title: Hepatitic bile duct injuries in chronic hepatitis C: histopathologic and immunohistochemical studies.
abstract: Interlobular bile ducts are reported to be damaged in viral hepatitis. Such damages are called hepatitic duct injuries and mimic chronic nonsuppurative destructive cholangitis of primary biliary cirrhosis. In this study, hepatitic bile duct injuries were evaluated histopathologically and immunohistochemically in 149 needle liver biopsy specimens from patients with chronic hepatitis C and compared immunohistochemically with primary biliary cirrhosis. Fifty-one of the needle biopsies from patients with chronic hepatitis C (34.2%) showed hepatitic bile duct injuries which were distributed focally in the liver and showed variable epithelial damages such as cytoplasmic swelling, vacuolation and acidophilia, nuclear pleomorphism, and loss of nuclear polarity. Some of the injured bile ducts were embedded within lymphoid aggregates, whereas others were surrounded by lymphocytes as well as other inflammatory cells to varied degrees. The majority of lymphoid cells around hepatitic bile duct injury were B- and T-cells mixed in various proportions, and activated T-cells were occasionally found within the biliary epithelial layer. Histopathologic and serial section studies disclosed that bile duct loss was rare in chronic hepatitis C. Statistical analysis revealed that advancement of chronic hepatitis and the degree of necroinflammatory processes of the liver, particularly in the portal tracts, were positively correlated with the occurrence of hepatitic bile duct injuries. Immunohistochemical studies demonstrated that, whereas strong ectopic expression of HLA-DR and enhanced expression of HLA-A,B,C, and pyruvate dehydrogenase E2-complex in biliary epithelial cells were frequently observed in chronic nonsuppurative destructive cholangitis of primary biliary cirrhosis, such unusual expressions were generally absent or mild, even if present, in bile duct injuries in chronic hepatitis C.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pathology (II), Kanazawa University School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kaji
authors.forename: Y
authors.initials: Y
authors.lastname: Nakanuma
authors.forename: M
authors.initials: M
authors.lastname: Sasaki
authors.forename: M
authors.initials: M
authors.lastname: Unoura
authors.forename: K
authors.initials: K
authors.lastname: Kobayashi
authors.forename: A
authors.initials: A
authors.lastname: Nonomura
authors.forename: K
authors.initials: K
authors.lastname: Tsuneyama
authors.forename: J
authors.initials: J
authors.lastname: Van de Water
authors.forename: M E
authors.initials: ME
authors.lastname: Gershwin
mesh_terms: D000328:Adult; D000368:Aged; D001652:Bile Ducts / Q000473:pathology*; D001707:Biopsy, Needle; D002908:Chronic Disease; D051047:Dihydrolipoyllysine-Residue Acetyltransferase; D005260:Female; D006680:HLA Antigens / Q000032:analysis; D006526:Hepatitis C / Q000473:pathology*; D006801:Humans; D007124:Immunoenzyme Techniques; D008105:Liver Cirrhosis, Biliary / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011768:Pyruvate Dehydrogenase Complex / Q000032:analysis
chemical_list: D006680:HLA Antigens; D011768:Pyruvate Dehydrogenase Complex; D051047:Dihydrolipoyllysine-Residue Acetyltransferase