Disease relevance of Terlipressin

• Terlipressin in patients with cirrhosis and type 1 hepatorenal syndrome: a retrospective multicenter study [1].
• Terlipressin seems to be an effective rescue therapy, which is able to restore blood pressure in patients with catecholamine-resistant septic shock, without obvious complication [2].
• Terlipressin or somatostatin for acute variceal hemorrhage [3].
• Terlipressin and albumin for the hepatorenal syndrome [4].
• The effect of terlipressin (N-alpha-triglycyl-8-lysine-vasopressin) in bleeding esophageal varices was evaluated in a prospective placebo-controlled study [5].

Psychiatry related information on Terlipressin

• After 5 days of recovery VP was applied (terlipressin 0.1 mg/kg i.p.) The gastric motility was measured by means of balloon introduced into the stomach through the fistula.The gastric electrical and motor activity were recorded by the PowerLab/8SP system and software [6].

High impact information on Terlipressin

• Sclerotherapy was not superior to terlipressin, somatostatin, or octreotide for any outcome and to vasopressin for rebleeding, blood transfusions, death, and adverse events; it was superior to vasopressin for the control of bleeding in a single trial flawed by a potential detection bias [7].
• Terlipressin and albumin for HRS: an advance in therapy [8]?
• Double-blind randomized controlled trial comparing terlipressin and somatostatin for acute variceal hemorrhage. Variceal Bleeding Study Group [9].
• Although terlipressin produces systemic vasoconstriction, it produces cerebral vasodilatation and may increase cerebral blood flow (CBF) [10].
• Worsening of cerebral hyperemia by the administration of terlipressin in acute liver failure with severe encephalopathy [10].

Chemical compound and disease context of Terlipressin

• Thus, the aim of this study was to investigate the effects of terlipressin administration (a vasopressin analog) on in vivo LPS-induced aortic iNOS in rats with cirrhosis [11].
• A randomized trial was undertaken to determine the efficacy of nitroglycerin in addition to terlipressin infusion to improve the control of acute variceal hemorrhage compared with balloon tamponade [12].
• The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome [13].
• BACKGROUND: An enhancement of the haemodynamic effects of terlipressin by octreotide (and vice versa) may be useful in the treatment of portal hypertension [14].
• OBJECTIVE: To compare, in patients with hyperdynamic septic shock, the effects of norepinephrine or terlipressin on hemodynamic variables and renal function [15].

Biological context of Terlipressin

• BACKGROUND & AIMS: Terlipressin and somatostatin decrease portal pressure and have been used to treat variceal hemorrhage, but they have not been adequately compared [9].
• Three patients in the terlipressin group and three in the albumin group developed decreased arterial blood volume [16].
• At 30 min of terlipressin administration, the hepatic venous pressure gradient (1 mg: -16+/-9%, 2 mg: -21+/-11%; p<0.01) and azygos blood flow (1 mg: -19+/-13%, 2 mg: -25+/-17%; p<0.05) were significantly reduced [17].
• At 4 h, neither arterial pressure nor peripheral vascular resistance was significantly modified by either dose of terlipressin [17].
• Octreotide preinfusion significantly increased the responsiveness of arterial pressure and heart rate to terlipressin [18].

Anatomical context of Terlipressin

• In portal vein stenosed rats but not in cirrhotic rats, the addition of terlipressin to propranolol induces acidemia [19].
• In a subgroup of 21 patients, changes in hepatic vein waveform and HVPG were evaluated after intravenous administration of 2 mg of terlipressin [20].
• Fluid challenge significantly (p <.05) increased mesenteric vein blood flow in both the EF and EFT groups, and terlipressin had no detrimental effect on mesenteric blood flow [21].
• Terlipressin significantly (p <.05) increased ileal microcirculation in fluid-challenged endotoxic rats (EF and EFT) but not in hypodynamic endotoxic rats (E and ET) [21].
• Terlipressin restored the hepatic artery buffer response, which led to an increase in hepatic artery flow, ultimately resulting in well-maintained liver oxygen delivery, oxygen uptake, and all other variables of regional metabolism and organ function [22].

Associations of Terlipressin with other chemical compounds

• Bleeding was managed in a standardized protocol using octreotide or terlipressin with sclerotherapy or band ligation for active bleeding at endoscopy [23].
• Forty-seven bleeding episodes in 34 cirrhotic patients were included, with terlipressin plus sublingual nitroglycerin in 23 episodes (group I) and balloon tamponade in 24 episodes (group II) [12].
• As paracentesis induces arteriolar vasodilation which plays a role in the development of decreased effective arterial blood volume, administration of a vasoconstrictor (terlipressin) could prevent circulatory alterations due to paracentesis [16].
• In patients with HRS (n=6) treatment with terlipressin and albumin was associated with a marked improvement in circulatory and renal function and marked suppression of NPY and norepinephrine levels [24].
• Of the available drugs, somatostatin has the least side effects and is as effective as vasopressin, terlipressin and the combination of vasopressin and an organic nitrate vasodilator [25].
• Single variant analysis showed treatment with terlipressin, MELD score, and baseline serum creatinine to be predictive of HRS reversal [26].
• Noradrenaline was less expensive than terlipressin (p<0.05) [27].

Gene context of Terlipressin

• We present the first evidence that this effect of terlipressin may also occur clinically, in a patient with Child-Pugh class C cirrhosis, endotoxaemia, a raised circulating TNF-alpha concentration, and marked systemic vasodilatation with refractory arterial hypotension [28].
• Terlipressin has recently been shown in an animal model of cirrhosis to suppress endotoxin-induced TNF-alpha-mediated upregulation of iNOS, thereby preventing overproduction of nitric oxide and restoring normal vascular tone [28].
• Our findings suggest that terlipressin may be the vasopressor agent of choice in patients with decompensated cirrhosis and provide a rationale for combination terlipressin and MARS therapy when the therapeutic response to either treatment alone is suboptimal [28].
• RESULTS: Success of therapy was similar with terlipressin (80%) and somatostatin (84%) [9].
• Terlipressin (2-20 microg x k(-1)) and arginine vasopressin (3-300 pmol x min(-1) x kg(-1)) dose-dependently reduced, and at the highest doses, even abolished, the difference in mesenteric blood flow (MBF) between PVL and SHAM rats [29].

Analytical, diagnostic and therapeutic context of Terlipressin

• Thirteen patients underwent liver transplantation (92 +/- 95 days after HRS onset), 10 of whom had received terlipressin and had had improved renal function [1].
• 80 were randomized to receive (double-blind) intravenous terlipressin (2 mg/4 h) and 81 to receive somatostatin (continuous infusion of 250 micrograms/h after an intravenous injection of 250 micrograms) [9].
• Multicenter randomized controlled trial of terlipressin versus sclerotherapy in the treatment of acute variceal bleeding: the TEST study [30].
• Patients in the terlipressin group required fewer transfusions, the balloon needed to be inflated for a shorter time and the duration of bleeding was shorter than in the control group [5].
• Terlipressin in bleeding esophageal varices: a placebo-controlled, double-blind study [5].

References