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)

Since previous reports have suggested that somatostatin may be of value in the control of acute variceal haemorrhage, we compared its efficacy with that of injection sclerotherapy in a randomised controlled clinical trial. Eighty consecutive patients with endoscopically-proven severe variceal bleeding were randomised to injection sclerotherapy (n = 41) or somatostatin (n = 39) given as a continuous infusion of 250 micrograms/h for 5 days plus daily bolus administration of 250 micrograms. The efficacy of injection sclerotherapy and somatostatin infusion in controlling haemorrhage and preventing rebleeding (censored at 5 days), mortality (censored at 28 days) and complications was compared. The aetiology of the portal hypertension and transfusion requirements was similar between the two groups, but there were more patients with severe liver disease (Child's C) in the somatostatin group. There was no significant difference between the two treatments in the initial (p = 1.0) or overall control of bleeding (p = 0.58). Furthermore, somatostatin was as effective as injection sclerotherapy in controlling bleeding in patients with severe liver disease or in those actively bleeding at the time of their endoscopy. The relative risk of rebleeding whilst receiving somatostatin compared to injection sclerotherapy was 1.39 [95% Confidence Interval (CI) 3.73; 0.52], but this was reduced to 0.98 (95% CI 0.37; 2.67) when readjusted for Child's grading, the only prognostic factor shown to be of significance. Mortality was not significantly different between the two groups of patients (p = 0.31). The relative risk of dying whilst receiving somatostatin compared to injection sclerotherapy was 1.6 (95% CI 3.93; 0.66) but was reduced to 1.03 (95% CI 0.47; 2.47) when adjusted for Child's grading, the only significant prognostic factor. Complications in the somatostatin group were minor and less frequent than after injection sclerotherapy. The results of this study indicate that somatostatin is a safe treatment, which is as effective an endoscopic injection sclerotherapy for acute variceal bleeding.
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PMID:A prospective randomised controlled trial comparing the efficacy of somatostatin with injection sclerotherapy in the control of bleeding oesophageal varices. 136 32

Variceal bleeding is the most important complication of portal hypertension. Mortality due to the first variceal bleeding is very high (50%) and of those surviving a variceal bleeding episode, up to 80% may rebleed. Proper management of the acute variceal bleeding episode, the prevention of rebleeding and primary prophylaxis for variceal haemorrhage are therefore mandatory in order to improve the morbidity and mortality of cirrhotic patients with variceal bleeding. Injection sclerotherapy would be the treatment of choice for acute variceal bleeding. Drug treatment in the form of either a combined vasopressin-nitroglycerin regimen or somatostatin may be used as an alternative. Patients not responding to these treatments should be referred for surgery. For the prevention of variceal rebleeding, non-selective beta-blockers should be tried first, reserving long-term injection sclerotherapy for patients with contraindications or intolerance to beta-blockers or in whom beta-blocker therapy has failed. Surgical rescue in the form of either shunt surgery or lever transplantation should be considered if either treatment fails. A new technique, transjugular intrahepatic portosystemic stent-shunt (TIPSS) may replace shunt surgery in the future. Beta-blockers is the treatment of choice for primary prophylaxis of variceal haemorrhage and has a role in preventing acute and chronic bleeding from congestive gastropathy. However, the above sequential approach from the least invasive to the more invasive therapeutic options may not be appropriate for all cirrhotic patients with variceal bleeding.
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PMID:Management of variceal haemorrhage. 136 89

Following the demonstration that somatostatin lowered portal pressure in cirrhotic patients with portal hypertension, 2 uncontrolled reports suggested that the hormone might be useful in the control of acute variceal haemorrhage. Subsequently, a number of randomised controlled trials have indicated that somatostatin may have an efficacy as good as or better than either vasopressin or combined vasopressin and nitroglycerin therapy and is associated with fewer side effects. Somatostatin has an efficacy comparable to balloon tamponade, histamine-2-receptor antagonists and injection sclerotherapy. One double-blind randomised controlled trial demonstrated a significant benefit of somatostatin over placebo in the control of variceal bleeding whereas a second did not show any significant difference between treatments. In all the controlled trials, the average control rate achieved with somatostatin administration was 69% and it was not associated with any major side effects. Somatostatin administration has also been shown in uncontrolled series to be very effective in controlling postinjection sclerotherapy bleeding from the varices per se, and from oesophageal ulcers and oesophagitis. Few data are available on the long acting analogue of somatostatin, octreotide, but preliminary data suggest that it may be as effective and safe as the native hormone in controlling the acute variceal bleeding and postinjection sclerotherapy haemorrhage. It is concluded that there may be a case for instituting somatostatin therapy as soon as the patient enters hospital to facilitate sclerotherapy, and for continuing treatment for 5 days after sclerotherapy when the risk of recurrent bleeding is highest.
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PMID:Somatostatin in acute bleeding oesophageal varices. Clinical evidence. 138 69

