A 54-year-old woman infected with HCV genotype 1a and HIV with FibroScan of 28.4 kPa (cirrhosis) and grade A Child-Pugh.
Antiretroviral therapy since August 2007 with tenofovir+emtricitabine+atazanavir/ritonavir.
PR showed normal values before starting treatment for HCC.
In February 2008, she was treated with pegIFNα + RBV for 48 weeks, resulting in partial response to treatment.
During treatment PRs were reduced to 51x109/L (thrombocyth grade II).
Before starting the second treatment episode for HCC, the patient had normal aminotransferase levels (AST = 45 IU/mL; ALT = 45 IU/mL; GGT = 48 IU/mL); platelet count x 109dL).
The basal CVH was 10,900,000 copies/mL and the CVHIV was undetectable.
In September 2012, treatment for HCC was initiated with pegIFN-α2a + RBV + TVR (135 mcg/week, 800 mg/day and 750 mg/8hours) and switched to atazanavir/saquinavir.
Concomitantly, and given the thrombocytopenia manifested during the previous treatment episode, eltrombopag 50mg/day was initiated.
At week 10 of treatment, she presented PR = 13 x 109/L, TVR was suspended and eltrombopag was increased to 75 mg/day, continuing treatment with pegIFN-α2a (135 mcg/week)
At week 17 and for a generalized pancytopenia response (weeks Hb = 9.1g/dL; Neutrophils = 1 x 109/L; PR = 18 x 109/L), pegIFNα + Rpag was discontinued.
