Wright State University Boonshoft School of Medicine Beavercreek, OH
Tahir Khan, MD1, Zahoor Ahmad, 2, Maimoona Zubair, 3, Ubaid Khan, 4, Drew Triplett, DO5 1Wright State University Boonshoft School of Medicine, Beavercreek, OH; 2Peshawar Medical College, Peshawar, North-West Frontier, Pakistan; 3Khyber Medical College, Peshawar, North-West Frontier, Pakistan; 4pak Internation Medical College, Peshawar, North-West Frontier, Pakistan; 5Wright State University Boonshoft School of Medicine, Dayton, OH Introduction: Vanishing Bile Duct Syndrome (VBDS) is an uncommon but severe form of chronic liver disease, defined as loss of intralobular bile ducts in >50% of portal areas of the liver. Development of VBDS has been associated with drugs, herbs, and natural supplements, infectious diseases including Hepatitis B, Hepatitis C, EBV, and CMV and immune-mediated reactions, though it can also have genetic causes. All etiologies are marked by chronic cholestasis and destruction of intrahepatic bile ducts. Progressive destruction and disappearance of intrahepatic bile ducts can lead to ductopenia. Here, we report a case of VBDS in the setting of valproic acid use
Case Description/
Methods: A 64-year-old male on divalproex acid for bipolar disorder presented with acute  jaundice with bilateral flank pain. Laboratory evaluation revealed total bilirubin of 6.3 mg/dl; direct bilirubin of 5.1 mg/dL, indirect bilirubin of 1.2 mg/dL; alkaline phosphatase 674 U/L; AST 189 U/L; ALT 170 U/L. Viral hepatitis panel was negative. Anti-smooth muscle, Alpha-1 Antitrypsin, and antimitochondrial antibody were negative. A right upper quadrant ultrasound showed mildly dilated common bile duct measuring 8mm. CT of the abdomen and pelvis showed mild intrahepatic ductal dilation. MRCP was negative for obstruction and re-confirmed mild dilation of the common bile duct with no significant intrahepatic biliary dilation. Given rising bilirubin without a cause, liver biopsy was obtained which showed acute cholestasis with ductular reaction and lymphocytic inflammation, thought to be secondary to medications. Histologic changes of autoimmune hepatitis were not appreciated. With concern for hepatic injury secondary to divalproex sodium use, the medication was tapered and switched to paliperidone. L- Carnitine was not initiated due to chronic exposure to divalproex sodium Discussion: This case highlights the importance of Divalproex as a potential cause of VBDS. Progressive destruction and disappearance of intrahepatic bile ducts can lead to ductopenia, a hall mark of VBDS. Providers should have increased awareness regarding the possibility of VBDS in patients chronically exposed to divalproex sodium since the progression of this syndrome can lead to an overall paucity of bile ducts with the potential to progress to cholestatic liver disease and possibly biliary cirrhosis.
Disclosures: Tahir Khan indicated no relevant financial relationships. Zahoor Ahmad indicated no relevant financial relationships. Maimoona Zubair indicated no relevant financial relationships. Ubaid Khan indicated no relevant financial relationships. Drew Triplett indicated no relevant financial relationships.
Tahir Khan, MD1, Zahoor Ahmad, 2, Maimoona Zubair, 3, Ubaid Khan, 4, Drew Triplett, DO5. P1798 - Vanishing Bile Duct Syndrome in the Setting of Valproic Acid Use: A Case Report of Progressive Ductopenia, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.
