Published online Aug 28, 2015. doi: 10.4254/wjh.v7.i18.2177
Peer-review started: November 20, 2014
First decision: December 12, 2014
Revised: March 17, 2015
Accepted: July 21, 2015
Article in press: July 23, 2015
Published online: August 28, 2015
Processing time: 282 Days and 20.2 Hours
AIM: To evaluate virological response to telaprevir or boceprevir in combination with pegylated interferon and ribavirin and resistance mutations to NS3/4A inhibitors in hepatitis C virus-human immunodeficiency virus (HCV-HIV) coinfected patients in a real life setting.
METHODS: Patients with HCV genotype 1-HIV coinfection followed in Nice University Hospital internal medicine and infectious diseases departments who initiated treatment including pegylated interferon and ribavirin (PegIFN/RBV) + telaprevir or boceprevir, according to standard treatment protocols, between August 2011 and October 2013 entered this observational study. Patient data were extracted from an electronic database (Nadis®). Liver fibrosis was measured by elastometry (Fibroscan®) with the following cut-off values: F0-F1: < 7.1 kPa, F2: 7.1-9.5 kPa, F3: 9.5-14.5 kPa, F4: ≥ 14.5 kPa. The proportion of patients with sustained virological response (SVR) twelve weeks after completing treatment, frequency and type of adverse events, and NS3/4A protease inhibitor mutations were described.
RESULTS: Forty-one patients were included: 13 (31.7%) patients were HCV-treatment naïve, 22 (53.7%) had advanced liver fibrosis or cirrhosis (Fibroscan stage F3 and F4); none had decompensated cirrhosis or hepatocellular carcinoma; all were receiving antiretroviral treatment, consisting for most them (83%) in either a nucleoside reverse-transcriptase inhibitor/protease inhibitor or/integrase inhibitor combination; all patients had undetectable HIV-RNA. One patient was lost to follow-up. SVR was achieved by 52.5% of patients. Five patients experienced virological failure during treatment and four relapsed. Seven discontinued treatment due to adverse events. Main adverse events included severe anemia (88%) and rash (25%). NS3/4A protease mutations were analyzed at baseline and at the time of virological failure in the 9 patients experiencing non-response, breakthrough or relapse. No baseline resistance mutation could predict resistance to HCV protease inhibitor-based treatment.
CONCLUSION: Telaprevir and boceprevir retain their place among potential treatment strategies in HIV-HCV coinfected patients including those with advanced compensated liver disease and who failed previous PegIFN/RBV therapy.
Core tip: Data regarding treatment of hepatitis C virus (HCV) infection with triple combination regimen including interferon/ribavirin and a protease inhibitor (telaprevir or boceprevir) among difficult to treat human immunodeficiency virus (HIV)-HCV co-infected patients are lacking. Most of the patients included in this single-center observational study had already failed a previous dual treatment course and had severe liver fibrosis, one out of six being both cirrhotic and non-responder to prior therapy. More than one of two patients displayed sustained virological response, suggesting that in low-income countries, telaprevir and boceprevir may retain their place among potential treatment strategies in HIV-HCV coinfected patients.