Liver biopsy at 19 days after LDLT revealed mild ACR, but it reso

Liver biopsy at 19 days after LDLT revealed mild ACR, but it resolved without any specific treatment. At 23 months after LDLT, she developed recurrent hepatitis C with mild activity and severe fibrosis on liver biopsy (METAVIR score, A1 F3). The HCV genotype was 2b and the serum HCV RNA level was 7.2 log IU/mL, as detected by a real-time polymerase chain reaction-based quantitation method. Antiviral therapy with 100 μg/week pegylated interferon-α-2b and 400 mg/day ribavirin was initiated (Fig. 2a). At that time, 50 mg/day cyclosporin and 15 mg/day prednisolone were used for immunosuppression. LBH589 supplier The prednisolone dose was reduced to 10 mg/day after 3 months

of antiviral therapy. HCV RNA was undetectable in serum; however, treatment was discontinued after 21 weeks because of severe general fatigue. The transaminase levels were reduced and maintained within the reference range from 3 weeks to the end of antiviral therapy, but worsened 2 months after the termination of the treatment to an AST level of 136 IU/L and an ALT level of 152 IU/L. The serum IgG level increased to 1719 mg/dL, from 641 mg/dL before the antiviral therapy.

She was negative for ANA and anti-LKM-1 throughout her clinical course. Liver biopsy revealed the features of AIH, including portal inflammation with plasma cell-rich lymphoid aggregates, interface hepatitis and centrilobular inflammation (Fig. 2b,c). As HCV RNA was undetectable in serum; the International AIH Group score was 14, suggesting AIH;[9] and the total score on the histological scoring system for PCH was 10,[6] the patient was diagnosed with PCH. selleckchem Methylprednisolone was started 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. The treatment was terminated on the seventh day, followed by the initiation of 10 mg/day prednisolone. The transaminase levels decreased and normalized after 2 months

of steroid administration, and liver biopsy 19 months after the initiation of steroid therapy showed the remission of hepatitis. She was considered to have achieved SVR on the basis of a negative HCV RNA result at 24 weeks after the termination of antiviral therapy. IN THIS REPORT, we demonstrated the cases of two patients who developed PCH just after the termination of antiviral Amine dehydrogenase therapy for recurrent hepatitis C after LDLT. The diagnosis of PCH in the present cases is definite because both patients achieved SVR and recovered after steroid therapy. Termination of antiviral therapy likely induced PCH in these patients, as both patients had no other trigger for PCH, such as reduction of immunosuppression. At our institute, 125 HCV-infected liver transplant recipients were treated with standard interferon and/or pegylated interferon in combination with ribavirin for recurrent hepatitis C after LDLT between January 2001 and December 2012.

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