Histologic injury caused by recurrent hepatitis C virus (HCV) has been reported in up to 90% of HCV-infected patients who undergo liver transplantation with a cadaveric graft. However, the natural history of HCV after living donor liver transplantation (LDLT) is not well described. We performed a retrospective analysis of 68 consecutive HCV-infected adult patients: 45 recipients of cadaveric grafts (CAD) were compared with 23 LDLT patients. Elevated serum transaminases, positive HCV RNA, and liver biopsy consistent with histologic evidence of HCV defined recurrence. When comparing CAD with LDLT, both the incidence of HCV recurrence and time to recurrence were not different. The overall incidence of severe sequelae of HCV recurrence, either cholestatic hepatitis, grade III-IV inflammation, and/or HCV-induced graft failure requiring retransplantation, was also not different when comparing CAD with LDLT. However, when comparing CAD versus LDLT, no CAD patient developed cholestatic hepatitis C, compared with 17% of LDLT who developed this complication (P ‫؍‬ .001). Thus, in this patient population, the timing and incidence of HCV recurrence were not different when comparing CAD versus LDLT, but the incidence of cholestatic hepatitis was significantly greater in patients with HCV who underwent LDLT. (Liver Transpl 2003;9:1028-1035.) E nd stage liver disease caused by hepatitis C virus (HCV) is the most common indication for liver transplantation in the United States. However, complications caused by recurrent HCV infection are increasingly being recognized; in patients with active HCV replication before transplantation, reacquisition of viremia after transplantation is universal, and allograft hepatitis caused by HCV occurs in up to 90% of patients followed for 5 years. 1-9 Although histologic injury in the allograft caused by HCV is exceedingly common, disease progression after the development of hepatitis is variable, with some patients experiencing indolent disease and others rapidly progressing to cirrhosis and liver failure. In patents who develop HCV-associated cirrhosis posttransplantation, rapid decompensation is a common occurrence. It has been reported that up to 42% of patients with HCV-associated cirrhosis posttransplantation develop decompensation manifested as ascites, encephalopathy, or hepatic hydrothorax, and fewer than 50% of patients survive more than 1 year after the development of decompensation. 10-12 Thus, both prospective and retrospective data are emerging that indicate that the progression of HCV after orthotopic liver transplantation is accelerated when compared with nontransplantation patients. This has been attributed to multiple factors, including the impact of immunosuppression on viral replication and host defenses. 13 Several lines of anecdotal evidence suggest that HCV recurrence might be more severe in recipients of living donor liver transplantation (LDLT). We hypothesize that postoperative liver regeneration in the partial graft procured from living donors may facilitate HCV repli...

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The MTD for weekly paclitaxel plus daily PTK/ZK is 75 mg/m(2) and 750 mg. PK analysis revealed a significant drug-drug interaction, with an increase in paclitaxel clearance. This combination was well tolerated with evidence of anti-cancer activity and provides guidance for phase 2 planning.