Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal hypertensive colopathy (PHC) is a recently described entity in patients with portal hypertension which can cause even life-threatening lower gastrointestinal bleeding. In contrast to variceal bleed, there is no standardized treatment for the control of bleeding from these lesions. We report a case of alcoholic cirrhosis with portal hypertension, in whom bleeding from colonic angiodysplasia-like lesions was effectively controlled by somatostatin infusion.
 ...
PMID:Severe acute bleeding from portal colopathy controlled by somatostatin: a case report. 1568 64

The complications of portal hypertension are totally prevented if hepatic venous pressure gradient is decreased below 12 mm Hg. Besides, if this target is not achieved, a 20% decrease in portal pressure from baseline levels offers an almost total protection from variceal bleeding. This sets the rationale for drug therapy to reduce portal pressure in portal hypertension. Pharmacological therapy to decrease portal pressure includes vasoconstrictors to decrease portal blood inflow, vasodilators to decrease hepatic resistance, and combination therapy. Oral agents, such as beta-adrenergic blockers and organic nitrates, are used for long-term prevention of variceal bleeding, while parenteral agents, such as somatostatin (and analogues) and terlipressin, are used for the treatment of acute variceal bleeding.
 ...
PMID:Variceal bleeding: pharmacological therapy. 1592 Mar 22

Portal hypertension can lead to life-threatening hemorrhage, ascites, and encephalopathy. This paper reviews the pathophysiology and multidisciplinary management of portal hypertension and its complications, including the indications for and techniques of the various surgical shunts. Variceal bleeding is the most dreaded complication of portal hypertension. It may occur once the portal-systemic gradient increases above 12 mm Hg, occurs in 30% of patients with cirrhosis, and carries a 30-day mortality of 20%. Treatment of acute variceal bleeding includes resuscitation followed by upper endoscopy for sclerosis or band ligation of varices, which can control bleeding in up to 85% of patients. Medical therapies such as vasopressin and somatostatin can also be useful adjuncts. Shunt therapy, preferably the placement of a TIPS, is indicated for refractory acute variceal bleeding. Recurrent variceal bleeding is common and is associated with a high mortality. Therapies to prevent recurrent variceal bleeding include chronic endoscopic therapy, nonselective beta-blockade, operative or nonoperative (TIPS) shunts, devascularization operations, and liver transplantation. Recommendations and a treatment algorithm are provided, taking into account both the etiology and the manifestations of portal hypertension.
 ...
PMID:Current management of portal hypertension. 1613 97

Portal hypertension (PHT) is responsible for the more severe and often lethal complications of cirrhosis such as bleeding oesophageal varices, ascites, renal dysfunction and hepatic encephalopathy. Because of the combined impact of these complications, PHT remains the most important cause of morbidity and mortality in patients with cirrhosis. Over the years, it has become clear that a decrease in portal pressure is not only protective against the risk of variceal (re)bleeding but is also associated with a lower long-term risk of developing complications and an improved long-term survival. A milestone in therapy was the introduction of non-selective beta-blockers for the prevention of bleeding and rebleeding of gastro-esophageal varices. However, in practice, less than half the patients under beta-blockade are protected from these risks, supporting the overall demand for innovation and expansion of our therapeutic armamentarium. Recent advances in the knowledge of the pathophysiology of cirrhotic PHT have directed future therapy towards the increased intrahepatic vascular resistance, which, in part, is determined by an increased hepatic vascular tone. This increased vasculogenic component provides the rationale for the potential use of therapies aimed at increasing intrahepatic vasorelaxing capacity via gene therapy, liver-selective nitric oxide donors and statines on the one hand, and at antagonizing excessive intrahepatic vasoconstrictor force through the use of endothelin antagonists, angiotensin blockers, alpha(1) adrenergic antagonists or combined alpha(1)- and non-selective beta-blockers or somatostatin analogues on the other. The focus of this review is to give an update on the pathophysiology of PHT in order to elucidate these potential novel strategies subsequently.
 ...
PMID:Portal hypertension: from pathophysiology to clinical practice. 1634 56

Cirrhosis results in portal hypertension in many patients. The major complications of portal hypertension include development of ascites and esophageal or gastric varices. Varices lead to hemorrhage and death in a significant proportion of patients. This review focuses on the pharmacologic approach to management of portal hypertension in patients at risk of variceal hemorrhage, or those who have already had variceal bleeding. Pharmacologic therapy is used for 1) primary prevention of bleeding, 2) management of acute bleeding, and 3) prevention of recurrent bleeding (secondary prophylaxis). For acute esophageal variceal hemorrhage, a variety of pharmacologic agents are used, including somatostatin, octreotide, vapreotide, lanreotide, terlipressin, and vasopressin (with nitrates). For primary and secondary prevention of esophageal variceal hemorrhage, beta-blockers remain the mainstay therapy.
 ...
PMID:Pharmacologic therapy for gastrointestinal bleeding due to portal hypertension and esophageal varices. 1651 29

The major concern of living donor liver transplantation is small-for-size graft injury at the early phase after transplantation. Novel therapeutic strategies should be developed. To investigate the protective effect of somatostatin related to hemodynamic stress on small-for-size liver graft injury, we applied a treatment regimen of low-dose somatostatin in a rat orthotopic liver transplantation model using small-for-size grafts (median, 38.7%; range, 35-42%). Somatostatin was given at 5 minutes before total hepatectomy and immediately after reperfusion in the recipient (20 microg/kg). Graft survival, portal hemodynamics, intragraft gene expression and hepatic ultrastructural changes were compared between the rats with or without somatostatin treatment. Seven-day graft survival rates in the somatostatin treatment group were significantly improved compared to the control group (66.7% vs. 16.7%, P = 0.036). In the treatment group, portal pressure and hepatic surface blood flow were significantly decreased within the first 30 minutes after reperfusion, whereas in the control group, transient portal hypertension and excessive hepatic blood flow were observed. Intragraft expression (both messenger RNA and protein) of endothelin-1 was significantly downregulated accompanied with upregulation of heme oxygenase-1 and A20. Better preservation of liver function was found in the treatment group. Hepatic ultrastructure, especially the integrity of sinusoids, was well protected in the treatment group. In conclusion, low-dose somatostatin rescues small-for-size grafts from acute phase injury in liver transplantation by attenuation of acute-phase shear stress that resulted from transient portal hypertension.
 ...
PMID:Attenuation of acute phase shear stress by somatostatin improves small-for-size liver graft survival. 1655 22

