Abstract Body

There is scarce data regarding efficacy and safety of new direct antiviral agents (DAA) in cirrhotic HCV-HIV coinfected patients.

Multicenter prospective cohort analysis carried-out in 13 Spanish hospitals between January and December 2015. Inclusion criteria: 1) Cirrhosis diagnosed by transient elastography (TE>14.6KPa) or by sonographic, endoscopic and/or clinical data. 2) HCV-treatment based on DAA according to drug availability and physician discretion. 3) HCV-HIV coinfection with stable ART and controlled HIV infection. Primary endpoint: Overall efficacy, defined as the percentage of patients with undetectable HCV-RNA at week 12 after treatment (SVRS12). Secondary endpoints: Safety (percentage of withdrawal due to toxicity and/or hepatic decompensation) and efficacy according to regimen used and HCV genotype. Change in TE value after HCV treatment was also evaluated.

A total of 201 patients started treatment. Mostly, male (n=150; 74.3%), Caucasian (n=198; 98%) and ex-IDUs (n=165; 81.7%). Genotypes: Gt-1a, 75 (37.1%); Gt-1b, 27 (13.4%); Gt-4, 51 (25.2%) and Gt-3, 38 (18.8%). Baseline median TE was 20.7KPa (IQR 16.1-33) and HCV-RNA log10 6.1UI/mL (IQR 5.7-6.6). Most patients had Child-Pugh A class score (n=153; 75.7%) and 36 (17.8%) of them suffered prior hepatic decompensation. There were 104 (51.5%) pretreated patients, of whom 40.4% (n=42) with null response. SVR12 data was available in 170 (84.6%) patients. More commonly used regimens: SOF/LDV+RBV, 43 (25.3%) patients; SOF+SMV+RBV, 34 (20%); SOF/LDV, 26 (15.3%) and SOF+DCV+RBV, 25 (14.7%). Overall, 92.9% (158/170) of patients achieved SVR12, without differences between genotypes (Table 1). A significant lower SVR12 was observed in pretreated as compared to naive patients (88.8% vs. 97.5%; p=0.026). Causes of treatment failure were: 7 (4.1%) relapses, 2 (1.2%) lost to follow-up, 1 (0.6%) toxicity-related discontinuation, 1 (0.6%) hepatic decompensation and 1 (0.6%) viral breakthrough. RBV dose modification was needed in 20 (16.3%) cases, mainly due to anemia (n=17). On-treatment hepatic decompensation was seen in 4 (2.4%) patients (encephalopathy and ascites, 2 each). At week 12 after treatment, TE decreased a mean of 5.6 KPa (95%CI 1.8-9.2; p=0.004) as compared with baseline.

In our cohort, 92.9% of cirrhotic HCV-HIV coinfected patients achieved SVR12, which was associated with a significant decrease in TE. Only 2 (1.2%) patients had to stop treatment due to adverse events.