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Topics/Liver Transplantation/Deceased Donor Liver Transplantation Increases Risk of Biliary Cast Syndrome Liver Transplantation | April 2026

Deceased Donor Liver Transplantation Increases Risk of Biliary Cast Syndrome Liver Transplantation | April 2026

Clinical knowledge base curated and reviewed by GastroAGI TeamLast updated April 1, 2026

Quick Answer

Introduction Biliary cast syndrome (BCS) is an uncommon but clinically significant biliary complication after liver transplantation, characterized by the formation of obstructive biliary debris within the graft biliary tree. It has traditionally been associated with ischemic biliary injury, biliary strictures, and hepatic artery compromise, and may contribute to recurrent cholangitis, graft dysfunction, and, in severe cases, graft loss.


Introduction

Biliary cast syndrome (BCS) is an uncommon but clinically significant biliary complication after liver transplantation, characterized by the formation of obstructive biliary debris within the graft biliary tree. It has traditionally been associated with ischemic biliary injury, biliary strictures, and hepatic artery compromise, and may contribute to recurrent cholangitis, graft dysfunction, and, in severe cases, graft loss. However, contemporary data defining its risk profile—particularly across living donor and deceased donor liver transplantation—remain limited.

Problem Statement

The determinants of BCS after liver transplantation are incompletely understood, especially whether the risk differs meaningfully between living donor liver transplantation (LDLT) and deceased donor liver transplantation (DDLT). This distinction is clinically important because donor type influences ischemic exposure, biliary vulnerability, and postoperative management. Clarifying the major predictors of BCS and its long-term clinical impact may improve surveillance strategies and guide early intervention.

Summary

In this single-center retrospective study of 469 adult liver transplant recipients, BCS developed in 6.6% of patients. The risk was markedly higher after DDLT than LDLT, identifying deceased donor grafts as the strongest independent predictor of BCS. Additional major risk factors included biliary stricture, hepatic arterial complications, and older donor age, reinforcing the central role of ischemic and biliary injury in BCS pathogenesis. Despite its clinical relevance, BCS did not adversely affect long-term graft or overall survival when managed appropriately. Endoscopic intervention appeared effective in controlling disease progression and preserving outcomes, even in patients with established BCS. These findings highlight DDLT recipients as a higher-risk population requiring closer biliary surveillance and support early endoscopic management as a key strategy to maintain favorable long-term transplant outcomes.

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