Acute allograft rejection is most commonly seen at 7 to 14 days. The incidence of acute rejection varies from 40 to 80 percent during the first posttransplant year. After several months, the incidence of acute rejection decreases steadily, but it may be triggered at any time by tapering of immunosuppressive agents. 12 Though frequently subtle in presentation, a syndrome of acute rejection includes fever, liver tenderness, lymphocytosis, eosinophilia, liver enzyme elevation, and a change in bile color or production. In the perioperative period, the differential diagnosis must include infection, acute biliary obstruction, and vascular insufficiency. The diagnosis can be made with certainty only by excluding other causes of graft dysfunction and biopsy, which usually requires referral back to the transplant center for management and follow-up. Acute rejection is typically treated by high-dose glucocorticosteroid bolus followed by a rapid taper over 5 to 7 days. Ihis treatment is effective in 65 to 80 percent of transplant recipients.3 Secondary therapy includes the infusion of antilymphocyte globulin (e.g., OKI3), which is accompanied by a variety of potential side effects. Both these therapies are best managed at an experienced transplant center.

Chronic allograft rejection occurs in approximately 5 to 10 percent of recipients and is a major cause of late graft failure. Ihe primary manifestation of chronic rejection is a persistently cholestatic liver injury pattern with elevated serum alkaline phosphatase and bilirubin, which can be associated with pruritus. Significant loss of hepatic synthetic function is often not evident until late in the course of chronic rejection. Ihe diagnosis is made by biopsy.

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