Portal hypertension is a common complication of hepatic cirrhosis, and is responsible for much of the mortality and morbidity associated with advanced liver disease. Esophageal varices are a common occurrence, and esophageal variceal hemorrhage carries a high mortality. Endoscopic therapies have proven effective in treating active bleeding and preventing recurrence, but several pharmacological agents are useful adjuncts to endoscopy in both acute bleeding and in the primary and secondary prophylaxis of variceal hemorrhage. In acute hemorrhage, vasoconstricting agents such as vasopressin, terlipressin, somatostatin, and octreotide have been demonstrated to add benefit to endoscopic therapy. Secondary prophylaxis includes endoscopic therapy to eradicate varices, usually combined with oral beta-blockers. Primary prophylaxis is typically used in patients with medium or large varices, and consists of oral beta-blockers, at times combined with oral nitrates. This paper the reviews the pharmacological principles behind these therapies, and the clinical trial data that has led to their widespread use.
 ...
PMID:Pharmacological therapy for the treatment of esophageal varices. 1655 91

Portal hypertensive gastropathy (PHG) is the term used to describe the endoscopic appearance of gastric mucosa seen in patients with cirrhotic or non-cirrhotic portal hypertension with a characteristic mosaic-like pattern with or without red spots. The prevalence of PHG varies from 50% to 98%, this variation of the prevalence being perhaps related to patient selection, inter- and intra-observer variation and absence of uniform criteria and classification. About 8% of the upper digestive hemorrhages in the cirrhotic patients are secondary to PHG. There is no general consensus on the endoscopic classification of PHG (the most New Italian Endoscopy Club). The exact pathogenesis of PHG is not completely understood, but the portal hypertension is the main factor involved in its development and not the severity of the hepatic disease. Gastric Antral Vascular Ectasia (GAVE) is a term used for the typical endoscopic findings of red stripes, separated by normal mucosa, most frequently seen in the gastric antrum or proximal stomach. Current therapy of PHG includes beta blockers, somatostatin and derivates, endoscopic and surgical methods including hepatic transplantation.
 ...
PMID:Portal hypertensive gastropathy. 1673 61

Oesophageal and fundic varices belong to the most frequent complications of cirrhosis and portal hypertension. Due to their significant morbidity and mortality, bleedings from oesophageal or fundic varices represent a challenge for the emergency medical team as well as for the gastroenterologist. The patient with a variceal bleeding should be accurately monitored and his/her hemodynamic parameters should be maintained stable with the administration of plasma expanders and blood units when indicated. An antibiotic prophylaxis in this setting--norfloxacin or ceftriaxon--has been demonstrated to significantly reduce morbidity and mortality. Additionally, the early administration of vasoactive compounds, such as terlipressin, somatostatin or octreotide, is associated with beneficial effects in reducing the bleeding. An upper gastrointestinal endoscopy should be generally performed within the first twelve hours from the beginning of the bleeding in order to obtain an accurate diagnosis and to provide an adequate treatment. Endoscopic procedures to control the bleeding include the rubber band ligation, the treatment of the varix with a sclerosing agent or the injection of tissue glue into the varix. In case of recurrent bleeding, beyond the above methods, different techniques, such as the transjugular porto-caval shunt, surgical shunt procedures, as well as embolisation of splanchnic blood vessels, represent additional therapeutic options. However, they are associated with very high mortality rates and their indication has to be discussed case by case by an interdisciplinary team of experts. Future therapies include the optimisation and the improvement of the current medical and endoscopic armamentarium, as well as the application of treatments to novel targets, such as the coagulation cascade.
 ...
PMID:[Oesophageal and fundic variceal bleeding]. 1673 87

Hepatic portoenterostomy or Kasai operation has been widely accepted as the standard therapy for biliary atresia. Recently, more female patients have grown up and reached adulthood; therefore, pregnancy in women with biliary atresia is sometimes inevitable. The authors report a 17-year-old woman with biliary atresia post Kasai operation at 3 months of age. After the operation, she became jaundice-free but developed portal hypertension with abnormal liver function. She had several episodes of esophageal variceal bleeding and was treated by beta-blocker and endoscopic sclerotherapy. Since then, she was lost to follow up for nearly 2 years. She came back again with 12 weeks of gestation with no symptoms of gastrointestinal bleeding for antenatal care. At 32 weeks of gestation, she presented with severe hematemesis from variceal bleeding and had thrombocytopenia from hypersplenism. She was treated with somatostatin analogue, fluid and blood component replacement and other supportive treatments. Cesarean section was performed when she was stable at 33 weeks of gestation. After the operation, her clinical status was improved and had no other complications. Her baby experienced complications of prematurity but improved after treatment. Pregnancy may affect the natural course of portal hypertension and worsen the clinical outcome. Pregnancy should be avoided in patients with portal hypertension, however it is not contraindicated. Pregnancy in biliary atresia patients needs intensive prenatal care.
 ...
PMID:Pregnancy in biliary atresia after kasai operation complicated by portal hypertension. 1720 81


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>