Published online Apr 18, 2017. doi: 10.4254/wjh.v9.i11.551
Peer-review started: June 23, 2015
First decision: September 21, 2015
Revised: February 10, 2017
Accepted: March 14, 2017
Article in press: March 17, 2017
Published online: April 18, 2017
To evaluate new therapies for hepatitis C virus (HCV), data about real-world outcomes are needed.
Outcomes of 223 patients with genotype 1 HCV who started telaprevir- or boceprevir-based triple therapy (May 2011-March 2012) at the Mount Sinai Medical Center were analyzed. Human immunodeficiency virus-positive patients and patients who received a liver transplant were excluded. Factors associated with sustained virological response (SVR24) and relapse were analyzed by univariable and multivariable logistic regression as well as classification and regression trees. Fast virological response (FVR) was defined as undetectable HCV RNA at week-4 (telaprevir) or week-8 (boceprevir).
The median age was 57 years, 18% were black, 44% had advanced fibrosis/cirrhosis (FIB-4 ≥ 3.25). Only 42% (94/223) of patients achieved SVR24 on an intention-to-treat basis. In a model that included platelets, SVR24 was associated with white race [odds ratio (OR) = 5.92, 95% confidence interval (CI): 2.34-14.96], HCV sub-genotype 1b (OR = 2.81, 95%CI: 1.45-5.44), platelet count (OR = 1.10, per x 104 cells/μL, 95%CI: 1.05-1.16), and IL28B CC genotype (OR = 3.54, 95%CI: 1.19-10.53). Platelet counts > 135 x 103/μL were the strongest predictor of SVR by classification and regression tree. Relapse occurred in 25% (27/104) of patients with an end-of-treatment response and was associated with non-FVR (OR = 4.77, 95%CI: 1.68-13.56), HCV sub-genotype 1a (OR = 5.20; 95%CI: 1.40-18.97), and FIB-4 ≥ 3.25 (OR = 2.77; 95%CI: 1.07-7.22).
The SVR rate was 42% with telaprevir- or boceprevir-based triple therapy in real-world practice. Low platelets and advanced fibrosis were associated with treatment failure and relapse.
Core tip: A cohort of 223 hepatitis C virus (HCV)-infected patients at a tertiary referral center was analyzed. All patients were treated with telaprevir and boceprevir. Using both logistic regression and a machine learning techniques we identified baseline and on-treatment factors associated with sustained virologic response and relapse. We found that both low platelet count and advanced fibrosis or cirrhosis were associated with treatment failure. Information of the effectiveness of these protease inhibitors could be used to inform clinical trials of future HCV direct-acting antivirals.