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Fig. 1 | BMC Gastroenterology

Fig. 1

From: Vanishing bile duct syndrome with hyperlipidemia after ibuprofen therapy in an adult patient: a case report

Fig. 1

The First Liver-Biopsy Specimens on Day 28. The specimen revealed seven peri-portal areas and lobular plates was intact. Hepatic lobule scattered moderate necrosis with granuloma formation and inflammatory infiltration around central veins. There were mild sinusoidal expansion with a small amount of sinus lymphocytes and eosinophil infiltration although a small quantity of DPAS-positive macrophages was present. In peri-portal area, mild to moderate expansion with mixed inflammatory cell infiltration including lymphocytes and eosinophils were noted. Eosinophilic changes were present in hepatocyte cytoplasm. In portal areas, there were accumulation of epithelium-like cells and interstitial cells, fibrous tissue hyperplasia, and interstitial fibrosis. In addition, interlobular bile duct injury with loss of bile duct structure around hepatic arteries was noticed in more than 50% of lobules. Bile salt deposition was visible among peripheral hepatocytes. The results of Immunohistochemistry stain were the followings: CD10 (+), CD38 (+), CK19 (+), CK7 (+), HBcAg (−), HBsAg (−), HCV (−), Mum-1 (+), Pre-S1 (−), ubiquitin (−); Patent staining results: DPAS (−), Masson (+), PAS (−), reticulocyte staining (+), copper and iron staining (−), rhodanine (−). Ishak grading:necroinflammatory activity score of 5 and fibrosis score of 2. The clinical implications of special markers are the followings: CD10 is a maker of bile canaliculus; CD38 and MUM1 are plasmacytic markers; CK7 and CK19 are biliary markers. CK7-positive hepatocytes indicate cholestatic hepatic changes

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