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)

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

The use of norepinephrine, and probably vasopressor therapy in general, in intensive care patients with hypotensive vasodilatation despite fluid resuscitation and evidence of acute kidney injury remains the subject of much debate and controversy. Although there is concern about the use of these drugs, these concerns are unfounded. At this time, the experimental and human data strongly suggest that, in these patients, vasopressor therapy is safe and probably beneficial from a renal, and probably general, point of view. On the basis of currently available evidence, in hypotensive vasodilated patients with acute kidney injury, restoration of blood pressure within autoregulatory values should occur promptly with noradrenaline and be sustained until such vasodilatation dissipates. The additional role of other vasopressors in these situations remains unclear. The addition of vasopressin may be helpful in individual patients, but widespread use is not supported by evidence. Alpha-dose dopamine has no advantages over noradrenaline and is not as reliably effective in restoring blood pressure and urine output. Its widespread use cannot be supported in patients with vasodilatation and acute kidney injury. Other vasopressor drugs such as epinephrine and phenylephrine may be similar in efficacy to noradrenaline. However, experience and available data with their use is vastly less than with noradrenaline. Adrenaline, in addition, is associated with hyperglycemia, hyperlactatemia, acidosis, and hypokalemia. Terlipressin appears useful in patients with acute kidney injury secondary to hepatorenal syndrome. Whether it is superior to noradrenaline in this setting remains uncertain, and more studies are needed before recommendations can be made.
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PMID:Vasoactive drugs and acute kidney injury. 1881 15

Terlipressin is a synthetic analogue of vasopressin, which has been used in the treatment of acute variceal hemorrhage. In contrast to vasopressin, terlipressin can be administered as intermittent injections instead of continuous intravenous infusion. Thus, it has a less adverse reaction than vasopressin. We report a case of ischemic skin complication in a cirrhotic patient treated with terlipressin. A 71-year-old man with liver cirrhosis was admitted because of hematemesis and melena. He was commenced on terlipressin at a dose 1 mg every 6 hours for the treatment of varicieal bleeding. After 36 hours of treatment, skin blistering and ecchymosis was noted on the skin of his upper thigh, scrotal area and trunk. We found that terlipressin was a possible cause of ischemic skin complication based on the skin biopsy finding. Terlipressin may induce a complication of the ischemic event. In spite of rarity, special attention needs to paid on the peripheral ischemic complication of terlipressin.
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PMID:[A case of ischemic skin necrosis after glypressin therapy in liver cirrhosis]. 1860 41

Terlipressin is an analog of the natural hormone arginine-vasopressin. It is used in the treatment of patients with cirrhosis and bleeding esophageal varices (BEV) and in patients with hepatorenal syndrome (HRS): two of the most dramatic and feared complications of cirrhosis. Terlipressin exerts its main pharmacological effect through stimulation of vasopressin-1 receptors. These receptors are located in vascular smooth muscle and mediate vasoconstriction. In patients with cirrhosis and portal hypertension, treatment with terlipressin increases mean arterial pressure and decreases portal flow and pressure within minutes of administration. Furthermore, in patients with ascites terlipressin improves glomerular filtration and excretion of sodium. Terlipressin decreases failure of initial hemostasis by 34%, decreases mortality by 34%, and is considered a first-line treatment for BEV, when available. Terlipressin in combination with albumin reverses type 1 HRS in 33%-60% of cases and is the only treatment with proven efficacy in randomized trials. The safety profile is favorable when considering the clinical efficacy and the high mortality of these clinical entities. Adverse events are mostly cardiovascular and related to vasoconstriction. Mortality and withdrawal of terlipressin due to adverse events occurs in less than 1% of cases. Mild adverse events related to terlipressin treatment occur in 10%-20% of patients. The benefit, however, of terlipressin on long-term survival in HRS remains to be determined. At present, treatment with terlipressin and albumin is considered the most efficient therapy and should therefore be recommended for the treatment of type 1 HRS-1.
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PMID:Efficacy and safety of terlipressin in cirrhotic patients with variceal bleeding or hepatorenal syndrome. 1901 83

Terlipressin, a vasopressin agonist, is a commonly used drug with different indications, particularly in patients with end-stage liver disease. As a V(1) receptor agonist, it increases systemic vascular resistance, particularly in the splanchnic area, resulting in a decrease of portal pressure. Besides the approved use for variceal bleeding, terlipressin also has beneficial effects in the treatment of hepatorenal syndrome and norepinephrine-resistant septic shock. In patients with cirrhosis and variceal bleeding, the use of terlipressin reduces the portal vein pressure and decreases the pressure in esophageal varices. This can save lives when skilled endoscopists are not immediately available. Hepatorenal syndrome is associated with vasodilation in the mesenteric circulation with arterial underfilling and consecutive renal vasoconstriction. Restoration of an effective arterial blood volume can be achieved by the combination of terlipressin and volume expansion. In some cases, a success rate of up to 75% is reported. The early use of terlipressin in catecholamine-resistant shock can improve organ perfusion.
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PMID:Pharmacology, clinical efficacy and safety of terlipressin in esophageal varices bleeding, septic shock and hepatorenal syndrome. 1907 11

Terlipressin is a splanchnic constrictor that is used to control variceal bleeding and is considered to have a very good safety profile compared to vasopressin. However, side effects such as hyponatremia and seizure, although very rare, can occur. Recently, the authors have experienced a case of hyponatremia induced by infusion of terlipressin which resulted in generalized seizure. On admission, the patient's sodium level was 141 mmol/l but, 4 days after the initiation of terlipressin, it plummeted to 114 mmol/l, with serum osmolality also having fallen to 243 mOsm/kg. Hyponatremia could not be corrected despite correction with hypertonic saline but, after withdrawal of terlipressin, the serum sodium level showed a dramatic increase almost to the normal range the following day. Therefore, it is necessary to carefully monitor patients' electrolyte levels during the course of terlipressin therapy.
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PMID:Terlipressin-induced hyponatremic seizure. 2030 35

