An Analysis of Virological Failure Patients Treated for Hepatitis C (HCV) with Direct Acting Anti-viral (DAA) Therapy in a Community Based Practice: Is the Real World Like Clinical Trials? 2016 ACG Category Award (Liver)

Introduction: The advent of new DAA therapies have transformed the landscape of HCV treatments in terms of use, side effects and sustained viral response (SVR) rates. Both clinical trials and multi-center real world analyses report SVR of greater than 90% in all patients. Despite these high SVR rates, there are still patients who are not cured with treatment. We analyzed the 410 patients that were treated in our office in calendar year 2015 and had 12 weeks of post-treatment follow up to assess the characteristics of those patients (pts) NOT achieving an SVR. Methods: We reviewed the characteristics of all HCV pts treated with DAA therapies in our office in 2015 and analyzed the pts that did not have an SVR. We reviewed their age, gender, fibrosis stage, genotype, treatment history, baseline viral load, resistance associated variants, and presence/absence of HIV Results: 410 pts started treatment in our office in 2015 and completed therapy by March 2016. 14/410 (3.4%) did not acheive an SVR. 13 pts relapsed after cessation of therapy and 1 had viral breakthrough at week 20. This patient was GT 1a, treatment experienced with cirrhosis who was treated with PrOD/RBV. Relapsers were as follows: 9 Sofosbuvir (SOF)/ledipasvir (LDV) 9 [7 GT 1a, 2 GT 1b], PrOD 1 [GT1b], SOF/RBV 1 [GT 3a], SOF/daclatasvir (DAC)1 [GT 3a], PrOD/RBV 1 [GT1a]. Average age was 59 yrs (46-71). Gender was 9 male (64%), 5 female (36%). 9 5/14 (36%) were treatment naive. 9/14 (64%)were treatment experienced. Of the treatment experienced patients, 6 were previously treated with PEG-interferon plus RBV, 2 were treated with PEG-interferon/RBV and telaprevir and 1 was prevously treated with SOF/simeprevir. Genotypes were as follows: 1a 9, 1b 3, 3a 2. 8/14 (57%) were cirrhotic, 2/14 F3 (14%), F2 1/14 (7%), F1 (7%). One cirrhotic GT 3a patient was co-infected with HIV. The remaining 13/14 were HIV negative. No patient was tested for resistance associated (RAV) mutations prior to iintiating therapy. 6/14 (42%) were found to have RAVs following relapse. One treatment experienced GT 1a cirrhotic, previously treated with SOF/simeprevir, developed hepatocelluar carcinoma while on PrOD treatment. Conclusion: We describe a 97% SVR rate with a 3% viral failure rate in our real world, community based practice. The majority of our relapse patients were genotype 1a with cirrhosis. While RAV's developed in 43% of our viral failure pts, the majority of our relapse pts did not have detectable RAVs which questions the reason that these pts had a relapse.