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Liver transplantation in adults: Overview of immunosuppression

Norman L Sussman, MD
John M Vierling, MD, FACP
Section Editor
Robert S Brown, Jr, MD, MPH
Deputy Editor
Kristen M Robson, MD, MBA, FACG


In 1994, the US Multicenter FK506 Liver Study Group published a paper comparing cyclosporine and tacrolimus for immunosuppression after liver transplantation [1]. The study was a landmark in the evolution of liver transplantation. First, the introduction stated that rejection remained an important cause of graft loss and death. Second, the paper reported that survival with cyclosporine and tacrolimus was similar but that tacrolimus was associated with fewer episodes of steroid-resistant rejection. Third, it reported that tacrolimus was associated with excess adverse events, including nephrotoxicity and neurotoxicity.

Liver transplantation has evolved substantially since that publication, and we have addressed many of the issues outlined in the 1994 study. Acute rejection is usually easy to manage, and we now try to balance the risk of rejection with the risk of drug toxicity. Our focus has shifted to avoiding the long-term complications of immunosuppression and recurrent liver disease. Tacrolimus has become first-line immunosuppression in most liver transplant programs, and a number of supplemental drugs allow us to customize immunosuppression.

This topic will provide an overview of the drugs used for immunosuppression following liver transplantation. The diagnosis and treatment of acute cellular rejection are discussed elsewhere. (See "Liver transplantation: Diagnosis of acute cellular rejection" and "Treatment of acute cellular rejection in liver transplantation".)


Organ rejection is a multistep process that includes alloantigen recognition, lymphocyte activation, clonal expansion, and graft inflammation (figure 1 and figure 2).

Signal I: Alloantigen recognition — Alloantigen recognition requires presentation of a foreign alloantigen along with a host major histocompatibility complex (MHC) molecule. Presentation is done by an antigen-presenting cell (APC). The antigen, bound to an MHC molecule, binds to the T-cell receptor. This is the first of three signals that are required for T-cell maturation and can be aborted by antilymphocyte antibodies. (See 'Antibody therapy' below.)


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Literature review current through: Aug 2017. | This topic last updated: Sep 19, 2017.
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