Research Article Recipient Hyperbilirubinemia May Reduce Ischemia-Reperfusion Injury but Fails to Improve Outcome in Clinical Liver Transplantation Mihai Oltean, 1,2 Christian Barrenäs, 2 Paulo Ney Martins, 3 Gustaf Herlenius, 1,2 Bengt Gustafsson, 1,2 Styrbjörn Friman, 1,2 and William Bennet 1,2 1 Te Transplant Institute, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden 2 Sahlgrenska Academy, Te University of Gothenburg, Gothenburg, Sweden 3 Department of Surgery, Transplant Division, University of Massachusetts, Worcester, MA 01655, USA Correspondence should be addressed to Mihai Oltean; mihai.oltean@surgery.gu.se Received 2 February 2016; Accepted 24 April 2016 Academic Editor: Edna F. S. Montero Copyright © 2016 Mihai Oltean et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Exogenous bilirubin may reduce experimental ischemia-reperfusion injury (IRI) due to its antioxidant properties. We studied if early graf exposure to high bilirubin levels in the recipient afects the early IRI and outcomes afer liver transplantation (LTx). Methods. In 427 LTx patients, the AUROC curve based on bilirubin and AST at day 1 identifed a cutofof 2.04 mg/dL for the recipient pretransplant bilirubin. Recipients were grouped as having low (group L,  = 152) or high (group H,  = 275) bilirubin. Both groups had similar donor-related variables (age, preservation time, donor BMI > 28, and donor risk index (DRI)). Results. Alanine (ALT) and aspartate (AST) aminotransferase levels were higher in group L at day 1; ALT levels remained higher at day 2 in group L. LTx from high risk donors (DRI > 2) revealed a trend towards lower transaminases during the frst two days afer transplantation in group H. One month and 1-year patient survival were similar in groups L and H. High preoperative bilirubin did not afect the risk for early graf dysfunction (EGD), death, or graf loss during the frst year afer transplantation nor the incidence of acute rejection. LTx using donors with DRI > 2 resulted in similar rates of EGD in both groups. Conclusion. Increased bilirubin appears to reduce the early IRI afer LTx yet this improvement was insufcient to improve the clinical outcome. 1. Introduction Ischemia-reperfusion injury (IRI) of the liver graf reemerges as a major issue as the pressure of ever increasing waiting lists requires the use of extended criteria donor livers with steatosis, older, and non-heart-beating donors. Tese grafs are more susceptible to IRI with up to 10% of the procured livers not being transplanted due to the risk of primary graf nonfunction or dysfunction and ischemic type cholan- giopathy [1]. Several protective strategies aimed at inducing biological protective mechanisms in the graf or recipient before the injurious chain of events in the graf occurs (i.e., ischemic or pharmacologic preconditioning) have been explored both in clinical and in experimental settings [2– 5]. Although promising, many of these approaches rely on complex protocols or toxic chemicals or are technically demanding and expensive (machine perfusion). Tis ofen renders them unpractical and limits their clinical applicabil- ity. Bilirubin is a byproduct of heme catabolism occurring through the heme oxygenase-1 pathway. Bilirubin has been shown to have potent antioxidant properties [6, 7] and exoge- nous administration of bilirubin in several models of isolated organ perfusion has been shown to have a protective efect against IRI when administered before or during the ischemic event [8, 9]. Experimental evidence indicates that even a brief contact with bilirubin is sufcient to confer protection against IRI [8]. Furthermore, a clinical report suggests a protective efect of increased endogenous bilirubin against develop- ment of late graf failure afer kidney transplantation [10]. Although the protective mechanisms were unidentifed, the protective efect could be due to the reduction of the oxidative Hindawi Publishing Corporation Gastroenterology Research and Practice Volume 2016, Article ID 6964856, 6 pages http://dx.doi.org/10.1155/2016/6964856