{'fraction_non_alphanumeric': 0.027929743737402823, 'fraction_numerical': 0.027929743737402823, 'mean_word_length': 5.010380622837371, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The successful use of telaprevir to treat hepatitis C recurrence after liver transplantation in an HIV co-infected patient.

The protease inhibitors, telaprevir (TVR) and boceprevir, have revolutionized the treatment of chronic hepatitis C virus (HCV) genotype 1 infection (1). Both medications are substrates and inhibitors of the cytochrome P450 3A (CYP3A) which are important for the metabolism of many commonly used medications including those used to treat human immunodeficiency virus (HIV) infection and immunosuppressive agents (2). Therefore, these protease inhibitors are not currently approved by the Food and Drug Administration for use in orthotopic liver transplantation (OLT) recipients or HIV co-infected patients because of concerns about serious drug interactions. Limited data are available on using TVR-based triple therapy to treat HCV recurrence after OLT (3) and in HIV co-infected patients (4). Since the introduction of highly active antiretroviral therapy (HAART), chronic HCV infection has become a major cause of morbidity and mortality in the HIVinfected population, and OLT has been performed in selected HIV-HCV coinfected patients (5, 6). HCV recurrence after OLT in co-infected patients is a major issue with significant effect on transplant outcomes (7, 8). This provides rationale for treating HCV recurrence with the highly effective protease inhibitors despite concerns about interactions with both immunosuppressive and HIV medications. Here we report our experience in treating recurrent HCV after OLT in a patient with HIV co-infection with TVRbased triple therapy. A 62-year-old white man with a history of HIV infection, chronic HCV genotype 1b infection complicated by the development of cirrhosis, and hepatocellular carcinoma underwent OLT in August 2011. He developed recurrent hepatitis C with a grade 2/4 inflammation, and stage 2/4 fibrosis disease was found on his liver biopsy approximately 9 months after transplantation. HAART regimen included emtricitabine-tenofovir 200 to 300 mg daily, etravirine 200 mg twice daily, and darunavir-ritonavir 600 to 100 mg twice daily owing to failure of several previous regimens and development of significant HIV resistance. His CD4 count was 461 cells/KL and he was negative for HIV-1 RNA by polymerase chain reaction. His immunosuppression regimen consisted of tacrolimus 0.5 mg every 15 days (because he was on HIV protease inhibitors) and mycophenolate mofetil 500 mg twice daily. His transaminases were in the 150 to 300 U/L range. His baseline HCV RNA was at 4,920,000 IU/mL, and his interleukin 28B genotype was CT. Before starting TVR-based triple therapy, we stopped his darunavir-ritonavir and started raltegravir 400 mg twice daily to avoid having the patient on both HCV and HIV protease inhibitors. His tacrolimus level was increased to 0.5 mg twice daily during the transitioning period. On day 1 of TVR-based therapy, the patient was started on TVR 750 mg thrice daily, ribavirin 400 mg twice daily, and pegylated interferon >2a 180 Kg weekly. In addition, he took 0.5 mg of tacrolimus, and the tacrolimus level was checked at 12 and 24 hours and every other day thereafter for 2 weeks to assess tacrolimus pharmacokinetics. No additional tacrolimus was given until the level was around 4 to 6 ng/mL. The mean area under the concentration time curve (AUC) for tacrolimus while on TVR was 348 ngIhr/mL compared to an TABLE 1. Laboratory tests and virological responses