S3322 Vanishing Bile Duct Syndrome Following Cholecystectomy and ERCP: A Complex Case of Drug-Induced Cholestatic Liver Injury

Introduction: Vanishing bile duct syndrome (VBDS) is a rare and potentially severe condition characterized by the progressive loss of intrahepatic bile ducts, leading to cholestasis. While VBDS can arise from various etiologies, drug-induced liver injury (DILI) remains a significant contributor. Certain antibiotics, such as cephalosporins and metronidazole, have been implicated in VBDS. The pathogenesis often involves immune-mediated mechanisms, including T-cell-mediated injury to cholangiocytes. Diagnosis is confirmed via liver biopsy demonstrating ductopenia, and management primarily involves withdrawal of the offending agent and supportive care. Ursodeoxycholic acid (UDCA) has been utilized for its hepatoprotective properties, though its efficacy varies. Case Description/Methods: A 35-year-old woman with a history of hypertension presented with persistent abdominal pain and elevated liver enzymes. She had recently undergone laparoscopic cholecystectomy for gallstone pancreatitis and subsequently required endoscopic retrograde cholangiopancreatography (ERCP) with biliary stent placement. Despite these interventions, her liver function tests (LFTs) remained abnormal, with uptrending bilirubin, AST, ALT, and alkaline phosphatase levels. Extensive workup, including autoimmune and viral hepatitis panels, was unremarkable. A liver biopsy revealed ductopenia and cholestasis, consistent with VBDS. Potential etiologies included recent exposure to ceftriaxone and metronidazole, both known to cause DILI. Additionally, the patient had been on fluoxetine and omeprazole, medications with reported associations to VBDS. These medications were discontinued, and UDCA therapy was initiated. Subsequently, her bilirubin levels began to decline, and LFTs showed improvement. Discussion: This case underscores the complexity of diagnosing VBDS, particularly in the context of recent surgical interventions and multiple medication exposures. The temporal relationship between drug administration and onset of cholestasis, along with histological confirmation, supports a diagnosis of drug-induced VBDS. Early recognition and withdrawal of potential offending agents are crucial to prevent progression to liver failure. While UDCA has shown benefits in some cases, its role remains adjunctive, and outcomes can vary. This case highlights the need for vigilance in monitoring liver function in patients receiving hepatotoxic medications and the importance of considering VBDS in differential diagnoses of cholestatic liver injury.