title: Relevant histopathologic findings that distinguish acute cellular rejection from cholangitis in hepatic allograft biopsy specimens.
abstract: OBJECTIVE
  Histopathologic differential diagnosis of acute cellular rejection (ACR) and cholangitis continue to pose important problems following liver transplantation. The purpose of the present study was to evaluate the histopathologic features of ACR versus cholangitis.
  
  
  METHODS
  The following variables were evaluated among 36 hepatic allograft biopsy specimens, consisting of 21 with ACR (group 1) and 15 with cholangitis (group 2) for ductal neutrophilic infiltration, presence/density of portal eosinophilia, centrilobular necrosis, central/portal vein endothelialitis, pericentral inflammation, hepatocyte ballooning, hepatocanalicular/ductular cholestasis, hepatocyte apoptosis, lobular inflammation, ductular proliferation, periductal fibrosis/edema, ductular epithelial damage, and portal inflammation. Only the first biopsy samples of the ACR group were included in this study.
  
  
  RESULTS
  The incidences of ductal neutrophilic infiltration (93.3% vs 19%), hepatocanalicular cholestasis (86.7% vs 47.6%), ductular cholestasis (60% vs 0%), ductular proliferation (93.3% vs 4.8%), and periductal fibrosis/edema (93.3% vs 19%) were significantly greater in group 2 than group 1 (P < .05). In contrasts the incidences of portal eosinophilia (mean +/- SD, 3.37 +/- 3.9 vs 0.73 +/- 0.8), dense portal eosinophilia (mean +/- SD, 0.33 +/- 0.31 vs 0.11 +/- 0.16), central vein endothelialitis (0% vs 57.1%), portal vein endothelialitis (20% vs 95.2%), apoptosis (40% vs 71.4%), and necroinflammation (0% vs 90.5%) were significantly higher in group 1 (P < .05). The other parenchymal histopathologic changes and features of portal inflammation were similar in the 2 groups.
  
  
  CONCLUSIONS
  In the differential diagnosis, ductal changes (cholestasis, neutrophilic infiltration, proliferation, and periductal fibrosis/edema) favor cholangitis, whereas the presence and density of portal eosinophilia favor ACR. Portal inflammation is not a distinctive morphological finding.
authors.affiliation: Department of Pathology, Başkent University School of Medicine, Ankara, Turkey. banubil@yahoo.com
authors.forename: B
authors.initials: B
authors.lastname: Bilezikçi
authors.forename: B
authors.initials: B
authors.lastname: Demirhan
authors.forename: A
authors.initials: A
authors.lastname: Kocbiyik
authors.forename: Z
authors.initials: Z
authors.lastname: Arat
authors.forename: M
authors.initials: M
authors.lastname: Haberal
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D001706:Biopsy; D006528:Carcinoma, Hepatocellular / Q000601:surgery; D016009:Chi-Square Distribution; D002761:Cholangitis / Q000473:pathology*; D002779:Cholestasis / Q000601:surgery; D005260:Female; D006084:Graft Rejection / Q000473:pathology*; D006509:Hepatitis B / Q000601:surgery; D006527:Hepatolenticular Degeneration / Q000601:surgery; D006801:Humans; D008103:Liver Cirrhosis / Q000601:surgery; D008113:Liver Neoplasms / Q000601:surgery; D016031:Liver Transplantation / Q000473:pathology*; D008297:Male; D011183:Postoperative Complications / Q000473:pathology*; D012189:Retrospective Studies