Recurrence and Accelerated Progression of Hepatitis C following Liver Transplantation

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Abstract
A 68-year-old woman underwent orthotopic liver transplantation (OLT) in July 1998 for hepatocellular carcinoma, which developed in an HCV related cirrhotic liver. The tumor had been previously chemoembolized. Hepatitis C was diagnosed in 1982, but had never been treated. During the immediate postoperative period, she developed severe hypoxia, successfully treated by almitrine. On day 8, she was extubated. She received a classical triple immunotherapy regimen including tacrolimus, azathioprine and prednisolone and additional prophylactic anti -CMV treatment. She was transiently put on insulin and a carbohydrate diet to control diabetes which appeared post-operatively. On day 13, liver function tests were grossly normal (Table [ 1 ]). On day 25 postOLT, she was discharged, free of insulin. On that day, mild elevation of serum transminases were noted for the first time (Table [ 1 ]). Thereafter, several clinical and biological abnormalities were observed during follow-up (Table [ 1 ]): episodes of hyperglycemia with or without ketoacidosis, which required insulin; arterial hypertension, which was treated, and a persistent rise in serum transaminases and a mild elevation in conjugated bilirubin starting 2 months postoperatively. Azathioprine was stopped on day 29, and tacrolimus was replaced by cyclosporine on day 210. Differential Diagnosis A rise in serum transaminases and a mild elevation in bilirubin starting 2 months postoperatively could be due to several etiologies. First, it was important to look systematically for the following causes, which could require specific treatment. There was no obvious endothelialitis and interlobular bile ducts were normal on liver biopsies ruling out the diagnosis of acute and chronic rejection. The absence of bile duct proliferation on biopsies and the absence of dilatation of the intrahepatic biliary tree on MR-cholangiogram rule out the diagnosis of biliary obstruction. Doppler ultrasound was normal making the diagnosis of vascular obstruction unlikely. Finally, the patient was not exposed to known drugs that could explain the biochemical and pathological data. In favor of the diagnosis of recurrent hepatitis C were the following arguments:

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