Lee – Consulting: Bristol Myers Squibb, Gilead, Roche, Janssen, Vertex, Genentech, Merck, Abbvie; Grant/Research Support:

BMS, Gilead, Roche, Janssen, Merck, Vertex, Abbvie; Speaking and Teaching: BMS, Gilead, Roche, Merck, Vertex Sandra S. Lovell – Employment: AbbVie Guy Neff – Employment: AbbVie Paul Y. Kwo – Advisory Committees or Review Panels: Abbott, Novartis, Merck, Gilead, BMS, Janssen; Consulting: Vertex; Grant/Research Support: Roche, Vertex, GlaxoSmithKline, Merck, BMS, Abbott, Idenix, Vital Therapeutics, Gilead, Vertex, Merck, Idenix; Speaking and Teaching: Merck, Merck The following people have nothing to disclose: David J. Mutimer, Leticia Canizaro, Roger Trinh Background & Aim The availability of interferon-free regimens has ushered in a new era in BIBW2992 cell line the treatment of chronic hepatitis C. However, real-life data in cirrhotic patients, especially in patients with clinically significant portal hypertension (CSPH), are limited. We aimed to investigate the impact of Palbociclib portal pressure measured by hepatic venous pressure gradient (HVPG) on early viral kinetics

and on-treatment virologic response in patients treated with interferon-free regimens outside of clini cal trials. Patients & Methods Eighteen patients with chronic hepatitis C, cirrhosis and available information on HVPG treated with either sofosbuvir/daclatasvir (hepatitis C virus (HCV)-genotype (GT)1), simeprevir/daclatasvir (HCV-GT1 or 4), or sofosbuvir/ribavirin (HCV-GT3) were included in this retrospective study. HCV-RNA was assessed at baseline (BL), treatment day 2 (D2), week 1 (W1), week 2 (W2), week 3 (W3) and week 4 (W4) using the Abbott RealTime HCV quantitative assay. Rapid virologic response (RVR) was defined as target not detectable HCV-RNA at W4. HVPG >10mmHg Casein kinase 1 was considered as CSPH. Results Nine patients (50%) were infected with HCV-GT1 (subtype 1a:4[22%], 1a:5[28%]), 8 patients (44%) with HCV-GT3 and one patient (6%) with HCV-GT4. The majority of patients were Child-Pugh stage A (11/18[61%]), while stage B was observed in

7 patients (39%). No patients had stage C cirrhosis. Fourteen patients (78%) had CSPH, with a median HVPG of 12.5mmHg. HCV-RNA log-drop was not statistically significantly correlated with HVPG at any time point: D2:r=−0.099,P=0.715; W1:r=−0.297,P=0.247; W2:r = −0.042,P = 0.8 83; W3:r = −0.019,P = 0.95; W4:r=0.014,P=0.959. Moreover, the proportion of patients with HCV-RNA below the lower limit of quantification was comparable between patients with (high) and without (low) a HVPG above the median: W1: low:0/8(0%), high:1/9(11%); W2: low:2/8(25%), high:1/7 (14%); W3: low:1/7(14%), high:1/6(17%); W4: low:5/9 (56%), high:4/6(67%). RVR was observed in 2 out of 15 patients (13%), who both had a HVPG below the median.