CROI 2015 Program and Abstracts

Abstract Listing

Poster Abstracts

TUESDAY, FEBRUARY 24, 2015 Session P-N2 Poster Session

Poster Hall

2:30 pm– 4:00 pm HCV Therapy: Observations From Cohort Studies 643 Statins Improve SVR, Reduce Fibrosis Progression and HCC Among HCV+ Persons Adeel A. Butt 1 ; PengYan 2 ; Obaid Shaikh 2 ; Shari Rogal 2 1 University of Pittsburgh/VA Pittsburgh Healthcare System, Pittsburgh, PA, US; 2 VA Pittsburgh Healthcare System, Pittsburgh, PA, US Background: Statins have been variably noted to affect HCV treatment response, fibrosis progression, and hepatocellular carcinoma (HCC) incidence. However, this has not been evaluated in a large national cohort while controlling for important confounders. Methods: Within Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), we identified those Veterans initiated on HCV treatment with a follow up of at least 24 months after treatment completion. We excluded those with HIV coinfection, hepatitis B surface antigen positivity, and those with missing data to determine SVR rates or FIB-4 score. Our main outcome measures were: 1) Liver fibrosis progression as measured by FIB-4 scores; 2) SVR rates, defined as proportion of participants with undetectable HCV RNA 12-48 weeks after completion of treatment; 3) incident HCC. Results: Among 7,248 eligible subjects, 46%were taking statins. Statin use was significantly associated with attaining SVR (39.2% vs. 33.3%, p<0.01), decreased fibrosis progression, and decreased HCC incidence (1.2% vs. 2.6%, p<0.01). In multivariable models, statins remained significantly associated with SVR (OR=1.44, 95%CI=1.29,1.61) and progression to cirrhosis (HR=0.56, 95%CI-0.50,0.63) Other factors significantly associated with the development of cirrhosis included SVR attainment, alcohol abuse, diabetes, HCV genotype and viral load, age, and race. Statin use was significantly associated with decreased HCC (HR=0.51, 95% CI=0.34,0.76) when adjusting for baseline fibrosis and controlling for other relevant clinical factors.

Poster Abstracts

Conclusions: In this large, national cohort of persons who initiated anti-HCV treatment, administration of statins in addition to anti-HCV therapy significantly improved SVR, reduced fibrosis progression and reduced incidence of HCC. 644 Sofosubuvir, Simeprevir, +/- Ribavirin in HCV Protease Inhibitor-Experienced Patients Kristen M. Marks ; Ethan M.Weinberg; Sonal Kumar; Carrie Down;Ype P. de Jong; Leah A. Burke; Mary C. Olson; Ira M. Jacobson Weill Cornell Medical College, New York, NY, US Background: Little data exists on use of HCV protease inhibitors (PIs) as part of a treatment (Rx) regimen for PI-experienced G1 patients (pts). Since polymorphisms associated with PI-resistance decrease to baseline levels over time in most studied subjects, sofosbuvir (SOF) + simeprevir (SMV) +/- ribavirin (RBV) represents a potential retreatment option for PI-experienced pts. Methods: We compiled a retrospective cohort of HCV PI-experienced G1 pts treated with SOF+SMV+/-RBV at our center. Baseline factors including prior regimen & Rx response, fibrosis stage, HCV genotype & resistance testing (population-based) data, viral RNA levels, demographic data as well as on Rx response, SVR4, and SVR12 were collected and reported. Results: In 2014, 15 pts with genotype 1 and prior PI experience initiated Rx because of clinical need with 12 wks SOF+SMV with (10) or without (5) RBV . Median age was 61 yrs (range 26-73), baseline HCV RNA 6.5 log IU/ml (5.5-7.0 log), 12 were male, and 10 had cirrhosis. PI Rx occurred 26 (5-85) months prior and included telaprevir (10), boceprevir (3), ABT 450/r (1), GS9451 (1) as part of Rx regimen with 11 nonresponders, 1 relapser, and 3 intolerant of Rx. All had genotype and resistance testing performed prior to SOF+SMV+/- RBV. Of the 9 G1a pts, Q80K was detected in 4, Q80L in1. Of the 6 G1b pts, V36I and T54S were detected in 1 pt each. No other mutations associated with PI resistance were detected.

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CROI 2015