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)

Early detection of bleeding site by immediate endoscopy is the key of effective treatment in massive upper gastrointestinal (GI) bleeding. Upper GI endoscopy gives useful information about the risk, re-bleeding and mortality. Algorithm of treatment is also based on findings upon early endoscopy. Meta-analysis of prospective, randomized, multicenter clinical trials assessing H2-receptor antagonists and proton pump-inhibitors in the treatment of peptic ulcers suggest that these drugs cannot be justified for stopping bleeding or prevent re-bleeding. Other drugs, such as somatostatin, might be effective, but further studies are needed to prove their effectiveness. Both vasopressin and somatostatin are also successfully employed the treatment of bleeding related to portal hypertension, and a recent meta-analysis found significant benefit for beta-blockade in the prevention of recurrent bleeding. Although beta-blocker therapy does not improve survival, it reduces re-bleeding rate, therefore, it can be used as prophylactic therapy for esophageal varices. As for the treatment of erosions, none of the drugs currently employed are effective in reducing or preventing clinically significant bleeding.
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PMID:[Possibilities of drug therapy of acute hemorrhage of the upper digestive system]. 967 6

Esophageal varices are a life threatening cause of gastrointestinal bleeding. Management includes both primary prevention of variceal bleeding and treatment of actively bleeding varices. Evidence from randomized controlled trials indicates that beta blockers and nitrates may prevent the initial episode of bleeding varices. Ample data from randomized controlled trials indicate that band ligation is more effective than scleropathy for the treatment of bleeding esophageal varices. Somatostatin may decrease rebleeding rates with or without endoscopic therapy. No effective treatment has been developed for the treatment of patients who fail endoscopic therapy.
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PMID:An evidence-based approach to the treatment of esophageal variceal bleeding. 970 Apr 41

The efficacies of somatostatin and octreotide have been widely studied in the control of bleeding from oesophageal varices. It has also been suggested that these drugs may be useful for the control of non-variceal upper gastrointestinal (UGI) bleeding, including that from peptic ulcers. In approximately 80% of patients presenting with non-variceal UGI bleeding, haemorrhage ceases spontaneously and does not recur. However, the remaining 20% of patients require active treatment. Results from recent studies have indicated that somatostatin is an effective treatment for the control of non-variceal UGI bleeding in high-risk patients, i.e. those in whom haemorrhage does not cease spontaneously or is likely to recur. In contrast there is no good evidence available at present to support a role for octreotide in this indication. The efficacy of somatostatin in controlling bleeding in patients with non-variceal UGI bleeding at high risk of mortality upon admission, or rebleeding following endoscopy, coupled with an excellent safety and tolerability profile, suggests that it may be a valuable therapeutic option in the management of non-variceal bleeding.
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PMID:Somatostatin in the treatment of non-variceal upper gastrointestinal bleeding. 1022 37

In patients with cirrhosis, somatostatin or octreotide administration is followed by a transient decrease in the hepatic venous pressure gradient and azygos blood flow. Although no clear-cut changes in variceal pressure are observed and the exact mechanisms of acute hemodynamic changes induced by somatostatin or its derivatives are still unknown, this provided the rationale for its use in patients with variceal hemorrhage. The only known sustained hemodynamic effect of octreotide is to prevent increases in hepatic venous gradient or azygos blood flow in response to food intake. Somatostatin infusion can be as effective as sclerotherapy in the initial control of bleeding esophageal varices in patients with cirrhosis and is associated with fewer complications. Octreotide also seems to be as effective as endoscopic therapy in the control of acute variceal bleeding, although larger studies should be performed before its efficacy and safety profile can be fully evaluated. The combination of somatostatin or long-acting analogues to endoscopic therapy has recently been delineated as one of the most promising approaches in these patients. Early somatostatin administration with repeat boluses, starting several hours before sclerotherapy is combined, eases the endoscopic procedure and reduces bleeding control failure rate. Although two studies also showed that octreotide, when started at the time of sclerotherapy or variceal banding, also improves bleeding control, a conclusion on octreotide use in these patients is premature. Optimal administration schedules and doses of somatostatin or octreotide are still unknown. The safety of octreotide in patients with variceal bleeding, which has recently been challenged, should be assessed in larger trials. Recent data suggesting that octreotide combination to beta-blockers or sclerotherapy may represent a useful approach for long-term prevention of rebleeding in these patients will have to be confirmed.
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PMID:Somatostatin or octreotide in acute variceal bleeding. 1020 29

