Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Gastrointestinal bleeding is a frequent and severe complication of portal hypertension. The most frequent cause of the bleeding is variceal rupture. Despite improvements in prognosis after variceal bleeding over the past two decades, the 6-week mortality rate remains high, ranging from 15 to 30%. Patients die from uncontrolled bleeding, early rebleeding, infection, or renal failure within the first weeks of a bleeding episode. Poor hepatic function, severe portal hypertension with a hepatic venous pressure gradient (HVPG) >20 mmHg, and active bleeding at endoscopy are independently associated with poor prognosis. First-line treatment includes resuscitation, prophylactic antibiotic therapy, the combined use of vasoactive drugs (started as soon as possible), and an endoscopic procedure. Reconstitution of blood volume should be done cautiously to maintain the haematocrit between 25 and 30%. Terlipressin, somatostatin, or octreotide can be used, and drug therapy is maintained from 48 h to 5 days. Ligation is the endoscopic treatment of choice in bleeding oesophageal varices; in gastric varices, obturation with cyanoacrylate is preferable. Uncontrolled bleeding should be an indication for a salvage transjugular portosystemic shunt (TIPS). In patients with Child-Pugh score A, shunt surgery might be an alternative to TIPS. Trials are currently ongoing into the precise indications of early TIPS in selected patients with an HVPG >20 mmHg, and into the usefulness of administration of recombinant activated factor VII when there is an active bleeding at endoscopy.
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PMID:Management of acute bleeding from portal hypertension. 1722 94

Portal hypertension leads to special complications, which tend to progression. Increase in the size of varices, and variceal-wall tension may cause life-threatening bleeding, which affects mortality. Therefore the reduction of portal hypertension is essential. For prevention of the first bleeding (primary prevention) beta-blockers must be given. For estimation of the effectiveness of this drug, patients should be followed. In case of inefficiency or intolerability variceal ligation or sclerotherapy can prevent bleeding. In case of acute variceal hemorrhage, hemodynamic stabilization of the patient is the first step. Transfusion if necessary, somatostatin or terlipressin should be given for reduction of portal hypertension and also endoscopic treatment of varices is mandatory. Early antibiotic administration for prophylaxis or treatment of infections is associated with a significant reduction in mortality. Up to now in absence of exact data, correction of haemostasis is suggested by the administration of fresh frozen plasma. For secondary prevention i. e. to prevent repeated bleeding beta-blockers (probably with nitrates) can be used. If necessary, drug administration should be complemented with varix ligation or sclerotherapy. In case of inefficiency TIPS implantation or liver transplantation must be considered.
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PMID:[Prevention and treatment of esophageal variceal bleeding]. 1737 64

Variceal bleeding in liver cirrhosis is a medical emergency with a high mortality. The therapeutic options in patients with portal hypertension are: treatment of acute bleeding from varices, prevention of the first bleeding episode and prevention of rebleeding. Treatment of acute bleeding from varices includes: blood volume restitution, use of antibiotics for preventing bacterial infections, vasoactive drug therapy (terlipressin, somatostatin, vapreotide, octreotide), endoscopic band ligation for acute esophageal bleeding and endoscopic therapy with tissue adhesive (cyanoacrylate) for acute gastric variceal bleeding. Endoscopic treatments are best used in association with pharmacological therapy. In primary prophylaxis non-selective beta- blocker therapy and endoscopic band ligation are useful. Beta blockers, band ligation or both should be used for prevention of recurrent bleeding. In patients who fail endoscopic and pharmacological treatment for prevention of rebleeding TIPS and transplantation should be considered.
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PMID:[Variceal upper digestive bleeding--an ever new complication in liver cirrhosis]. 1759 42

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are two distinct gastric mucosal lesions that may cause acute and/or chronic upper gastrointestinal hemorrhage in patients with cirrhosis. Whereas PHG is associated with portal hypertension, GAVE may present in patients without portal hypertension or liver disease. Diagnosis is made upon visualization of the characteristic lesions with upper gastrointestinal endoscopy, although the differential may be difficult at times. PHG is characterized endoscopically by a mosaic pattern with or without red signs and a proximal distribution. PHG mainly causes chronic blood loss and anemia in patients with cirrhosis but also can cause acute hemorrhage. First-line therapy for chronic hemorrhage from PHG is a nonselective beta-blocker (propranolol or nadolol) and iron supplementation. If bleeding/anemia are not controlled with these measures and the patient is transfusion-dependent, shunt therapy (transjugular intrahepatic portosystemic shunt or shunt surgery) should be considered. Management of acute bleeding from PHG, an infrequent event, should be accomplished with a vasoactive drug, somatostatin (or its analogues) or terlipressin. If bleeding responds, the patient must be switched to a nonselective beta-blocker. Shunt therapy should be considered in patients who rebleed or continue to bleed despite adequate beta-blocker therapy. GAVE is less common than PHG. It is characterized by red spots without a background mosaic pattern, typically in the gastric antrum. When lesions have a linear distribution, the lesion is called "watermelon stomach." GAVE is a cause of chronic gastrointestinal bleeding and anemia in patients with cirrhosis. If lesions are localized, first-line therapy is argon plasma coagulation. In more diffuse lesions, therapy with argon plasma coagulation is more complicated. Preliminary data suggest that cryotherapy may be a reasonable option for diffuse GAVE lesions. Neither beta-blockers nor TIPS reduces the bleeding risk in patients with GAVE and thus should not be used in this setting.
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PMID:Treatment of gastropathy and gastric antral vascular ectasia in patients with portal hypertension. 1822 9

