2425 A Rare Case of Alloimmune Hepatitis Induced After Direct-Acting Antiviral Treatment in a Liver Transplant Patient

Abstract

INTRODUCTION: Cases of autoimmune hepatitis induced after Direct-acting antiviral (DAA) in patients undergoing treatment for hepatitis C virus (HCV) infection have been reported in the literature. This is a case report of alloimmune hepatitis in a post-liver transplant patient shortly after starting DAA treatment for recurrent hepatitis C in the graft. CASE DESCRIPTION/METHODS: A 56-year-old Egyptian woman with history of liver cirrhosis secondary to chronic HCV, genotype 4, complicated by hepatocellular carcinoma underwent orthotopic liver transplant. Two months later, an increase of the aminotransferases and the HCV viral load of 734,703 IU/mL were noted. Liver biopsy was suggestive of recurrent HCV infection. Treatment was started with sofosbuvir, velpatasvir, and voxilaprevir. Repeat HCV viral load was 537 IU/mL 2 weeks after starting DAA. At this point she presented with jaundice, nausea, and vomiting. Vital signs were normal. Scleral icterus and moderate abdominal tenderness were noted. AST 1,395 U/L, ALT 1,359 U/L, ALP 601 U/L, total bilirubin 12.2 mg/dL, direct bilirubin 9.6 mg/dL, and INR 1.5 were noted. Liver biopsy showed hepatitis with abundant plasma cells and interface activity, compatible with an alloimmune process. The patient was started on IV methylprednisolone and N-acetyl cysteine. Her symptoms resolved and liver enzymes normalized on subsequent follow up. She achieved sustained viral response. DISCUSSION: Alloimmune hepatitis is a rare cause for graft dysfunction that can occur among patients who have undergone liver transplantation for other reason than autoimmune hepatitis. The exact pathogenesis is not fully understood but believed to share similar mechanisms with classical autoimmune hepatitis. Calcineurin inhibitors may cause impairment of the regulatory T-cells function by reducing the production of IL-2, a cytokine important for the regulatory T-cells proliferation. The treatment of recurrent HCV with interferon can stimulate the activation of T-cells, which enhance the presentation and release of antigens. With DAA therapy's anti-HCV activity and its potential to stimulate host immunity, it has been suggested that rapid elimination of HCV might favor a dysregulation of immune surveillance, which precipitates alloimmune process. In summary, we report a rare case of alloimmune hepatitis in a liver transplant patient with recurrent HCV responding to DAAs and steroid. Thorough follow up of patients undergoing DAA therapy after liver transplantation for alloimmune hepatitis is warranted.