Oren Shaked1, Jack Demetris2, Josh Levitsky3, Sandy Feng1, Bao-Li Loza4, Jeff Punch5, Jorge Reyes6, Goran Klintmalm7, Whitney Jackson8, Michele DesMarais9, Peter Sayre9, Abraham Shaked4, K Rajender Reddy10. 1. Department of Surgery, University of California San Francisco, San Francisco, CA. 2. Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA. 3. Division of Hepatology and Comprehensive Transplant Center, Northwestern Memorial Hospital, Chicago, IL. 4. Department of Surgery, University of Pennsylvania, Philadelphia, PA. 5. Department of Surgery, University of Michigan, Ann Arbor, MI. 6. Department of Surgery, University of Washington, Seattle, WA. 7. Baylor Simmons Transplant Institute, Baylor University Medical Center, Dallas, TX. 8. Division of Gastroenterology and Hepatology, University of Colorado Denver, Aurora, CO. 9. Immune Tolerance Network, San Francisco, CA. 10. Division of Gastroenterology and Hepatology, University of Pennsylvania, Philadelphia, PA.
Abstract
BACKGROUND: Deceased donor and recipient predictors of posttransplant steatosis/steatohepatitis and fibrosis are not well known. Our aim was to evaluate the prevalence and assess donor and recipient predictors of steatosis, steatohepatitis, and fibrosis in liver transplantation recipients. METHODS: Using the immune tolerance network A-WISH multicenter study (NCT00135694), donor and recipient demographic and clinical features were collected. Liver biopsies were taken from the donor liver at transplant, and from recipients per protocol and for-cause (ie, abnormal transaminases and to rule out rejection) and were interpreted by a central pathologist. RESULTS: One hundred eighty-three paired donor/recipients liver biopsies at the time of transplant and posttransplant follow-up (median time 582 d; average time to last biopsies was 704 d [SD ± 402 d]) were analyzed. Donor steatosis did not influence recipient steatosis or fibrosis. Ten of 183 recipients had steatohepatitis on the last biopsy. Recipient body mass index at the time of liver biopsy was the most influential factor associated with posttransplant steatosis. Both donor and recipient metabolic syndrome features were not associated with graft steatosis. Untreated hepatitis C viral (HCV) infection was the most influential factor associated with the development of allograft fibrosis. CONCLUSIONS: In a large experience evaluating paired donor and recipient characteristics, recipient body mass index at the time of liver biopsy was most significantly associated with posttransplant steatosis. Untreated HCV etiology influenced graft fibrosis. Thus relative to untreated HCV, hepatic fibrosis in those with steatosis/steatohepatitis is less common though long-term follow-up is needed to determine the course of posttransplant fibrosis. Emphasis on recipient weight control is essential.
BACKGROUND: Deceased donor and recipient predictors of posttransplant steatosis/steatohepatitis and fibrosis are not well known. Our aim was to evaluate the prevalence and assess donor and recipient predictors of steatosis, steatohepatitis, and fibrosis in liver transplantation recipients. METHODS: Using the immune tolerance network A-WISH multicenter study (NCT00135694), donor and recipient demographic and clinical features were collected. Liver biopsies were taken from the donor liver at transplant, and from recipients per protocol and for-cause (ie, abnormal transaminases and to rule out rejection) and were interpreted by a central pathologist. RESULTS: One hundred eighty-three paired donor/recipients liver biopsies at the time of transplant and posttransplant follow-up (median time 582 d; average time to last biopsies was 704 d [SD ± 402 d]) were analyzed. Donor steatosis did not influence recipient steatosis or fibrosis. Ten of 183 recipients had steatohepatitis on the last biopsy. Recipient body mass index at the time of liver biopsy was the most influential factor associated with posttransplant steatosis. Both donor and recipient metabolic syndrome features were not associated with graft steatosis. Untreated hepatitis C viral (HCV) infection was the most influential factor associated with the development of allograft fibrosis. CONCLUSIONS: In a large experience evaluating paired donor and recipient characteristics, recipient body mass index at the time of liver biopsy was most significantly associated with posttransplant steatosis. Untreated HCV etiology influenced graft fibrosis. Thus relative to untreated HCV, hepatic fibrosis in those with steatosis/steatohepatitis is less common though long-term follow-up is needed to determine the course of posttransplant fibrosis. Emphasis on recipient weight control is essential.
Authors: Abraham Shaked; Michele R DesMarais; Heather Kopetskie; Sandy Feng; Jeffrey D Punch; Josh Levitsky; Jorge Reyes; Goran B Klintmalm; Anthony J Demetris; Bryna E Burrell; Allison Priore; Nancy D Bridges; Peter H Sayre Journal: Am J Transplant Date: 2018-12-31 Impact factor: 8.086
Authors: Michael R Charlton; Justin M Burns; Rachel A Pedersen; Kymberly D Watt; Julie K Heimbach; Ross A Dierkhising Journal: Gastroenterology Date: 2011-07-02 Impact factor: 22.682
Authors: Stefano Gitto; Nicola de Maria; Fabrizio di Benedetto; Giuseppe Tarantino; Valentina Serra; Lorenzo Maroni; Matteo Cescon; Antonio D Pinna; Filippo Schepis; Pietro Andreone; Erica Villa Journal: Eur J Gastroenterol Hepatol Date: 2018-07 Impact factor: 2.566
Authors: Vatche G Agopian; Fady M Kaldas; Johnny C Hong; Meredith Whittaker; Curtis Holt; Abbas Rana; Ali Zarrinpar; Henrik Petrowsky; Douglas Farmer; Hasan Yersiz; Victor Xia; Jonathan R Hiatt; Ronald W Busuttil Journal: Ann Surg Date: 2012-10 Impact factor: 12.969