Of these 39 patients, 21 were nonresponders and nine were relapsers, whereas the remaining nine patients had discontinued previous anti-HCV therapy voluntarily or due to adverse effects. During follow-up, 93 (39%) patients started therapy against HCV with pegylated interferon plus ribavirin. At the end of study period, 11 out of these 93 patients were still receiving

such therapy. SVR was achieved in 19 (23%) of the remaining 82 patients. Thirty-one (13%, 95% CI: 9%-17%) patients developed a hepatic decompensation and/or HCC during the follow-up. The density of incidence of Bafilomycin A1 in vitro hepatic decompensation and/or HCC was 6.7 per 100 person-years (95% CI: 4.7%-9.6%). The probability of developing a decompensation and/or HCC at 1 year, 2 years, and 3 years was 7%, 10%, and 15%, respectively. Ascites was the most common type of first decompensation, appearing in 21 (68%) patients. PGHB occurred in four (13%) patients, HE in one (3%), SBP in one (3%), and HRS in one (3%). HCC was diagnosed in three (10%) patients. The median (Q1-Q3) time

to development of liver decompensation and/or HCC was 19 (range: 3-37) months. Two patients of those who developed ascites PKC412 mw as the initial decompensation presented a concomitant clinical event, PGHB in one case and HE in the other. The factors associated with the emergence of a hepatic decompensation and/or HCC in univariate analyses are shown in Table 2. Higher baseline LS values were associated with developing a first hepatic event and/or HCC (Table 2, Fig. 1A). The probability of remaining free of decompensations and HCC at 1 year, medchemexpress 2 years, and 3 years was 97%, 93%, and 81%, respectively, for patients with a baseline LS < 40 kPa, whereas it was 80%, 74%, and 63% for patients with a baseline LS above or equal to 40 kPa. Figure 1B and Supporting Fig. 1A,B show the probability of remaining free of a decompensation and HCC according to baseline CTP stage, therapy against HCV during follow-up and MELD score, respectively. Figure 1C,D shows the probability of this event according

to different categories of LS combined with baseline CTP stage and MELD score. Multivariate Cox regression analyses demonstrated a statistical interaction between CTP and MELD scores. On the contrary, there were no interactions between CTP stage and LS or MELD score and LS. Thus, Cox regression analyses were stratified by the baseline MELD score. After multivariate analyses, baseline plasma HCV viral load, hepatitis B virus coinfection, CTP stage, and LS were independently associated with developing a liver decompensation and/or HCC (Table 2). Additionally, we compared the ability of LS, CTP stage, and MELD score to predict the primary outcome. Thus, multivariate models including either LS or CTP stage or MELD score were done and their respective AUROC computed. The AUROC (95% CI) for CTP stage including multivariate model was 0.76 (range: 0.65-0.