Semin Liver Dis 2014; 34(02): 194-204
DOI: 10.1055/s-0034-1375959
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Drug-Induced Liver Injury with Autoimmune Features

Andrew S. deLemos
1   Department of Medicine, Center for Liver Diseases and Transplantation, Carolinas Medical Center, Charlotte, North Carolina
,
David M. Foureau
2   Immune Monitoring Core Laboratory, Carolinas Medical Center, Charlotte, North Carolina
,
Carl Jacobs
3   Department of Pathology, Carolinas Medical Center, Charlotte, North Carolina
,
Will Ahrens
3   Department of Pathology, Carolinas Medical Center, Charlotte, North Carolina
,
Mark W. Russo
1   Department of Medicine, Center for Liver Diseases and Transplantation, Carolinas Medical Center, Charlotte, North Carolina
,
Herbert L. Bonkovsky
1   Department of Medicine, Center for Liver Diseases and Transplantation, Carolinas Medical Center, Charlotte, North Carolina
› Author Affiliations
Further Information

Publication History

Publication Date:
31 May 2014 (online)

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Abstract

Drug-induced liver injury (DILI) with features of autoimmunity (AI) represents an important category of hepatotoxicity due to medication exposure. Drugs repeatedly associated with AI-DILI include diclofenac, α-methyl DOPA, hydralazine, nitrofurantoin, minocycline, and more recently statins and anti-TNF-α agents. Usually, symptoms of acute liver injury occur within a few months after initiation of a culprit medication, but a longer latency period is possible. Like idiopathic autoimmune hepatitis, circulating autoantibodies and a hypergammaglobulinemia are frequently present in sera from patients with AI-DILI. If performed, a liver biopsy should demonstrate interface hepatitis with a prominent plasma cell infiltrate. The severity of AI-DILI is variable, but a complete resolution after withdrawal of the offending medication is the expectation. A response to corticosteroid therapy supports the diagnosis, whereas a lack of recurrence of symptoms or signs following corticosteroid cessation distinguishes AI-DILI from idiopathic autoimmune hepatitis.