Hepatorenal syndrome (HRS) is a reversible form of functional renal failure that occurs with advanced hepatic cirrhosis and liver failure. Despite mounting research in HRS, its etiology and medical therapy has not been resolved. HRS encompasses 2 distinct types. Type 1 is characterized by the rapid development of renal failure that occurs within 2 wk and involves a doubling of initial serum creatinine. Type 2 has a more insidious onset and is often associated with ascites. Animal studies have shown that both forms, in particular type 1 HRS, are often precipitated by bacterial infections and circulatory changes. The prognosis for HRS remains very poor. Type 1 and 2 both have an expected survival time of 2 wk and 6 mo, respectively. Progression of liver cirrhosis and the resultant portal hypertension leads to the pooling of blood in the splanchnic vascular bed. The ensuing hyperdynamic circulation causes an ineffective circulatory volume which subsequently activates neurohormonal systems. Primarily the sympathetic nervous system and the renin angiotensin system are activated, which, in the early stages of HRS, maintain adequate circulation. Both advanced cirrhosis and prolonged activation of neurohormonal mechanisms result in fatal complications. Locally produced nitric oxide may have the potential to induce a deleterious vasodilatory effect on the splanchnic circulation. Currently medical therapy is aimed at reducing splanchnic vasodilation to resolve the ineffective circulation and maintain good renal perfusion pressure. Terlipressin, a vasopressin analogue, has shown potential benefit in the treatment of HRS. It prolongs both survival time and has the ability to reverse HRS in the majority of patients. In this review we aim to focus on the pathogenesis of HRS and its treatment with terlipressin vs other drugs.
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PMID:Terlipressin and hepatorenal syndrome: what is important for nephrologists and hepatologists. 2104 48

Hepatorenal syndrome (HRS) is the most frequent life threatening complication of advanced liver failure and cirrhosis. HRS results from a functional renal dysfunction due to circulatory disturbances in patients with advanced liver disease and portal hypertension. Reduction in the effective circulating blood volume and hence hypoperfusion of the kidney is the basic underlying common pathogenetic mechanism for the development of hepatorenal syndrome. The prognosis for HRS remains very poor with types 1 and 2-both having an expected survival time of 2 weeks and 6 months, respectively. Although the available data are derived from studies including a limited number of patients mainly affected by type 1 HRS, vasoconstrictor drugs, in particular the vasopressin analog Terlipressin, seem to be the most effective approach for the management of HRS. Associated with albumin infusion, these drugs have been shown to lead to reduced mortality and improved renal function in HRS. Terlipressin administration significantly increases mean arterial pressure and systemic vascular resistance; while the heart rate, cardiac output, HVPG and portal venous blood flow decrease significantly. This decrease correlates well with the decrease in plasma renin activity. Thus the vasoconstrictor effect of Terlipressin reverses the basic pathology of HRS by reducing the plasma renin activity. The improvement in hemodynamics with Terlipressin is associated with an increase in glomerular filtration rate and deactivation of the vasoconstrictor and sodium-conserving hormones with reduced activity of the RAAS resulting in increased natriuresis. Terlipressin thus reverses HRS and is useful in bridging the patient to liver transplantation and may hence indirectly improve survival. Patients with HRS who show an improvement in renal function with Terlipressin and albumin seem to have an excellent post-transplantation outcome similar to that of patients without HRS. Thus, the use of Terlipressin has been shown to be safe, with minimal side effects that usually disappear after dose reduction, and results in an improved outcome in patients with HRS.
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PMID:Terlipressin in hepatorenal syndrome: Evidence for present indications. 2119 21

This article reviews the role of arginine-vasopressin and the vasopressin analogue terlipressin as potent alternative vasoconstrictors in the treatment of fluid and catecholamine-refractory septic shock. Terlipressin is the most selective, clinically available V1 receptor agonist, and may be more potent than arginine-vasopressin in restoring catecholamine refractory septic shock. Recent experimental and clinical studies on terlipressin, as well as the possible benefit of selective V1a receptor agonists, are discussed.
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PMID:Vasopressin analogues and V1a receptor agonists in septic shock. 2131 51

Safety in the use of small volumes of hypertonic saline solution for hypovolaemic shock and in the treatment of intracranial hypertension has been demonstrated in studies in the field of resuscitation. There is little experience of this for septic shock in humans. Beneficial immunomodulatory effects have been detected in pre-clinical studies. Interactions with the pituitary-adrenal axis and with the secretion of anti-diuretic hormone are varied and suggestive, but are not sufficiently understood. On the other hand, vasopressin has cardiovascular, osmoregulatory, and coagulation effects, and also acts on the hypothalamic-pituitary-adrenal axis. There is a relative deficit of vasopressin in septic shock. Its use in these patients does not seem to have any advantages as regards mortality, but may be beneficial in patients at risk from acute renal failure, or those who receive corticosteroids. Terlipressin is a vasopressin analogue that has also been studied. The synergy between vasopressin and hypertonic saline is a hypothesis that is mainly supported in pre-clinical studies. The use of hypertonic saline solution in septic shock, although promising, is still experimental, and must be restricted to the field of controlled clinical trials.
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PMID:[Septic shock. Update of treatment using hypertonic saline and antidiuretic hormone-vasopressin]. 2277 Jul 59


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