Abstract

A 50-year-old man, paraplegic from a motor vehicle accident in 1973, contracted hepatitis C virus (HCV) through multiple blood transfusions at the time of his severe injuries relating to his accident. He was diagnosed with HCV when he sought care for fatigue in 2003. In August 2004, he developed ascites and peripheral edema and was treated locally for several months. He had no variceal bleeding, no encephalopathy, and no other evidence of decompensated liver disease. He was otherwise healthy. He had never smoked and only drank 1-2 alcoholic beverages at a time every 4-8 weeks. He was an active individual who used a manual wheelchair, performed mechanical work with moderate lifting, and drove all-terrain vehicles. He was listed for a liver transplant in May 2005. He was a blood group A and was stable on diuretics and sodium restriction, with no other evidence of further decompensation through his follow-up on the waiting list. On October 17, 2005, the patient underwent a cadaveric liver transplantation without major complications. His preoperative Model for End-Stage Liver Disease score was 15. Both the donor and recipient were negative for cytomegalovirus. A duct-to-duct anastomosis was performed. The immunosuppression protocol at our institution consists of basiliximab 20 mg intraoperatively, then repeated on day 4 of the postoperative course; cyclosporine A (CyA) intravenously, changed to oral administration when the patient is eating well with a goal of cyclosporine blood level 2 hours after dose (C2) between 1000 to 1200 g/L; and mycophenolate mofetil (MMF) started when eating well. Corticosteroids are not used to treat our patients with hepatitis B and C. This patient received intravenous CyA for 4 days, and changed to oral dose on day 5. At that time, he also initiated MMF treatment. He spent a total of 3 uneventful days in the intensive care unit and was transferred to the ward. Postoperatively, his transaminases peaked on day 2 with an alanine aminotransferase (ALT) 1646 U/L (normal [N] 54) and an aspartate aminotransferase (AST) 1358 U/L (N 41). His bilirubin peaked on day 5 at 105 mol/L (6.2 mg/dL), as did his alkaline phosphatase (AP) at 208 U/L (N 92) and his gammaglutamyl transferase (GGT) at 239 U/L (N 50). The only complications throughout his postoperative course were mild fluid overload during early postoperative days 2-5, which was easily managed with diuretics; a urinary tract infection; and a superficial heel ulcer. His renal function remained stable throughout his posttransplantation course. His transaminases normalized by day 13 after transplant (ALT 18 U/L, AST 24 U/L; Table 1). At that time, his bilirubin continued to be mildly abnormal at 68 mol/L (4 mg/dL) and his alkaline phosphatase 129 U/L, but he steadily improved over the next few weeks. His creatinine was 60-90 mol/L (0.8-1 mg/ dL) and CyA C2 levels were 1000-1500 g/L. He was discharged from the hospital on November 9, 2005, with cyclosporine 450 mg twice a day (bid), MMF 1 g bid, acyclovir 400 mg bid, dapsone 100 mg daily, aspirin, and Prilosec 20 mg daily. On November 30, 2005 (1 month after transplantation), he underwent blood work, the results of which were as follows: ALT 222 U/L, AST 112 U/L, AP 97 U/L, GGT 48 U/L, bilirubin 29 mol/L, and CyA 1800-2300 g/L. Doppler ultrasonography revealed nothing abnormal. His CyA and MMF doses were decreased, and his liver biochemistry improved over the next few weeks to the following: ALT 153 U/L, AST 65 U/L, AP 91 U/L, GGT 39 U/L, and bilirubin 22 mol/L (1.3 mg/dL). On December 28, 2005 (2 months after transplanta-

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