Post-Transplant Plasma Cell Hepatitis in a Patient with Hepatitis C

Abstract

Purpose: Post-transplant plasma cell hepatitis (PCH) is a rare reported cause of acute cellular rejection in patients with underlying HCV. It must be differentiated from de novo autoimmune hepatitis (AIH) and histologic evaluation is key in differentiating the two entities. The treatment includes aggressive modification of the patient's immunosuppressive regimen but corticosteroids must be used judiciously due to the increased risk of aggressive HCV recurrence. PCH is a negative prognostic factor for allograft survival and is a subsequent cause of morbidity and mortality. A 56 year old Hispanic man with a history of OLT in 2006 due to HCV cirrhosis and secondary hepatocellular carcinoma presented with acute elevation of his liver function tests 58 months post-transplant. Specifically, his indices included ALT of 274, AST of 195, total bilirubin of 1.5 and alkaline phosphatase of 145; prior AST/ALT had been within the 50-60 range consistent with his history of recurrent HCV. Liver biopsy revealed severe acute cellular rejection with dense plasma cell infiltrates, interface activity, perivenular hemorrhage and necrosis. Serum autoimmune markers including antinuclear antibody (ANA) and anti-smooth muscle antibody (ASMA) were negative while immunoglobulin G (IgG) level was elevated at 2220 (reference range 694-1618 mg/dL). The patient was treated with a course of IV steroids and his immunosuppression regimen was augmented. Repeat biopsy one week after initiation of treatment showed near complete resolution of rejection and no signs of active HCV. In addition, his LFTs normalized to his baseline and his IgG level decreased to 1350 mg/dL. Plasma cell hepatitis must be considered in the differential for acute cellular rejection after liver transplantation in patients with underlying HCV and must be differentiated from de novo AIH. While AIH is associated with high titers of ASMA and IgG levels, PCH typically only presents with elevated IgG levels. PCH tends to be associated with poorer long-term outcomes and as such, these patients need to be identified early and managed with appropriate changes in their immunosuppression regimen given their predisposition for hepatic decompensation.