Variceal bleeding is one of the most severe complications of portal hypertension related to liver cirrhosis. Primary prophylaxis is considered mandatory in patients with cirrhosis and high-risk oesophageal varices, and once varices have bled, every effort should be made to arrest the haemorrhage and prevent further bleeding episodes. In acute variceal bleeding, vasoactive drugs that lower portal pressure should be started even before endoscopy, and should be maintained for up to 5 days. The choice of vasoactive drug should be made according to local resources. Terlipressin, somatostatin and octreotide can be used; vasopressin plus transdermal nitroglycerin may be used if no other drug is available. In variceal bleeding, antibiotic therapy is also mandatory. In primary and secondary prophylaxis, beta-blockers are the mainstay of therapy. In secondary prophylaxis (but not in primary prophylaxis) these drugs can be combined with organic nitrates.
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PMID:Acute variceal bleeding: pharmacological treatment and primary/secondary prophylaxis. 1834 84

To clarify the effects of long-term ocreotide (a long-acting somatostatin analogue) treatment on mucosal changes in a rat model of portal hypertensive enteropathy, groups of male Swiss albino rats (n=15 each) were randomly assigned to one of three treatment arms. These were: sham laparotomy+twice daily subcutaneous saline 0.5 mL (Group 1); portal hypertension induction+twice daily subcutaneous saline 0.5 mL (Group 2); and portal hypertension induction+subcutaneous ocreotide 100 microg/kg/12h (Group 3). After 12 weeks of treatment, jejunal and ileal tissue specimens were obtained and evaluated histopathologically (villus/crypt ratio, mean diameter of dilated vessels, mucosal edema, and fibromuscular proliferation in the lamina propria) and immunohistochemically (vascular endothelial growth factor (VEGF), von Willebrand factor (F8), and cluster of differentiation 34 (CD34) labelling). In jejunal specimens, the villus/crypt ratio was markedly lower in Group 2 (2.38+/-0.46 microm) than in Group 1 (5.07+/-2.25 microm) or Group 3 (4.97+/-2.19 microm); mean diameter of dilated vessels was markedly higher in Group 2 (43.30+/-5.71 microm) than in Group 1 (33.53+/-4.00 microm) or Group 3 (36.76+/-3.96 microm); mucosal edema and fibromuscular proliferation were universally absent in Group 1 when compared with the other groups. There were statistically significant differences (p<0.05) between Groups 1 and 2 for villus/crypt ratio, mean diameter of dilated vessels, VEGF immunolabelling intensity, and CD34 immunolabelling intensity; between Groups 1 and 3 for mean diameter of dilated vessels, VEGF immunolabelling intensity, and CD34 immunolabelling intensity; and between Groups 2 and 3 for villus/crypt ratio, mean diameter of dilated vessels, and VEGF immunolabelling intensity. In ileal tissue specimens, the villus/crypt ratio was markedly lower in Group 2 (5.51+/-0.67 microm) than in either Group 1 (7.19+/-2.18 microm) or Group 3 (7.62+/-2.58 microm); mean diameter of dilated vessels was markedly higher in Group 2 (46.36+/-4.77 microm) than in either Group 1 (36.43+/-4.57 microm) or Group 3 (41.31+/-4.70 microm); while mucosal edema was absent in Group 1, it was present in Group 2 and Group 3; and fibromuscular proliferation was universally absent. There were statistically significant differences (p<0.05) between Groups 1 and 2 for villus/crypt ratio and mean diameter of dilated vessels; between Groups 1 and 3 for mean diameter of dilated vessels; and between Groups 2 and 3 for villus/crypt ratio, mean diameter of dilated vessels, and VEGF immunolabelling intensity. Together, these findings indicate that ocreotide treatment ameliorates histomorphological changes in a rat model of portal hypertensive enteropathy.
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PMID:Effects of ocreotide on intestinal mucosa in rats with portal hypertensive enteropathy. 1855 88