Somatostatin, a naturally occurring peptide, displays a wide range of biological actions, mainly inhibitory ones, that can make it an appropriate drug for the treatment of a variety of digestive diseases. The marked effect of the peptide on splanchnic hemodynamics together with its inhibitory action on acid-peptic and pancreatic exocrine secretions represent the rationale for the use in upper gastrointestinal (GI) bleeding and surgical conditions of the pancreas. Besides the hemodynamic effects, other pharmacological actions of somatostatin may contribute to its therapeutic efficacy in active variceal bleeding. The peptide indeed increases lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood into the submucous venous plexus of the esophagus and hence into the esophageal varices. Through its inhibitory action on acid-peptic secretion, somatostatin may also inhibit peptic digestion of the clot at the site of hemostasis on the varix itself. In addition, the natural peptide was shown to enhance human platelet aggregation in vitro, whose stimulation can activate the hemostatic process. Since its short half-life makes continuous intravenous infusion mandatory, several long-acting analogs have been synthesized. Amongst the hundreds of cyclic peptides synthesised, octreotide (which binds mainly to SSTR-2 and SSTR-5 receptor subtypes) has been the most extensively investigated. A thorough analysis of the pharmacological activities and therapeutic efficacy of the native somatostatin and the synthetic analogs reveals that the biological actions of these peptides are not always identical. These differences appear to be related to the different affinities of the natural hormone and synthetic derivatives for the different receptor subtypes. The fading of the pharmacological effect, which has yet been observed only with analogs, has never been reported with the natural peptide and may be due to down-regulation of specific receptor subtypes. The safety profile of both natural somatostatin and synthetic analogs is today well established. Most adverse reactions to these peptides are merely a consequence of their pharmacological activity and consist mainly of gastrointestinal complaints and effects on glucose metabolism. They are often of little clinical relevance, especially in the short term. Native somatostatin and its synthetic analogs are therefore safe and effective drugs for the treatment of a variety of GI disorders. While the native peptide is the drug of choice in the acute hospital setting, the synthetic derivatives are better indicated, on outpatient basis, for the long-term management of chronic conditions.
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PMID:Somatostatin for upper gastrointestinal hemorrhage and pancreatic surgery. A review of its pharmacology and safety. 1056 84

The efficacy of somatostatin and octreotide have been widely studied in the control of bleeding from oesophageal varices. It has also been suggested that these drugs may be useful for the control of non-variceal upper gastrointestinal (UGI) bleeding, including that from peptic ulcers. In approximately 80% of patients presenting with non-variceal UGI bleeding, haemorrhage ceases spontaneously and does not recur. However, the remaining 20% of patients require active treatment. Results from recent studies have indicated that somatostatin is an effective treatment for the control of non-variceal UGI bleeding in high-risk patients, i.e. those in whom haemorrhage does not cease spontaneously or is likely to recur. In contrast there is no good evidence available at present to support a role for octreotide, histamine (H(2) antagonists) or proton pump inhibitors in this indication. The efficacy of somatostatin in controlling bleeding in patients with non-variceal UGI bleeding at high risk of mortality upon admission, or rebleeding following endoscopy, coupled with an excellent safety and tolerability profile, suggests it may be a valuable therapeutic option in the management of non-variceal bleeding.
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PMID:Drug therapy for non-variceal upper gastrointestinal bleeding. Assessment of options. 1056 88

Endoscopic treatments for bleeding gastroesophageal varices include injection sclerotherapy, variceal obturation with tissue adhesives, and variceal rubber band ligation. Acute injection sclerotherapy remains a quick and simple technique for the control of active bleeding from esophageal varices. Although few trials have been published so far, some evidence suggests that the early administration of vasoactive drugs (somatostatin, octreotide, or terlipressin) is safe and may increase the efficacy of endoscopic treatments. Banding ligation is the optimal endoscopic treatment for the prevention of rebleeding from esophageal varices. The use of tissue adhesives and thrombin as injectates to treat bleeding fundal gastric varices and esophageal varices not responding to vasoactive drugs or sclerotherapy is promising but needs further assessment by means of randomized controlled trials. As of today, endoscopic treatments are not recommended for the primary prophylaxis of variceal bleeding.
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PMID:Endoscopic treatments for portal hypertension. 1064 28

