One-year protocol liver biopsy can stratify fibrosis progression in liver transplant recipients with recurrent hepatitis C infection (original) (raw)
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HCV-related fibrosis progression following liver transplantation: increase in recent years
Journal of Hepatology, 2000
to-event analysis, the expected median duration to cirrhosis was 10 years The rate of it-~ansplantation fibrosis progression was significantly higher than pre-tra~pl~tation (0.2/year (0.09-M) p<O.OOOl), and higher in Spanish than US centers (0.48 (0.01-2.19) vs 0.28 (0.004-2.08); p=O.O9) despite similar progression rates prior to transplantation. Variables independently associated with post-transplantation progression included year of ~anspl~tation ~=O.O~l), race &=0.02), number of methyl-prednisolone boluses &=0.03), and HCV RNA levels at ~anspl~tation (p=O.Ol). Conclusions: HCV-related disease progression is accelerated in immunocompromised compared to immunocompetent patients, with a progressive increase in patients who have recently undergone liver transplantation. Changes in patient management posttransplantation over time and between ~ansplant centers may account for the increase in fibrosis progression observed in recent years.
Liver Transplantation, 2008
Hepatitis C recurs universally after liver transplantation (LT). Whether its progression differs after live donor liver transplantation (LDLT) and deceased donor liver transplantation (DDLT) is still debated. We retrospectively analyzed 201 consecutive LTs performed at our institution for hepatitis C–related end-stage liver disease between April 2000 and December 2005 (46 LDLTs and 155 DDLTs). Patients were followed with protocol biopsies for medians of 29 (LDLT) and 39 months (DDLT; P = 0.7). Although overall graft and patient survival did not differ, the mean fibrosis stage (Metavir) was significantly higher at 12 to 48 months post-LT (all P < 0.05), and the rate of fibrosis progression tended to be faster after DDLT than LDLT (0.19 versus 0.11 stage/year, P = 0.05). In univariate analysis, donor age, cold ischemic time, and DDLT were significantly associated with a fibrosis stage ≥ 1 at 1 year and a fibrosis stage of 3 or 4 at 2 years post-LT. In multivariate analysis, however, donor age was the sole variable independently associated with both surrogate outcomes. Thus, donor age > 45 years carried a relative risk of 8.17 (confidence interval = 2.6–25.5, P = 0.001) for reaching fibrosis stage 3 or 4 at 2 years post-LT. In conclusion, donor age, rather than the transplant approach, determines the progression of recurrent hepatitis C after LT. LDLT, allowing for the selection of younger donors, may particularly benefit hepatitis C patients. Liver Transpl 14:1778–1786, 2008. © 2008 AASLD.
Liver International, 2007
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 Ludwig and Batts. A Cox's proportional hazard regression model was used to 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, and 81% and 52% for patients who received a non-steatotic liver. Donor macrovesicular steatosis (5-45%) was found to have no impact on HCV recurrence (P = 0.47). Donor age (P = 0.02) and cold ischaemia time (P = 0.01) were found to increase the relative risk of HCV recurrence. The estimated risk of HCV recurrence increased by 23% for every 10-year increase in donor age. Similarly the risk of recurrence increased by 13% for every 1-h increase in cold ischaemia time. 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 HCV recurrence.
Transplantation, 2011
Background. Hepatitis C virus (HCV) recurrence is universal after liver transplantation (LT). Whether the progression of recurrent HCV is faster after live-donor LT (LDLT) compared with deceased-donor LT (DDLT) is debatable. Methods and Results. We retrospectively examined 100 consecutive LTs (65 DDLTs and 35 LDLTs) performed between July 2000 and July 2003. A total of 147 liver biopsies were performed between 6 months post-LT and last follow-up. Mean donor age and model for end-stage liver disease (MELD) score were significantly lower in LDLT (PϽ0.01). On a mean follow-up of 86.6Ϯ6.8 months, overall patient and graft survivals were 61% (51% DDLT vs. 77.1% LDLT; Pϭ0.026) and 56% (46.2% DDLT vs. 71.4% LDLT; Pϭ0.042), respectively. Eight of 39 (20.5%) deaths (7 DDLT and 1 LDLT) and two of nine (22.2%) retransplants (one in each group) were related to recurrent HCV. Mean fibrosis scores for DDLT and LDLT were 1.9Ϯ1.7 and 1.6Ϯ1.4, respectively (Pϭ0.01). When donor age less than 50 years and MELD score less than 25 were matched among 64 patients (32 DDLT and 32 LDLT), the overall patient and graft survivals were 73.4% (68.8% DDLT vs. 78.1% LDLT; Pϭ0.439) and 71.9% (71.9% DDLT vs. 71.9% LDLT; Pϭ0.978), respectively. Conclusions. Long-term survival rates were better, and fibrosis scores were lower for LDLT. The survivals between LDLT and DDLT were comparable for patients with MELD score less than 25 and donor age less than 50 years.
