Sustained virological response with telaprevir in 1078 patients with advanced hepatitis C: The international telaprevir access program

Pharmacokinetic interactions between telaprevir and antiretroviral drugs in HIV/HCV-coinfected patients with advanced liver fibrosis and prior HCV non-responders

“…Although the TVR C min was not lower than the reported 90% inhibitory concentration (IC 90 ) of 564 ng/mL [15] in any of the study patients, since the pharmacokinetics of HCV PIs, particularly the concentration at the end of the dosage interval (C trough ), was described as the best predictive parameter of HCV-RNA decline during phase 1 and 2 studies [16,17], even a small reduction of TVR plasma levels should raise a concern. Indeed, in this small case file the SVR12 rate was 53.3%, in line with previous studies on patients not responding to prior pegIFN + RBV treatment [18], also considering the high proportion of prior null or partial responders among our patients. We extend previous findings by documenting for the first time that no clinically relevant drug-drug interactions between TVR and highly active antiretroviral therapy can be expected not only when looking at total drug amount but also at the single TVR isomers, which are the most active forms [8,19].…”

Assessing safety and efficacy of sofosbuvir for the treatment of hepatitis C

“…Not only the need for PR backbone, who renders triple therapy contraindicated in a significant number of patients [43], but also TVR and BOC-associated AEs limit the applicability of these therapeutic options ( Table 4) [44][45][46][47]. In field practice, anemia was clinically relevant, since it has been associated with frequent RBV dose reduction, epoetin supplementation and blood transfusions [5,48]. Safety profile is even worse in patients with poorly compensated cirrhosis, with albumin values < 3.5 g/dl and a platelet count below 100.000 mm 3 in whom therapy was associated with the lowest chances of achieving an SVR and an increased risk of severe complications, thus including death.…”

Management of direct-acting antiviral agent failures

“…The efficacy of firstgeneration protease inhibitors depends on the viral sensitivity to interferon. Therapy failures have been reported in 20% of naive patients and 80% of previous P/RBV null responders, particularly those with liver cirrhosis [17][18][19][20][21][22][23][24]. Patients who fail to respond to TPV harbor resistance-associated variants (RAVs) that have a profile of cross resistance to BOC and vice versa.…”