Boga S, Munoz-Abraham AS, Rodriguez-Davalos MI, Emre SH, Jain D, Schilsky ML. Host factors are dominant in the development of post-liver transplant non-alcoholic steatohepatitis. World J Hepatol 2016; 8(15): 659-664 [PMID: 27239259 DOI: 10.4254/wjh.v8.i15.659]
Corresponding Author of This Article
Salih Boga, MD, Postdoctoral Fellow, Division of Digestive Diseases, Section of Transplantation and Immunology, Department of Medicine and Surgery, Yale University School of Medicine, 333 Cedar Street, LMP 1080, New Haven, CT 06520, United States. salihboga@yahoo.com
Research Domain of This Article
Transplantation
Article-Type of This Article
Case Report
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Hepatol. May 28, 2016; 8(15): 659-664 Published online May 28, 2016. doi: 10.4254/wjh.v8.i15.659
Host factors are dominant in the development of post-liver transplant non-alcoholic steatohepatitis
Salih Boga, Armando Salim Munoz-Abraham, Manuel I Rodriguez-Davalos, Sukru H Emre, Dhanpat Jain, Michael L Schilsky
Salih Boga, Michael L Schilsky, Division of Digestive Diseases, Section of Transplantation and Immunology, Department of Medicine and Surgery, Yale University School of Medicine, New Haven, CT 06520, United States
Armando Salim Munoz-Abraham, Manuel I Rodriguez-Davalos, Sukru H Emre, Department of Surgery, Section of Transplantation and Immunology, Yale-New Haven Transplantation Center, Yale University School of Medicine, New Haven, CT 06520, United States
Dhanpat Jain, Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, United States
Author contributions: Boga S and Munoz-Abraham AS collected the data from patients’ file, reviewed literature and drafted manuscript; Jain D evaluated the biopsy specimens from pathologic points of view, prepared demonstrative pathology pictures; Rodriguez-Davalos MI, Emre SH and Schilsky ML supervised in designing and drafting the manuscript, revised the manuscript critically for important intellectual content; Emre SH and Schilsky ML presented patients’ clinical data, constituted the final form of manuscript; all authors read and approved the final manuscript.
Institutional review board statement: This case report was exempt from the Institutional Review Board standards at Yale University.
Informed consent statement: The patients involved in this report gave their written informed consents authorizing use and disclosure of their protected health information.
Conflict-of-interest statement: All the authors have no conflicts of interests to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Salih Boga, MD, Postdoctoral Fellow, Division of Digestive Diseases, Section of Transplantation and Immunology, Department of Medicine and Surgery, Yale University School of Medicine, 333 Cedar Street, LMP 1080, New Haven, CT 06520, United States. salihboga@yahoo.com
Telephone: +1-203-7371592 Fax: +1-203-7856645
Received: January 25, 2016 Peer-review started: January 25, 2016 First decision: February 29, 2016 Revised: March 30, 2016 Accepted: May 7, 2016 Article in press: May 9, 2016 Published online: May 28, 2016 Processing time: 115 Days and 10.7 Hours
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a recognized problem in patients after orthotopic liver transplantation and may lead to recurrent graft injury. As the increased demand for liver allografts fail to match the available supply of donor organs, split liver transplantation (SLT) has emerged as an important technique to increase the supply of liver grafts. SLT allows two transplants to occur from one donor organ, and provides a unique model for observing the pathogenesis of NAFLD with respect to the role of recipient environmental and genetic factors. Here we report on two recipients of a SLT from the same deceased donor where only one developed non-alcoholic steatohepatitis (NASH), suggesting that host factors are critical for the development of NASH.
Core tip: Split liver transplantation provides a unique model of the pathogenesis of non-alcoholic fatty liver disease with respect to the role of recipient environmental risk factors and genetic background because the same donor graft is shared by two distinct recipients. Here we present two recipients of a split liver transplantation from same deceased donor, with one developing nonalcoholic steatohepatitis and the other without any evidence of hepatic steatosis three years after they were transplanted. These cases provide a unique natural experiment to explore host factors that contributed to the development of nonalcoholic steatohepatitis after liver transplantation.
