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)

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

1. The haemodynamic and hormonal changes following glucose ingestion (1 g/kg) were determined before and after pretreatment with either placebo or the somatostatin analogue, octreotide (SMS 201-995, 50 micrograms subcutaneously), in seven patients with chronic autonomic failure. 2. In the placebo phase, after glucose, there was a marked and prolonged fall in blood pressure with no change in cardiac index and peripheral blood flow. Plasma insulin and neurotensin levels increased, whereas glucagon, vasoactive intestinal polypeptide, noradrenaline and adrenaline levels were unchanged. 3. Octreotide transiently raised blood pressure and prevented glucose-induced hypotension. There were no changes in cardiac index or peripheral blood flow. Plasma insulin and neurotensin levels did not rise. Plasma glucose levels increased more slowly but reached a similar level to the placebo phase. 4. We conclude that in autonomic failure patients, glucose-induced hypotension was not accompanied by changes in cardiac index or peripheral blood flow, indicating a lack of compensation to probable splanchnic vasodilatation. The hypotension was prevented by the peptide release inhibitor, octreotide, with no change in cardiac index or in peripheral blood flow, suggesting an effect on the splanchnic vasculature, probably through inhibiting release of vasodilatatory pancreatic and gut peptides.
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PMID:Prevention of glucose-induced hypotension by the somatostatin analogue octreotide (SMS 201-995) in chronic autonomic failure: haemodynamic and hormonal changes. 269 Nov 74

The purpose of this study was to evaluate the therapeutic potential of the somatostatin analog octreotide in patients with orthostatic hypotension. Octreotide was administered sc, and its pressor effect was assessed while the patients were semirecumbent and on the tilt table. We also studied the effect of octreotide on blood pressure while patients walked. The efficacy of therapy was assessed by measuring the duration of walking (walking time) before the onset of hypotension. Low doses of octreotide (0.2-0.4 micrograms/kg) had a pressor effect in all patients with progressive autonomic failure (n = 7), multiple system atrophy (n = 7), and diabetic autonomic neuropathy (n = 8), but not in patients with sympathotonic orthostatic hypotension (n = 6). Larger doses (0.4-1.6 micrograms/kg) resulted in a sustained (greater than or equal to 50 min) increase in blood pressure during walking in four of six patients with progressive autonomic failure and in one of six patients with multiple system atrophy. Some patients in whom octreotide failed to stabilize upright blood pressure had a satisfactory response to the drug after pretreatment with dihydroergotamine (10 micrograms/kg, sc). Patients with diabetic autonomic neuropathy, although sensitive to the pressor effect of octreotide, often developed nausea or abdominal cramps after moderate doses (greater than 1.0 micrograms/kg). These results indicate that the pressor effect of octreotide is sufficiently potent to prevent orthostatic hypotension in some patients with autonomic neuropathy. Others require treatment with both dihydroergotamine and octreotide to achieve a stable upright blood pressure.
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PMID:Treatment of orthostatic hypotension with octreotide. 272 26

We have determined the haemodynamic responses to a balanced liquid meal in eight normal subjects, before and after administration of the somatostatin analogue, Octreotide (SMS 201-995), which inhibits the release of gastrointestinal peptides. In the absence of Octreotide ingestion of the meal caused a marked increase in superior mesenteric artery (SMA) blood flow. Blood pressure was maintained, presumably by a compensatory rise in cardiac output and forearm vascular resistance. After Octreotide there was a fall in SMA blood flow alone, with no further changes after food ingestion. We conclude that Octreotide prevents the haemodynamic changes following food ingestion, probably by inhibiting the release of those gastrointestinal peptides that induce splanchnic vasodilatation.
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PMID:The peptide release inhibitor, Octreotide (SMS 201-995), prevents the haemodynamic changes following food ingestion in normal human subjects. 279 66

Somatostatin, a 14 amino acid peptide hormone, is a potent inhibitor for secretion of gastrointestinal hormones from endocrine cells. The clinical use of somatostatin for treatment of endocrine gastrointestinal tumours was limited due to its short half-life (2-3 min). Octreotide (Sandostatin), a long-acting somatostatin analogue, has been developed for subcutaneous use with an elimination half-life of about 45 min. This offers a new way of long-term treatment for patients with endocrine gastrointestinal tumours. The effect of octreotide in various forms of these diseases and its importance for the possible inhibition of tumour growth are described.
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PMID:[Treatment of gastrointestinal neuroendocrine tumors with the somatostatin analog octreotide (Sandostatin)]. 284 48