Oesophageal varices and ascites may develop when the hepatic venous pressure gradient (HVPG) increases above 10 mmHg, and variceal bleeding may occur when the HVPG rises above 12 mmHg. Pharmacological therapy of portal hypertension may prevent bleeding by reducing the HVPG below 12 mmHg. Even if this threshold level is not reached, the risk of bleeding decreases markedly with reductions in HVPG that are >20% from baseline.Endoscopic therapy is a local treatment that prevents bleeding by obliterating the varices, and has no effect on the pathophysiological mechanisms that lead to portal hypertension and variceal rupture. When used together, both pharmacological and endoscopic therapies may have an additive effect, which has been demonstrated in different clinical settings. In acute oesophageal variceal bleeding, vasoactive drugs (either terlipressin or somatostatin) should be started as soon as possible (before diagnostic endoscopy) and maintained for 2-5 days. The efficacy of pharmacotherapy is improved with the addition of emergency endoscopic therapy. Adding endoscopic variceal ligation (EVL) improves the efficacy and safety achieved with the combination of emergency sclerotherapy and vasoactive drugs. Antibacterial prophylaxis should be an integral part of therapy in acute bleeding.To prevent rebleeding, both EVL and the combination of beta-adrenoceptor antagonists (beta-blockers) and isosorbide mononitrate (ISMN) may be a valid first-line choice. Adding beta-blockers improves the efficacy of EVL alone. Haemodynamic responders to beta-blockers with or without ISMN (i.e. those with a decrease in HVPG to <12 mmHg or by >20% of baseline) have a reduction in the risk of haemorrhage to below 10% of patients and, consequently, will not need further treatment, while rescue therapies should be provided to nonresponders. Transjugular intrahepatic portosystemic shunts are the recommended rescue therapy when EVL and/or beta-blockers with or without ISMN fail. beta-Blockers significantly reduce the risk of a first haemorrhage in patients with large varices and improve survival. Compared with beta-blockers, EVL reduces the risk of first bleeding without any differences in mortality and should be offered to patients with large varices who have contraindications or an intolerance to beta-blockers.
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PMID:Variceal bleeding : pharmacological treatment and prophylactic strategies. 1897 95

Variceal bleeding is a life-threatening complication of portal hypertension. The recommended treatment includes the early administration of a vasoactive drug. Vapreotide is a somatostatin analogue with a different receptor affinity to octreotide. It decreases portal pressure and blood flow of collateral circulation in rats with cirrhosis. The pivotal study of early administration of vapreotide in patients with cirrhosis and variceal bleeding has shown a significant improvement in bleeding control and, in the subset of patients with significant bleeding, a significant reduction in mortality. In addition, a meta-analysis of four randomized studies has shown a significant improvement in bleeding control. Vapreotide administrated via the intravenous route is simple to use, with practically no contraindications and few, usually minor, side effects.
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PMID:Vapreotide acetate for the treatment of esophageal variceal bleeding. 1907 53

We report on the efficacy of octreotide acetate in two patients with intestinal phlebectasia and no evidence of portal hypertension or mesenteric thrombosis. Patient 1 was a 46-year-old woman with primary pulmonary arterial hypertension. She required repeated transfusions for recurrent episodes of gastrointestinal bleeding (GIB). Intraoperative enteroscopy revealed wide-spread small bowel phlebectasia and intestinal resection was not performed. Blue rubber-bleb syndrome, portal hypertension and mesenteric thrombosis were ruled out. Octreotide acetate long-acting release was started. A transient interruption in treatment was followed by severe overt GIB. This was effectively controlled with continuous infusion of octreotide acetate. After this episode, octreotide acetate long-acting release was resumed and no further episodes of GIB have been reported until the most recent follow up (total duration of 74 months). Patient 2 was a 51-year-old woman with a history of recurrent GIB requiring multiple blood transfusions since young adulthood with negative endoscopic investigations. An enteroscopy showed numerous submucosal serpiginous varices in the colon and the terminal ileum. All putative causes including portal hypertension or mesenteric thrombosis were ruled out. Monthly intramuscular injections of long-acting octreotide acetate were initiated, and no GIB occurred since then (27 months of follow up). Somatostatin analogues are known to reduce splanchnic blood flow, to increase vascular resistance, to enhance platelet aggregation; and are thus efficacious in preventing GIB secondary to various vascular lesions (portal hypertension, intestinal angiodysplasia and blue rubber-bleb syndrome). These case reports suggest that they are also effective in preventing GIB in intestinal phlebactasia without portal hypertension.
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PMID:Octreotide for recurrent intestinal variceal bleeding in patients without portal hypertension. 1938 Oct 96

We describe a case of obscure gastrointestinal bleeding in a male with noncirrhotic portal hypertension who required multiple admissions and repeated blood transfusions over a 5-month period. Upper and lower gastrointestinal endoscopy failed to establish a cause for bleeding which was eventually ascribed to universal portal hypertensive stigmata in stomach, small bowel and colon, which were not amenable to endoscopic therapy. On account of extensive venous thrombosis, neither surgical shunting nor interventional radiology was an option. Initial management with prothrombotic agents failed. Our patient was successfully stabilized on long-acting somatostatin (SMS) analogue therapy using lanreotide, resulting in avoidance of further admissions and blood transfusion and restoration of his independence and quality of life. The use of short-acting SMS analogues is recognised in acute variceal haemorrhage secondary to portal hypertension in cirrhosis, and long-acting SMS analogue therapy has been described in obscure gastrointestinal bleeding though secondary to angiodysplasia. However, the potential role of long-term SMS analogues in noncirrhotic portal hypertensive bleeding of this type has not been reported earlier. This case supports its use in this scenario in the absence of surgical options and when only palliative approaches are available.
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PMID:Long-acting somatostatin analogue therapy in obscure-overt gastrointestinal bleeding in noncirrhotic portal hypertension: a case report and literature review. 1949 95


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