Mild donor liver steatosis has no impact on hepatitis C virus fibrosis progression following liver transplantation.

Background: This study examines the impact of donor liver macrovesicular steatosis on recurrence of hepatitis C virus (HCV) disease after liver transplantation. Methods: Between 1998 and 2004, 113 patients underwent liver transplantation for HCV-related cirrhosis. Time to histologic recurrence (fibrosis score Z2) was the primary endpoint of the study. Recurrence was graded according to the system of Ludwigand Batts. ACox’s proportional hazard regressionmodelwas usedto analyse the association between donor liver steatosis and HCV recurrence. Results: Recurrence-free survival for patients who received steatotic grafts was 82% and 47% at 1 and 4 years, respectively, and81% and52% for patients who receiveda non-steatotic liver. Donor macrovesicular steatosis (5‐45%) was found to have no impact on HCVrecurrence (P=0.47).Donorage( P=0.02) and cold ischaemia time (P=0.01) were found to increase the relative risk of HCV recurrence. The estimated risk of HCVrecurrence increased by 23% for every 10-year increase in donor age. Similarly the riskofrecurrence increasedby 13% forevery 1-h increasein coldischaemiatime. Conclusion: Mild-moderate donor liver macrovesicular steatosis has no impact on HCV recurrence after liver transplantation for HCV-related cirrhosis. Cold ischaemia time and donor age increased the likelihood of HCVrecurrence. The extent of liver allograft fibrosis caused by severe recurrent hepatitis C appears to be increasing in recent years. Hepatitis C virus (HCV)-positive patients who have undergone liver transplantation after 1995 appear to be progressing more rapidly to cirrhosis than those who underwent transplantation before 1995 (1, 2). Reasons for this increasingly rapid progression to liver failure in HCV-infected liver transplant recipients include a putative increased susceptibility of ‘marginal’ and older donor livers to HCV-related injury, and a suggestion that the stronger immunosuppressive medications used since 1995 may decrease resistance to HCV aggressiveness. Recent reports also suggest that allografts from older donors, those with longer ischaemia times, and grafts from living donors are associated with an increased severity of HCVrecurrence (2‐4). The increasing demand for donor livers, in the face of a static supply, is reflected by the fact that the waiting list for donor livers has increased by over 600% from 2,902 to 17,692 from 1993 to 2005 (4). Many liver transplantation centres have been forced to modify their criteria for acceptable donor grafts in order to accommodate the increased demand. Modified or ‘expanded’ criteria include using older donors, donors with longer ischaemia times, donation after cardiac death, livers with certain viral infections, obese donors, and steatotic (fatty) livers (5). These donor livers, which were previously designated as ‘marginal’, are now being used commonly. Between 6% and 21% of donor livers now being used are steatotic and the most common causes for hepatic steatosis in the general population are alcohol abuse, diabetes, obesity, dyslipidaemias, pregnancy, and medications (6‐8). Markin et al. (9) showed in a landmark study that 1-year patient and graft survival is not affected by transplantation of donor livers with mild to moderate macrovesicular steatosis (o45%) when compared with patients transplanted with nonsteatotic donor livers . However, whether steatosis affects HCVrecurrence is unknown. No definitive relationship linking the use of mildmoderate steatotic donor livers with rapid progression of fibrosis, post-transplant liver failure, or decreased graft survival in patients with HCVexists. The aim of