Abstract

Liver transplantation (LT) is an established therapy for end-stage liver disease based on a substantial progress in surgical and immunological management of concomitant posttransplant phenomena. Apart from rejection and HCV-recurrence, the development of biliary strictures is one of the most serious complications observed after LT significantly affecting graft and patient survival [1, 2]. Frequently compared to Achilles foot, the dynamics of post-transplant biliary restitution may determine the overall transplant success and play the role of a critical step after LT. Post-transplant complications in the biliary system occur in 10-50% with significant mortality in up to 19% and re-transplantation rates of 6-12.5% [3-6]. Early post-transplant biliary complications are predominantly related to technical aspects of the operation regarding the insufficiency of bile duct anastomosis, biliary leaks or anastomotic stenosis [7]. One third of all biliary complications occur later than first two months after LT affecting intrahepatic integrity on donor side and functionality of distal parts of the biliary tree in the recipient including the bile duct anastomosis and the ampulla of Vater [1, 2, 8]. In contrast to the anastomotic strictures, which can be successfully treated endoscopically or surgically, non-anastomotic strictures represent a significant therapeutic problem [9, 10]. Non-anastomotic strictures of the bile duct may develop in up to 20% of all LTs. Untreated stricture-associated complications may lead to cholestasis, severe graft dysfunction, cholangiosepsis, secondary cirrhosis and even death [6, 8, 11, 12]. Non-anastomotic strictures may be classified according to their etiology into strictures related to PSC-recurrence (primary sclerosing cholangitis), strictures occurring due to vascular complications in case of a manifest hepatic artery thrombosis as ischemic biliary lesions (IBL), strictures occurring after prolonged ischemia (e.g. successfully treated hepatic artery thrombosis) and strictures occurring without an obvious vascular complication. In the presence of a macroscopically obviously undisturbed perfusion they are described as so-called ischemic type biliary lesions (ITBL). The occurrence of biliary lesions after primarily successful LT justifies the necessity to introduce ITBL as an independent pathologic entity. In spite of a certain descriptive inaccuracy, the terms “non-anastomotic strictures”, “intrahepatic biliary strictures” and “ischemic type biliary strictures” are usually used as synonyms for posttransplant strictures, diffuse dilatations and segmental ectasia of the biliary tract as a result of inflammation and fibrotic remodeling (figs. 1 and 2) [13]. Due to terminological diversity, the incidence of ITBL significantly varies among published studies between 1.4 and 26% [1, 5, 14]. The diagnosis “ITBL” may be made only after the exclusion of vascular (IBL) and immunologic pathologies (PSC-recurrence and chronic

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