Moreover, the histological features of PCH could not be completely distinguished from interface hepatitis because of HCV. Therefore, whether PCH is a real threat to the graft during antiviral therapy is controversial at present. Here, we describe the cases of two patients who developed PCH just after

termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation (LDLT). As both patients achieved sustained virological response (SVR) and had no history of AIH, the termination of antiviral therapy was the likely trigger for PCH in these patients. A59-YEAR-OLD WOMAN underwent LDLT, with her son as the donor, for HCV-related cirrhosis. Six months after the LDLT, her liver biopsy showed HCV recurrence with mild necroinflammatory activity and mild fibrosis (METAVIR score, A1 F1) without acute cellular rejection (ACR). The HCV genotype BGB324 was 1b and the serum HCV RNA level was 3570 kIU/mL on an Amplicor HCV assay. The serum immunoglobulin (Ig)G level was 1260 mg/dL (reference range, 826–1840) and she was negative for antinuclear antibodies (ANA). She started antiviral therapy with 80 μg/week pegylated interferon-α-2b BVD-523 and 600 mg/day ribavirin, together with 2 mg/day tacrolimus and 1 g/day mycophenolate mofetil (Fig. 1a). HCV RNA was undetectable in serum 2 months after the initiation of the treatment, and antiviral therapy was

continued for 14 months. The immunosuppressants administrated were not changed during and after the antiviral therapy. Before the termination of treatment, her transaminase levels remained normal; however, 1 month later, her aspartate aminotransferase (AST) and alanine aminotransferase

(ALT) levels reached 455 and 650 IU/L, respectively, IgG level increased to 2660 mg/dL, and she was positive for ANA at a titer of 1:40 with a speckled pattern. Type 1 liver–kidney microsomal antibodies (anti-LKM-1) was negative. Liver histology showed moderate necroinflammatory activity and moderate fibrosis (METAVIR score, A2 F2) with plasma cell-rich infiltration (Fig. 1b,c). As serum HCV RNA remained undetectable at that time; the International AIH Group score was 16, indicating definite AIH;[9] and the total DCLK1 score in the histological scoring system for PCH[6] was 11, we diagnosed the patient with PCH. Steroid therapy with methylprednisolone was initiated at a dose of 500 mg/day for 3 days, and then the dose was tapered from 250 mg/day on the fourth day to 62.5 mg/day on the sixth day. Then, the drug was switched to 50 mg prednisolone, which was tapered to 10 mg until the end of the sixth month. AST and ALT levels decreased immediately after the administration of steroid, and normalized during 2 months of the steroid therapy. Liver biopsy after 17 months of steroid therapy showed histological improvement. Serum HCV RNA was undetectable in serum at 24 weeks after the completion of antiviral therapy, and she was considered to have achieved SVR.