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. 2024 May 28;12(7):659–666. doi: 10.14218/JCTH.2023.00531

Table 1. Heterogeneity of hepatocyte and cholangiocyte damage in ALDs.

AIH PBC PSC
Main target cells Hepatocytes. Severe chronic hepatitis with intense portal and lobular inflammation, severe interface hepatitis, and many damaged hepatocytes Cholangiocytes (small interlobular and septal bile ducts). Non-suppurative destructive cholangitis. Cholangiocytes with swelling, vacuolated or eosinophilic cytoplasm, pyknotic nuclei, and proliferative changes with stratification Cholangiocytes (large intra- and extra-hepatic bile ducts). Cholangiocytes with features of degeneration and atrophy, resulting in strictures and eventually occlusions
Inflammatory cells Mainly lymphocytes, with a variable amount of plasma cells (especially the presence of plasma cell clusters). Some eosinophils and neutrophils may be seen Mainly lymphocytes and often numerous plasma cells (especially a coronal arrangement of plasma cells around the bile duct). Eosinophils may also be numerous, particularly at earlier stages In early disease, the changes are confined to portal tracts, with a mild mixed inflammatory cell infiltrate of lymphocytes, plasma cells, and neutrophils, usually more intense around bile ducts
Other parenchyma cells Ductular reaction, collateral, and inconspicuous bile duct injury Mild hepatocyte necrosis, acidophilic bodies, and even interface hepatitis. Feathery degeneration of hepatocytes in advanced disease stages Small duct PSC (3–5% of PSC patients). In the late phase, periportal or diffuse hepatocyte metaplasia
Typical histopathology Moderate-severe interface hepatitis, rosettes Florid duct lesion Onion skin fibrosis

ALDs, autoimmune liver diseases; AIH, autoimmune hepatitis; PBC, primary biliary cholangitis; PSC, primary sclerosing cholangitis.