Abstract
The vanishing bile duct syndrome (VBDS) is a condition secondary to inciting triggers resulting in destruction and eventual disappearance of intrahepatic bile ducts leading to cholestasis. The overall outcome varies and often depends on the nature of the precipitating cause. VBDS has been found to be associated with adverse drug reactions, infectious diseases, autoimmune diseases, ischemia, and humoral factors associated with malignancies and is often irreversible. The objective of this clinical case report is to highlight the need for a broad differential to include VBDS in similar scenarios to aid rapid diagnosis and management. We hope this could lead to a more favourable outcome for patients presenting with VBDS such as the one described in this case report with concurrent non-Hodgkin’s lymphoma and infection with hepatitis E virus. To the best of our knowledge, this is the first ever reported case of VBDS associated with non-Hodgkin’s lymphoma and hepatitis E virus infection.
Highlights
The vanishing bile duct syndrome (VBDS) is an acquired disorder associated with progressive destruction of intrahepatic bile ducts with resultant cholestasis [1]
The vanishing bile duct syndrome (VBDS) is a condition secondary to inciting triggers resulting in destruction and eventual disappearance of intrahepatic bile ducts leading to cholestasis
Non-Hodgkin lymphoma (NHL)-related VBDS has been reported as a rare occurrence, resulting in mortality associated with liver failure [4]
Summary
The vanishing bile duct syndrome (VBDS) is an acquired disorder associated with progressive destruction of intrahepatic bile ducts with resultant cholestasis [1]. We present a unique case of an 83-year-old man with non-Hodgkin’s lymphoma and co-infection with hepatitis E virus resulting in VBDS Following aggressive investigation, he was managed medically with resolution of symptoms and normalisation of biochemistry. Auto-immune profile was negative and his lactic acid dehydrogenase (LDH) was normal at 217 U/L (100-250 U/L) His serology tests did demonstrate evidence of acute hepatitis E virus, IgG and IgM reactive. As a result of his deranged liver function and acute infection, chemotherapy during his admission was not considered to be appropriate or safe He was managed on steroid monotherapy with prednisolone 40 mg once a day along with a proton pump inhibitor (PPI) (Omeprazole 40 mg once a day) for gastroprotection and vitamin Dcalcium supplement (Calcichew-D3 one tablet twice a day) for bone protection whilst on steroids. He attends regular outpatient appointments with the haematology team along with periodic blood tests, including liver function tests, for surveillance
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