The aim of this study was to determine the effects of the long-acting somatostatin analog, octreotide, on portal venous pressure and collateral blood flow in cirrhotic patients with portal hypertension during fasting and postprandial states. In a double-blind, placebo-controlled study, we investigated the effects of octreotide on the hepatic venous pressures and azygos blood flow of 21 patients before and after a standard liquid meal containing 40 gm of protein in 250 ml. Octreotide significantly reduced azygos blood flow from a mean of 499 +/- 65 ml/min to a mean of 355 +/- 47 ml/min (p < 0.01), but it had no effect on the hepatic venous pressure gradient. The hepatic venous pressure gradient of patients in the placebo group increased significantly, from a fasting mean of 16.4 +/- 1.6 mm Hg to a mean of 20.0 +/- 1.7 mm Hg 30 min after the meal (p < 0.01). In a second protocol hepatic venous pressures were measured in 20 patients at 30-min intervals for 2 hr after ingestion of the mixed meal. Again the placebo group showed a significant increase in the hepatic venous pressure gradient 30 min after the meal (20.4 +/- 1.5 mm Hg vs. 18.2 +/- 1.2 mm Hg; p < 0.05), but the group receiving octreotide showed no significant changes during the 2 hr of observation. We conclude that octreotide significantly reduces azygos blood flow, with little effect on portal venous pressure, and that it appears to inhibit postprandial increases in portal pressure in cirrhotic patients with portal hypertension.
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PMID:Octreotide inhibits the meal-induced increases in the portal venous pressure of cirrhotic patients with portal hypertension: a double-blind, placebo-controlled study. 142 56

Manipulation of hepatic blood flow may improve drug delivery to hepatic tumour. Somatostatin and its long acting analogues are known to elicit effects upon hepatic and splanchnic blood flow in experimental animals and patients with portal hypertension. This study investigates the effects of SMS 201-995 (sandostatin) infusion on hepatic, splanchnic and tumour blood flow in an experimental model of liver metastases. Hepatic tumour was induced by the intraportal inoculation of 10(6) HSN sarcoma cells and blood flow measured using the dual reference microsphere method before and after infusion of SMS 201-995. There was a significant decrease in hepatic arterial flow and a significant increase in the tumour:liver blood flow ratio associated with a marked reduction in blood flow to normal hepatic parenchyma. Portal venous inflow and tumour blood flow were not significantly affected. SMS 201-995 infusion may lead to preferential delivery of concomitantly injected cytotoxic drugs to hepatic tumour. In addition, the reduction in growth of hepatic tumour may be due to a reduction in nutritive, arterial blood flow to hepatic tumour.
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PMID:The effects of sandostatin (Octreotide, SMS 201-995) infusion on splanchnic and hepatic blood flow in an experimental model of hepatic metastases. 155 93

Whether the decrease of portal venous inflow and portal pressure induced by somatostatin is related to the effects of somatostatin in inhibiting the secretion of glucagon and other vasodilatory peptides that are increased in portal hypertension was investigated in the current study. Splanchnic vascular resistance and splanchnic blood flow were determined using radioactive microspheres in rats with portal hypertension caused by partial portal vein ligation. Somatostatin infusion significantly decreased portal pressure (from 13.1 +/- 1.9 to 12.1 +/- 2.2 mm Hg; P less than 0.05). This was associated with a significant decrease in portal venous inflow caused by splanchnic vasoconstriction, as evidenced by increased splanchnic vascular resistance, and with a marked suppression of glucagon secretion. The simultaneous infusion of somatostatin and glucagon (2.8 ng/min, a dose that prevented any decrease in circulating glucagon levels) abolished all the hemodynamic effects of somatostatin. This effect seems to be specific because no hemodynamic changes were noted in portal hypertensive rats receiving only the glucagon infusion.
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PMID:Glucagon hinders the effects of somatostatin on portal hypertension. A study in rats with partial portal vein ligation. 168 27