Liver Transplantation, 2007
In this retrospective study of hepatitis C virus (HCV)-infected transplant recipients in the 9-center Adult to Adult Living Donor Liver Transplantation Cohort Study, graft and patient survival and the development of advanced fibrosis were compared among 181 living donor liver transplant (LDLT) recipients and 94 deceased donor liver transplant (DDLT) recipients. Overall 3-year graft and patient survival were 68% and 74% in LDLT, and 80% and 82% in DDLT, respectively. Graft survival, but not patient survival, was significantly lower for LDLT compared to DDLT (P ϭ 0.04 and P ϭ 0.20, respectively). Further analyses demonstrated lower graft and patient survival among the first 20 LDLT cases at each center (LDLT 20) compared to later cases (LDLT Ͼ 20; P ϭ 0.002 and P ϭ 0.002, respectively) and DDLT recipients (P Ͻ 0.001 and P ϭ 0.008, respectively). Graft and patient survival in LDLT Ͼ20 and DDLT were not significantly different (P ϭ 0.66 and P ϭ 0.74, respectively). Overall, 3-year graft survival for DDLT, LDLT Ͼ20, and LDLT 20 were 80%, 79% and 55%, with similar results conditional on survival to 90 days (84%, 87% and 68%, respectively). Predictors of graft loss beyond 90 days included LDLT 20 vs. DDLT (hazard ratio [HR] ϭ 2.1, P ϭ 0.04), pretransplant hepatocellular carcinoma (HCC) (HR ϭ 2.21, P ϭ 0.03) and model for end-stage liver disease (MELD) at transplantation (HR ϭ 1.24, P ϭ 0.04). In conclusion, 3-year graft and patient survival in HCV-infected recipients of DDLT and LDLT Ͼ20 were not significantly different. Important predictors of graft loss in HCV-infected patients were limited LDLT experience, pretransplant HCC, and higher MELD at transplantation. Liver Transpl 13:122-129, 2007.
Scandinavian Journal of Gastroenterology, 2012
Objective. Survival following liver transplantation for hepatitis C virus (HCV) infection is affected by several factors. The aims of this single-center study were to evaluate survival from 1992 to 2006 in HCV-infected liver transplant recipients and to identify factors influencing patient and graft survival, with particular focus on donor liver histopathology. Material and methods. Survival among 84 patients transplanted for HCV-related liver disease at the Sahlgrenska University Hospital during the above period was evaluated. Median follow-up time was 57 months (range 28-87). A perioperative liver biopsy from the donor liver graft was available in 68 cases. Biopsies were assessed for fibrosis, necroinflammatory activity, and degree of steatosis. Patient and graft survival according to relevant factors including donor histopathology were analyzed by Kaplan-Meier analysis. Results. We found an association between donor liver fibrosis and patient survival (p = 0.016) as well as between graft survival and portal inflammation in the donor liver (p = 0.026). Both these associations remained significant in multivariate analysis (p = 0.007 and 0.017 respectively). Moreover, recipient age over 60 was found predictive of patient survival and repeated steroid boluses or steroid-resistant rejection of graft survival. Donor age was high throughout the study period. Conclusion. Histopathological features, especially portal inflammation and stage of fibrosis, in the donor liver may deleteriously affect graft and patient survival following HCV-related liver transplantation. Thus, pretransplant evaluation of donor histopathology may be of value in the selection of donors for transplantation of HCV-positive individuals, especially among donors older than 60 years.