Increased resistance to portal blood flow is the primary factor in the pathophysiology of portal hypertension, and is mainly determined by the morphological changes occurring in chronic liver diseases. This is aggravated by a dynamic component, due to the active-reversible- contraction of different elements of the porto-hepatic bed. A decreased synthesis of NO in the intrahepatic circulation is the main determinant of this dynamic component. This provides a rationale for the use of vasodilators to reduce intrahepatic resistance and portal pressure. Another factor contributing to aggravate the portal hypertension is a significant increase in portal blood flow, caused by arteriolar splanchnic vasodilation and hyperkinetic circulation. Splanchnic arteriolar vasodilation is a multifactorial phenomenon, which may involve local (endothelial) mechanisms as well as neurogenic and humoral pathways. Most pharmacological treatments have been aimed at correcting the increased portal blood inflow by the use of splanchnic vasoconstrictors, such as beta-blockers, vasopressin derivatives and somatostatin. Several studies have demonstrated that changes in the hepatic venous pressure gradient (HVPG) during maintenance therapy are useful to identify those patients who are going to have a variceal bleeding or rebleeding. The wide individual variation in the HVPG response to pharmacological treatment makes it desirable to schedule follow-up measurements of HVPG during pharmacological therapy. A priority for research in the forthcoming years is to develop accurate non-invasive methods to assess prognosis, which can be used to substitute or as surrogate indicators of the HVPG response. In the clinical management of portal hypertension, beta-blockers are at present the only accepted treatment for the prevention of variceal bleeding. Whether the association of isosorbide-5-mononitrate will improve the high efficacy of beta-blockers is questionable. The efficacy of more aggressive techniques, such as endoscopic band ligation, should be further tested against beta-blockers in patients with a high risk of bleeding. In the treatment of acute variceal bleeding, administration of somatostatin or terlipressin is an established therapy. It may be used alone or, preferably, as an initial treatment before sclerotherapy or endoscopic band ligation. No more than two sessions of endoscopic treatment should be used to control the bleeding. If the bleeding is not easily controlled, other alternatives such as transjugular intrahepatic portosystemic shunts (TIPS) or derivative surgery should be considered, the former being the best in patients with poor liver function. Recent studies suggest that early measurement of HVPG during variceal bleeding may be used as a guide for therapeutic decisions in the treatment of patients with acute variceal bleeding. Those patients with a high HVPG have a high risk of poor evolution, and may be candidates for more intensive and aggressive therapy, such as surgery or TIPS. Those with lower HVPG have a very high probability of an uneventful evolution, and may thus be managed more conservatively using medical and endoscopic treatments. Pharmacological agents (propranolol or nadolol), endoscopic treatment (preferably banding ligation) or surgery can be used to prevent rebleeding. A pending task for the new millennium is to assess whether the early treatment of asymptomatic, compensated cirrhotic patients with portal pressure reducing agents can prevent the development of esophageal varices and of other complications of portal hypertension.
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PMID:Complications of cirrhosis. I. Portal hypertension. 1072 1

The aim of this study was to compare the efficacy of somatostatin versus endoscopic sclerotherapy in the management of digestive bleeding caused by rupture of esophageal varices. Forty patients were evaluated; 21 were randomly assigned to receive somatostatin (initial 250 micrograms followed by a 48-hour continuous infusion of 250 micrograms/h and 250 micrograms 6/6 h bolus in the first 24 hours) and 19 to receive endoscopic sclerotherapy with ethanolamine oleate 5%. The patients were evaluated after 48 hours and after 7 days of treatment. Both groups of patients were similar in sex, age, gravity of the hemorrhage and liver dysfunction. Therapeutic failure occurred in 26.3% and 35.7% in the group of endoscopic sclerotherapy (48 h and 7 days respectively), and in 23.8% and 21.4% in the group of somatostatin. The need of blood transfusion (3.38 U in the group of endoscopic sclerotherapy and 2.42 U in the group of somatostatin) and the mortality rate (31.6% in the group of endoscopic sclerotherapy and 28.6% in the group of somatostatin) were also similar (P > 0.05). The authors conclude that somatostatin is as effective as endoscopic sclerotherapy and that it should be considered in the treatment of acute esophageal variceal bleeding.
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PMID:[Sclerotherapy versus somatostatin in the treatment of upper digestive hemorrhage caused by rupture of esophageal varices]. 1124 56

In the primary prevention of variceal hemorrhage, beta-blockers continue to be the first-line treatment. Newer nonselective beta-blockers with anti-alpha1-adrenergic activity, such as carvedilol, appear to have a better impact on reducing the hepatic venous pressure gradient than propranolol. The addition of isosorbide mononitrate appears to improve the effectiveness of beta-blockers in primary prophylaxis, but not that of somatostatin in the treatment of acute variceal hemorrhage. The use of vasoactive drugs alone in acute variceal bleeding has not proved to be more effective than endoscopic treatment. The advent of endoscopic variceal ligation (EVL) has strengthened the role of endoscopy in the management of bleeding esophageal varices. EVL has improved the results, particularly in terms of lowering the treatment-related morbidity, compared with endoscopic variceal sclerotherapy (EVS). However, the variceal recurrence rate after initial eradication with EVL is relatively high. In contrast to synchronous combined therapy with EVL plus EVS, metachronous combination of EVL and low-dose EVS may improve the results of EVL alone. For bleeding fundic varices, obliteration using cyanoacrylate is currently the treatment of choice. Endosonography (EUS) is coming into more widespread use in the assessment of variceal eradication and in further attempts to improve the results of endoscopic injection therapy. According to two meta-analysis studies, transjugular intrahepatic portosystemic shunt (TIPS) is not yet capable of replacing endoscopic treatment in the secondary prevention of variceal bleeding.
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PMID:Variceal bleeding and portal hypertension: still a therapeutic challenge? 1127 15


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