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Case Report
Copyright: ©Author(s) 2027.
World J Gastroenterol. Jan 7, 2027; 33(1): 123590
Published online Jan 7, 2027. doi: 10.3748/wjg.123590
Figure 1
Figure 1 Dynamic changes of bilirubin during the course of the patient's illness. DBIL: Direct bilirubin; TBIL: Total bilirubin.
Figure 2
Figure 2 Representative histopathological findings of the liver biopsy. A: Hematoxylin and eosin staining showed preserved hepatic plate architecture, prominent intrahepatocellular and canalicular cholestasis with bile thrombi, hepatocellular swelling and degeneration, and focal spotty necrosis; B: Cytokeratin 7 immunostaining highlighted biliary epithelial and ductular changes, supporting bile duct injury in a cholestatic pattern.
Figure 3
Figure 3 Genetic analysis of the UGT1A1 mutation. Pedigree showing biparental inheritance of the c.211G>A variant. Sanger sequencing chromatograms confirming homozygosity in the proband (c.211A/A) and heterozygosity in both parents (c.211G/A).
Figure 4
Figure 4 Abdominal computed tomography, magnetic resonance imaging, and magnetic resonance cholangiopancreatography findings before third endoscopic retrograde cholangiopancreatography. A: Axial abdominal computed tomography shows pneumobilia in the intrahepatic bile ducts and dilatation of the portal vein; B: Axial abdominal magnetic resonance imaging shows multiple hypointense intraductal lesions within the hepatic ducts and common bile duct (CBD), with the largest measuring approximately 5.2 mm in diameter; C: Coronal maximum-intensity projection magnetic resonance cholangiopancreatography demonstrates multiple intraductal filling defects involving the hepatic ducts and CBD, extending over a longitudinal length of approximately 66.68 mm.


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