Hemodynamic profile of terlipressin and octreotide in patients with cirrhosis and portal hypertension: A randomized, single-blind clinical trial

Abstract

Background and aims Continuous infusion (CI) of terlipressin may result in a more sustained reduction in portal pressure with fewer adverse effects than administered as a bolus. This study aimed to compare the hepatic and cardiopulmonary hemodynamic effects and safety profiles of bolus vs terlipressin CI. Methods This is a single-center, single-blinded, double-dummy, parallel-group, clinical trial in which 38 patients with cirrhosis and portal hypertension were randomized to receive: 1mg bolus of terlipressin + CI of placebo (TERLBOL n=12), bolus of placebo + CI of terlipressin (2mg/day or 4mg/day if <10% reduction in hepatic venous pressures gradient (HVPG) at 30min of infusion) (TERLINF n=14) or a bolus of octreotide (50mcg) + CI of octreotide (50mcg/h) (OCTR n=12) as an additional control group. HVPG, cardiopulmonary pressures and cardiac output were measured at baseline, after 30, 60 and 120 minutes. Results Sixty-eight percent of patients were male, with median age 59-years. There were no significant differences in baseline characteristics. TERLBOL group: there was a non-significant reduction in HVPG (at 120min, -4.9%; p:0.14), however, cardiopulmonary and mean arterial pressures significantly increased, while cardiac output and heart rate significantly decreased. TERLINF group: there were non-significant changes in cardiopulmonary hemodynamics or HVPG (NS) despite doubling the infusion dose after 30min in 13/14 patients. OCTR group: there was a non-significant reduction in HVPG (at 120min, -4.9%; p:0.08) and pulmonary capillary pressure significantly decreased. All treatments were well tolerated, and no adverse events were observed. Conclusion There were non-significant reductions in HVPG with the three therapeutic strategies. Further investigations are warranted to determine the optimal dosing strategy for CI of Terlipressin in patients with cirrhosis and portal hypertension.