Antibodies against cytokeratin 8/18 in a patient with de novo autoimmune hepatitis after living-donor liver transplantation

TLDR

Graft dysfunction resembling autoimmune hepatitis is a rare complication after liver transplantation for nonautoimmune disease, and the underlying mechanisms remain unknown. The authors sought to serially evaluate autoantibodies in a patient who developed de novo autoimmune hepatitis and in transplant recipients who did not. Autoantibody levels were measured repeatedly in both the de novo AIH patient and in controls without de novo AIH following transplantation. Anticytokeratin 8/18 antibodies emerged only in the de novo AIH patient, indicating that CK8/18 alterations may contribute to its pathogenesis. Liver Transplant 2005;11:504–507.

Abstract

Graft dysfunction mimicking autoimmune hepatitis rarely develops after liver transplantation for nonautoimmune disease. The mechanism(s) and causes of de novo autoimmune hepatitis are unknown. We examined autoantibodies serially in a patient with de novo autoimmune hepatitis and in patients without de novo autoimmune hepatitis after liver transplantation. Anticytokeratin 8/18 antibodies were detected in the first patient's sera after the onset of de novo autoimmune hepatitis, whereas other patients without de novo autoimmune hepatitis were seronegative throughout the follow-up period even with acute cellular rejection or other cause of liver dysfunction. In conclusion, the changes in cytokeratin 8/18 in hepatocytes might be one of the sources of pathogenesis of de novo autoimmune hepatitis after liver transplantation. (Liver Transpl 2005;11:504–507.)