Hemodynamic Effects of Terlipressin and High Somatostatin Dose during Acute Variceal Bleeding in Nonresponders to the Usual Somatostatin Dose

Villanueva, Càndid; Planella, Montserrat; Aracil, Carles; López-Balaguer, J.M.; González, Begoña; Miñana, Josep; Balanzó, Joaquím

doi:10.1111/j.1572-0241.2004.40665.x

Cited by 53 publications

(29 citation statements)

References 30 publications

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“…That is why it is recommended to start treatment by administering an intravenous bolus (250 mcg), repeated if necessary, followed by the continuous intravenous infusion of 250 mcg/h. A recent study showed that, in patients showing a very scarce response (<10 % fall in portal pressure) to 250 mcg/h of somatostatin, both the infusion of 500 mcg/h of somatostatin or the administration of 1 mg of terlipressin resulted in almost twice the decrease in portal pressure [43]. Moreover, a clinical study demonstrated that in patients actively bleeding at initial endoscopy, the infusion of 500 mcg/h of somatostatin achieved a greater control of hemorrhage, a reduced incidence of early rebleeding, and reduced the mortality at 1 and 6 weeks and the transfusional requirements, as compared with the standard dose of 250 mcg/h [44].…”

Section: Somatostatin and Somatostatin Analoguesmentioning

confidence: 97%

Optimizing General Management of Acute Variceal Bleeding in Cirrhosis

Villanueva

Escorsell

2014

Curr Hepatology Rep

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Section: Somatostatin and Somatostatin Analoguesmentioning

confidence: 97%

Optimizing General Management of Acute Variceal Bleeding in Cirrhosis

Villanueva

Escorsell

2014

Curr Hepatology Rep

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“…This response may improve by doubling the dose of somatostatin or switching to another agent (such as terlipressin). 50 …”

Section: Hvpg Measurements In Acute Variceal Hemorrhagementioning

confidence: 99%

Portal hypertension and variceal bleeding—Unresolved issues. Summary of an American Association for the study of liver diseases and European Association for the study of the liver single-topic conference

2008

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“…However, scant evidence exists that this reduction will affect the risk of a primary bleeding episode in PHG patients [72,103,104,269,270] . Propranolol is recommended regardless of the severity or presence of PHG in patients with esophageal varices because it treats both entities by reducing portal pressure [105][106][107]198,271,272] . Prophylaxis of bleeding from PHG is not recommended [260] .…”

Section: Preventionmentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Hemodynamic Effects of Terlipressin and High Somatostatin Dose during Acute Variceal Bleeding in Nonresponders to the Usual Somatostatin Dose

Cited by 53 publications

References 30 publications

Optimizing General Management of Acute Variceal Bleeding in Cirrhosis

Optimizing General Management of Acute Variceal Bleeding in Cirrhosis

Portal hypertension and variceal bleeding—Unresolved issues. Summary of an American Association for the study of liver diseases and European Association for the study of the liver single-topic conference

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

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