Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years the technique of selective portasystemic shunting (Warren procedure) and sclerotherapy, and also the possibility of lowering portal pressure with beta-blockers, have changed the approach to management of patients with bleeding esophageal varices. Treatment of these patients is reviewed in the light of experience of 204 cases and the literature. The advantages and disadvantages of vasopressin, balloon tamponade, sclerotherapy, transhepatic embolization and various shunt and non-shunt operations in the acute phase are presented. For elective cases the discussion centers mainly on treatment by distal splenorenal shunt and sclerotherapy.
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PMID:[Therapy of bleeding esophageal varices. Attempt at a position statement]. 352 44

Intravenous vasopressin is a commonly used modality for control of bleeding esophageal varices. The development of ischemic cutaneous complications is a recently described entity. In previous reports, cutaneous necrosis has occurred at sites of extravasation, at or proximal to intravenous catheter sites, or at isolated pressure points. We review the literature on vasopressin-induced cutaneous reactions and report a case of cutaneous necrosis and bulla formation in which multiple bullae formed during vasopressin therapy at sites distant from direct intravenous flow.
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PMID:Vasopressin-induced bullous disease and cutaneous necrosis. 352 22

Bleeding from esophageal varices remains a difficult clinical problem, carrying a high likelihood both of rebleeding and of mortality. The initial approach requires adequate but not overly vigorous volume replacement with blood and other fluids. Once the patient is resuscitated, upper gastrointestinal endoscopy should be performed to establish the source of bleeding. Both endoscopic variceal sclerotherapy and balloon tamponade appear to be effective in achieving temporary control of acute ongoing hemorrhage from esophageal varices. The value of intravenous vasopressin remains controversial. Rebleeding can be prevented in most patients by shunt surgery. However, surgery carries both considerable early morbidity and mortality (related mainly to the severity of the underlying liver disease) and substantial longer-term morbidity and mortality from hepatic encephalopathy and liver failure. The role of pharmacologic agents (eg, propranolol) intended to prevent variceal hemorrhage by reducing portal pressure remains to be established. At present, we recommend use of endoscopic variceal sclerotherapy for the control of active variceal bleeding, with employment of balloon tamponade and intravenous vasopressin if sclerotherapy is successful. Emergency shunt surgery should be reserved only for those patients whose bleeding cannot be controlled by these other means. For prevention of rebleeding in Child class C patients, we attempt to obliterate the varices by repeated endoscopic sclerotherapy. Patients who have two to three episodes of rebleeding despite this approach are considered for shunt surgery. For better-risk patients who do not have ascites, which is difficult to control, we are currently recommending a distal splenorenal shunt. Alternatively, repeated endoscopic variceal sclerotherapy is used for these better-risk patients (Child class A or B) in some centers, with shunt surgery reserved for patients who continue to rebleed. Which approach to preventing rebleeding in the better-risk patient is more effective, as well as the role of pharmacologic therapy with propranolol or other agents, remains to be settled by well-controlled randomized clinical trials.
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PMID:Management of the patient with hemorrhaging esophageal varices. 352 43

Acute injection sclerotherapy has been used in Belfast for 25 years and the results are reviewed. During this period 264 patients had injection sclerotherapy for acute bleeding from oesophageal varices during 396 admissions; a rigid oesophagoscope was used and 447 injections were performed. The series includes 19 children who received 69 injections. Thirty-eight had extrahepatic portal venous hypertension and the remainder had intrahepatic disease. Overall, 81 were Child's grade A (including the 38 extrahepatics), 82 were grade B and 101 were grade C. Of the 396 admissions, acute injection sclerotherapy controlled bleeding in 362 instances (control rate 91.4 per cent); control rate in the children's group was 97.1 per cent and in the adults 90.2 per cent. The hospital mortality was 14.9 per cent (57 adults and 2 children). Nineteen deaths were due directly to bleeding oesophageal varices, two from bleeding gastric varices and seven directly or indirectly from oesophageal leaks. Most of the remaining deaths were due to liver failure. We consider that sclerotherapy is valuable in the control of variceal haemorrhage where bleeding is uncontrolled or recurs after vasopressin or tamponade in any admission.
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PMID:Twenty-five years of injection sclerotherapy for bleeding varices. 387 51

A patient bleeding from oesophageal varices in whom injection sclerotherapy failed to control bleeding required peripheral vein vasopressin infusion for a total of five days. Three days after stopping the infusion she collapsed and died. Post mortem examination showed the cause of death to be intestinal infarction resulting from superior mesenteric and portal vein thrombosis. This complication has not previously been described in association with vasopressin infusion into peripheral veins. The duration of each infusion should be minimised and blood volume should be carefully monitored throughout. The condition should be suspected in patients who develop unexplained abdominal pain or collapse following vasopressin treatment.
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PMID:A lethal complication of peripheral vein vasopressin infusion. 387 20

