity was studied only after treatment. The hormonal assessment included repeated blood samples for estimation of IGF-I, IGFBP-3 and repeated OGTTs. In each case 100 sigma g octreotide (Sandostatin lambda, Sandoz, Basel) was injected to test the acute response of GH, IGF-I and IGFBP-3. Intraoperatively, GH levels were estimated to examine acutely the influence of tumour reduction on GH levels. Patients were considered cured when GH levels (GH60min) were less than 2 ng/ml during OGTT 4 weeks after surgery. The data outlined that in patients with normalized GH60min levels, normalized IGFBP-3 levels were noticed 4 weeks and 12 months post-operatively. In non-cured patients normalized IGFBP-3 concentrations were found in 11 out of 15 cases in the late post-treatment phase. In contrast only 1 of 7 cured patients had persistently elevated IGF-I levels within the first month post-operatively, whereas no case of the non-cured patients had IGF-I values in the normal range. Despite these observations a strong correlation of IGF-I and IGFBP-3 did not exist before one year post-operatively -- either in the cured or in the non-cured patients. Serum IGFBP-3 in patients with pituitary acromegaly does not provide a predictive value of appreciable magnitude concerning cure or non-cure from the disease- whether examined early or late in the post-operative period. Absolute levels of IGFBP-3 may thus cause misinterpretation concerning cure of acromegalics after surgery.
Exp Clin Endocrinol Diabetes 1998
PMID:Insulin-like growth factor binding protein-3 levels during early and late follow-up after surgery in acromegalic patients. 962 44

Glucagonomas are rare tumors originating in alpha-cells of the pancreas. The most common clinical presentation is the association of diabetes mellitus, necrolytic erythema, weight loss and anemia. The diagnosis of pancreatic tumor is usually made by abdominal computed tomography and/or endoscopic ultrasonography. Indium-labeled octreotide scanning is useful for the localization of most neuroendocrine tumors and their metastases. Glucagon release can be confirmed by a high concentration of plasma glucagon. We report the case of a 74-year-old patient who had a glucagonoma with particular presentation of neurological impairment and weight loss. The diagnosis was confirmed by usual imaging procedures and plasma glucagon level. Medical treatment was started with long-acting repeatable octreotide (Sandostatin(R) LAR). After a one-year follow-up, the patient remained well. The original presentation and benefit of a new, long-acting somatostatin analog for the treatment of inoperable glucagonoma are discussed.
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PMID:[Clinical response of an atypical glucagonoma treated with a long-acting somatostatin analog]. 1243 3


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