The main aim of conservative treatment of upper gastrointestinal bleeding in portal hypertension is aim to treat and prevent esophageal variceal hemorrhage. Controlled trials show that the hemostasis rate following vaso-active therapy (vasopressin and analogues, somatostatin) is only slightly superior to the spontaneous hemostasis rate. Complications caused by vasopressin treatment can be avoided by concomitant application of nitroglycerin or by alternative treatment with somatostatin. Balloon tamponade is slightly superior to vasopressin for arresting variceal hemorrhage. Injection sclerotherapy influences acute bleeding most positively. Analysis of controlled trials favors sclerotherapy for prophylaxis of rebleeding, but beta-adrenoceptor blockers appear to be almost equally good.
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PMID:Conservative treatment of upper gastrointestinal bleeding in portal hypertension. 168 47

There are three distinct phases during which treatment might influence the outcome in patients with portal hypertension and variceal bleeding: treatment of the active bleeding episode, the prevention of recurrent haemorrhage and perhaps most controversially the use of prophylactic therapy to avert the first bleeding episode. For the treatment of active haemorrhage injection sclerotherapy is almost certainly the treatment of choice when the expertise is available. In the absence of such, vasoconstrictor therapy continues to be widely adopted as a temporizing measure. The efficacy of vasopressin as a single agent has been limited by associated cardiovascular complications. The addition of nitroglycerin to a vasopressin regime has recently been shown to reduce such complications and to improve overall efficacy. Somatostatin represents an alternative vasoconstrictor with increasing evidence of efficacy in the absence of serious complications. Long-term injection sclerotherapy is widely accepted as the first line treatment to prevent recurrence of variceal haemorrhage although early rebleeding, prior to the obliteration of varices, represents an important limitation of therapy. Alternative local endoscopic therapy using tissue adhesives or banding of varices are under evaluation. The major claims of benefit initially attributed to oral propranolol for the prevention of rebleeding have now been considerably modified and a specific role remains to be defined. Both injection sclerotherapy and B-adreno-receptor have been proposed as prophylactic therapy to prevent the first variceal haemorrhage. Two extremely positive reports of prophylactic sclerotherapy have received little further support and there are now few protagonists of this approach.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A critical review of the medical treatment of portal hypertension. 198 46

The changes of humoral substances in the blood of cirrhotic rats were studied together with their effects on portal hemodynamics at different stages during the development of cirrhosis. The profiles of humoral substances and hemodynamics in two different cirrhotic rat models were also investigated. During the development of cirrhosis, glucagon increased markedly in all stages, histamine and vasoactive intestinal polypeptide (VIP) increased in the early stage, serotonin (5-HT) and somatostatin (SS) increased in the middle and late stages. There were different patterns of humoral substances in different cirrhotic models. Glucagon was the main humoral substance elevated in CCL4 induced cirrhosis, but histamine and 5-HT were mainly elevated in the blood in thioacetamide (TAA) induced cirrhosis. The hemodynamics altered differently in different stages during the development of cirrhosis and differently in the two cirrhotic rat models. Exchange transfusions between normal and cirrhotic rats resulted in an elevation of portal flow in normal rats, but no such changes were found after exchange pressure and an increase of portal blood transfusions between normal rats. The relationship between the humoral substances and portal hemodynamics is discussed. The results of this study strongly support the hypothesis of "humoral mechanism" in the pathogenesis of portal hypertension due to cirrhosis.
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PMID:Changes of blood humoral substances in experimental cirrhosis and their effects on portal hemodynamics. 212 49

The pathophysiology and treatment of esophageal varices are reviewed. The cause of esophageal varices is generally thought to be portal hypertension. The most common cause of portal hypertension in the United States is alcoholic liver disease. Other etiologies of portal hypertension include portal vein thrombosis, schistosomiasis, and inferior vena caval obstruction by tumor or thrombus. Although short-term balloon tamponade and vasopressin infusion will control acute variceal hemorrhage, they do not affect the underlying problem and are not indicated for long-term treatment of esophageal varices. Surgical procedures either ablate varices or lower portal vein pressure. Portal-systemic shunts have emerged as the preferred surgical technique, but the superiority of total versus selective shunts is unclear. Pharmacological management can include administration of vasopressin, somatostatin, verapamil, or isosorbide dinitrate for short-term treatment or verapamil, isosorbide dinitrate, or propranolol for prolonged treatment. Use of sclerotherapy for treatment and prevention of hemorrhage from esophageal varices has grown recently. Because there are several sclerosing agents and combinations of agents available for use, assessing their relative safety and efficacy is difficult. Innovative approaches to management of varices include a shunt procedure involving the left lung, use of a tissue adhesive, and laser treatment. Because of its effectiveness and ease of administration, sclerotherapy appears to be a rational method of treatment for acute hemorrhage from esophageal varices.
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PMID:Treatment of esophageal varices. 264 81


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