Liver blood flow (xenon-133 clearance method) and portal venous flow were measured in cirrhotic and non cirrhotic rats following the infusion of vasopressin at varying rates. At low rates of infusion, vasopressin had no significant effect on portal venous flow or liver blood flow in cirrhotic or non-cirrhotic rats. Infusion of vasopressin at a rate of 0.08 microU/g body wt/min in non-cirrhotic rats and 0.04 and 0.08 microU/g body wt/min in cirrhotic rats decreased portal venous flow and increased liver blood flow. At higher rates of infusion (0.2 microU/g body wt/min in non-cirrhotic rats and 0.16 microU/g body wt/min in cirrhotic rats) these effects were reversed. Furthermore, an infusion of 0.08 microU/g body wt/min vasopressin significantly reduced portal pressure in the cirrhotic rat. However, portal pressure was not significantly altered following an infusion of 0.16 microU/g body wt vasopressin. The implications of these findings in relation to the possible deleterious effects of high rates of vasopressin infusion in the management of portal hypertension and bleeding oesophageal varices is discussed.
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PMID:The effects of vasopressin on hepatic haemodynamics in the cirrhotic and non-cirrhotic rat. 404 83

Seventeen patients bleeding from oesophageal varices were treated by continuous infusion of vasopressin through a catheter inserted percutaneously and positioned in the superior mesenteric artery and in two other patients catheterization proved technically impossible. Bleeding was completely controlled on only four out of 18 occasions in the 17 patients treated. In seven patients, bleeding was controlled for two or more days but then recurred although the infusion was continued with an increased dose of vasopressin. There was a high incidence of complications, including bleeding from the site of catheter insertion in the groin and septicaemias. Sengstaken balloon tamponade and oesophageal transection had to be used to control bleeding in some patients but only six out of 17 survived to leave hospital.
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PMID:Treatment of bleeding oesophageal varices by infusion of vasopressin into the superior mesenteric artery. 454 Feb 94

In a randomised controlled trial the effect of intermittent bolus injection of triglycyl lysine vasopressin (terlipressin 'Glypressin') (2 mg that 6-hourly), an analogue of vasopressin, was compared with that of a constant peripheral intravenous infusion of vasopressin (0.4 units/Min) in the initial management of bleeding oesophageal varices in nineteen patients. Failure of vasopressin therapy was defined as continued bleeding of sufficient severity to necessitate the passage of a Sengstaken tube. Bleeding was controlled in 70% of patients treated with glypressin but in only 9% of patients given vasopressin. The glypressin group required significantly less blood after randomisation than the vasopressin group. Because of its efficacy, lack of side-effects, and ease of administration, glypressin appears to be valuable in the management of bleeding varices.
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PMID:Controlled trial of terlipressin ('Glypressin') versus vasopressin in the early treatment of oesophageal varices. 612 8

Ten patients with portal hypertension and esophageal varices had percutaneous transheptic portography with selective catheterization of the short gastric or left gastric vein. The effect was studied on variceal blood flow after injection of various drugs (vasopressin IV, pentagastrin IV, somatostatin IV, domperidone IV, and methylcholine SC). Vasopressin had no effect on variceal flow; pentagastrin gave a total occlusion of flow in five of nine patients; somatostatin interrupted the flow in one of four patients; domperidone obstructed flow completely in one patient, while another receiving the same dose was unaffected; methylcholine did not affect the flow in three patients examined.
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PMID:Pharmacologic manipulation of lower esophageal sphincter pressure. A possible means of treatment of variceal bleeding. 613 13

Selective catheterization of the left gastric vein was performed after percutaneous transhepatic portography (PTP) in patients with portal hypertension and esophageal varices. Following the hypothesis that drugs increasing the lower esophageal sphincter (LES) pressure may obstruct the variceal blood flow through the lower esophagus, the effect of different drugs (i.e., intravenous injection of vasopressin, pentagastrin, domperidone and somatostatin and subcutaneous injection of metacholine) on the variceal blood flow was examined. Vasopressin did not change the variceal blood flow; pentagastrin, with its known effect of increasing the LES pressure produced a total interruption of the flow in four of eight patients; domperidone, also known to increase the LES pressure obstructed the variceal blood flow in the only patient examined with this drug; somatostatin has no reported action on the LES but blocked the flow in one of two patients; and metacholine, reported to increase the LES pressure did not produce any change in the flow in the three patients examined. LES pressure was recorded before and during vasopressin infusion in seven patients with portal hypertension and esophageal varices. No reaction on the pressure was found. The patient number in the study is small and the results are nonuniform but still they suggest that drugs increasing the LES tonus might be useful to control variceal blood flow.
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PMID:Pharmacologic influence on esophageal varices: a preliminary report. 613 25


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