Octreotide, a potent long-acting somatostatin analogue, has been shown to have a wide range of physiological actions. We have demonstrated a somatostatin-like inhibition of the electrically evoked contractions of the mouse vas deferens and an opioid antagonistic property in the same tissue. In addition, pretreatment with octreotide reduced the potency of naloxone antagonism in vitro in the mouse vas deferens and in vivo in the mouse charcoal meal test. The latter effect suggests that the agonist receptor interactions are taking place on sites allosteric to the agonist site and that the conventionally accepted concept of opioid antagonism may have to be modified.
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PMID:Weakening of naloxone antagonism in vitro and in vivo with octreotide (SMS 201-995). 288 9

Intractable diarrhoea and flushing due to the malignant carcinoid syndrome is seldom relieved by conservative medical treatment. Octreotide (Sandostatin; Sandoz) is a long-acting analogue of somatostatin and a powerful inhibitor of endogenous peptide release. A patient with severe diarrhoea and flushing due to the malignant carcinoid syndrome, in whom symptomatic control with octreotide was achieved, is described, and the value of octreotide treatment in the malignant carcinoid syndrome is discussed.
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PMID:[Symptomatic treatment of the malignant carcinoid syndrome with octreotide]. 291 81

The response to GH releasing hormone (GHRH 1-29) and 24-h serum GH and IGF-I levels were measured in 9 insulin-dependent diabetics with retinopathy and 6 normal volunteers before and after different treatment regimens with octreotide, a long-acting somatostatin analogue. Octreotide, 50 micrograms by sc injection, completely suppressed GHRH-stimulated GH release in both groups. Thrice daily sc injections for up to 20 weeks were associated with variable plasma octreotide levels and failed completely to suppress GH secretion in either the patients or the normal controls. Three days of continuous sc pump infusion (500 micrograms/24-h) resulted in consistently high plasma octreotide levels and completely suppressed 24-h GH in 4 normal subjects, whilst treatment for up to 16 weeks only partially suppressed GH levels in 6 patients (AUC mU.l-1.h-1; 209 +/- 81 vs 121 +/- 82; P = 0.01). Mean +/- SD IGF-I levels (micrograms/l) in the patients (but not controls) were suppressed into the hypopituitary range by median 6 weeks (range 2-16) pump administration (203 +/- 62 vs 60 +/- 25; P = 0.02). Pump treatment achieved total GH suppression in normal subjects; diabetics with retinopathy seem more resistant to the GH suppressing effects of the drug. However, the reduction of serum IGF-I with prolonged treatment may be of clinical value in arresting the progress of diabetic retinopathy.
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PMID:Continuous subcutaneous octreotide infusion markedly suppresses IGF-I levels whilst only partially suppressing GH secretion in diabetics with retinopathy. 291 80

Octreotide is an investigational synthetic peptide exhibiting actions similar to those of endogenous somatostatin. It has a longer half-life than the native hormone and can be administered by subcutaneous injection. Octreotide inhibits the secretion of growth hormone and numerous regulatory peptides of the gastroenteropancreatic system. Trials evaluating the clinical utility of octreotide indicate efficacy in the management of symptoms associated with acromegaly and hypersecretory neuroendocrine tumors, and in the control of nontumoral secretory diarrheas. Octreotide therapy is well tolerated. This agent should prove useful in the symptomatic control of a number of rare hypersecretory disorders.
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PMID:Octreotide: a synthetic analog of somatostatin. 306 36

The process of bacterial translocation (BT) after ischemia/reperfusion (I/R) injury is reported to be mediated by local mucosal factors, the effects of pancreatic enzymes, epithelial disruption, and by dysfunctional intestinal motility. Octreotide (OCT), a somatostatin analog, has been postulated to protect against BT by influencing one or more of these factors. Twenty-two formula-fed piglets (weight, 3.5 +/- 0.5 kg; age, 20 +/- 5 days) were divided into four groups: control (no drug given; no I/R; n = 6), I/R (no drug given; n = 5), I/R plus low-dose OCT (LD OCT, 0.08 microgram/kg; n = 6), and I/R plus high-dose OCT (HD OCT, 8 micrograms/kg; n = 5). All experimental subjects had nonocclusive mesenteric ischemia induced by reversible pericardial tamponade with mesenteric flow decreased to 25 +/- 5% of baseline for 5 hours followed by 15 +/- 5 hours of reperfusion. Mesenteric lymph nodes (MLN), liver, spleen, blood, and peritoneum were harvested for blind microbial analysis. None of the animals in the control group experienced translocation to the tissues tested. All of the animals in the I/R group experienced BT to the MLN. The subjects in the LD OCT and HD OCT groups experienced BT to the MLN 66% and 80% of the time, respectively. Despite the reported clinical evidence that OCT can protect the intestinal mucosa from injury and increase the clearance of bacteria from the gastrointestinal tract, in this study in which variables other than I/R known to promote bacterial translocation were eliminated, OCT failed to modify or prevent the occurrence of translocation to the MLN after I/R injury.
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PMID:Octreotide does not prevent bacterial translocation in an infant piglet model of intestinal ischemia-reperfusion. 747 54


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