Beavers – Advisory Committees or Review Panels: Gilead, Janssen, Genentech; Grant/Research Support: Gilead, Roche, Gilead, Roche, BMS, Salix; Speaking and Teaching: Roche, Merck, Vertex, Roche, Merck, Vertex, Gilead, Salix Daniel Ganger – Grant/Research Support: merck, gilead, Ocera Paul J. Thuluvath – Advisory Committees or Review Panels: Bayer, Gilead, Vertex; Grant/Research Support: Gilead, Abbott, BMS, Isai, Salix; Speaking and Teaching: Bayer/Onyx, Vertex, Gilead Roberto J. Groszmann – Advisory Committees or Review Panels: Gilead The following people have
nothing to disclose: Brett E. Fortune, Guadalupe Garcia-Tsao, Maria Ciarleglio, Yanhong Deng, Adrian Reuben, Gary Abrams, Michele Bishop Lewis, James F. Trotter, Norman D. Grace Introduction: terlipressin, a vassopressin 1a (V1a) agonist, is used as vasoconstrictive therapy in cirrhotic patients with var-iceal bleeding buy AP24534 (VB) and hepatorenal syndrome (HRS). Terli-pressin is also a partial agonist of the V2 receptors in the kidney, inducing natriuresis. Recently, terlipressin was found to cause a significant reduction in serum sodium concentration in the majority of patients with acute variceal haemorrhage, who failed to other vasoconstrictor therapy. We hypothesize that terlipressin rarely causes significant and/or symptomatic hyponatremia in unselected patients treated for VB or HRS. Methods:
retrospective analysis of 69 consecutive patients with liver cirrhosis
find more treated with between 2007 and 2011: 22 patients were treated with terlipressin for VB; another 47 were treated with terlipressin and albumin for HRS. Terlipressin was used as a first line agent in all cases. Standard treatment regimen for patients with VB was an i.v. bolus of 2mg terlipressin followed by 1 mg every 4 hours for 5 days. Patients with HRS received terlipressin 0.5mg i.v. every 4 hours, with dose escalation every 3 days if there was no response. Serum sodium concentration was assessed at baseline and during treatment Terminal deoxynucleotidyl transferase for a maximum duration of 14 days. Results: Serum sodium concentration significantly decreased during terlipressin therapy with 1.27 ± 4.57 mmol/L (p=0.031). When considered per group based on indication, this significant decrease was restricted to the VB patients (139.15 ± 1.35 to 135.50 ± 1.50 mmol/L, p=0.008). In 7 of 43 patients (16%) with HRS and in 9 of 20 patients with VB (45%), serum sodium decreased ≥5mmol/L during terlipressin treatment. However, none of the patients had symptomatic hyponatremia. None of the baseline characteristics were found to influence the reduction in serum sodium concentration in any of the groups. Three-month survival was 70.0% in the VB group and 37.2% in the HRS group. Cumulative dose was 21.72 ± 10.82 mg (during 4.21 ± 2.