title: Histopathologic features, immunophenotyping, clonality, and eubacterial fluorescence in situ hybridization in cats with lymphocytic cholangitis/cholangiohepatitis.
abstract: Feline lymphocytic cholangitis is a poorly characterized disease complex with respect to histologic lesions, immunophenotype, and etiopathogenesis. Seventy-eight cases of feline lymphocytic cholangitis (n = 51) and feline hepatic lymphoma (n = 27) were reviewed using standardized histopathology, immunophenotyping (B cell and T cell), polymerase chain reaction for T-cell receptor (TCR) gene rearrangement, and fluorescence in situ hybridization (FISH) for eubacteria. Five histopathologic features in cases of lymphocytic cholangitis assisted in its differentiation from hepatic lymphoma: bile duct targeting (n = 32, 62.7%), ductopenia (n = 9, 17.6%), peribiliary fibrosis (n = 37, 72.5%), portal B-cell aggregates (n = 36, 70.6%), and portal lipogranulomas (n = 38, 74.5%). The majority of lymphocytic cholangitis cases (n = 35, 68.6%) were T cell predominant; 15 (29.4%) had an equal mix of B cells and T cells, and 1 (1.9%) had a B cell-predominant infiltrate; 66.6% of hepatic lymphoma cases were T-cell lymphomas. TCR clonality results were unexpected, with 17.1% of cases of lymphocytic cholangitis having clonal or oligoclonal populations and with T-cell lymphomas having variable TCR clonality (63.6% clonal or oligoclonal, 36.3% polyclonal). The majority of lymphocytic cholangitis (n = 32 of 36, 88.8%) and all hepatic lymphoma cases had no detectable eubacteria using FISH. As demonstrated here, bile duct targeting, ductopenia, peribiliary fibrosis, portal B-cell aggregates, and portal lipogranulomas are lymphocytic cholangitis features that, along with polyclonal TCR (83%), help differentiate it from hepatic lymphoma. No strong evidence was found implicating in situ bacterial colonization as an etiopathogenesis of lymphocytic cholangitis.
authors.affiliation: Department of Veterinary Clinical and Diagnostic Sciences, University of Calgary, Calgary, Canada. alwarren@ucalgary.ca
authors.forename: A
authors.initials: A
authors.lastname: Warren
authors.forename: S
authors.initials: S
authors.lastname: Center
authors.forename: S
authors.initials: S
authors.lastname: McDonough
authors.forename: R
authors.initials: R
authors.lastname: Chiotti
authors.forename: R
authors.initials: R
authors.lastname: Goldstein
authors.forename: E
authors.initials: E
authors.lastname: Meseck
authors.forename: M
authors.initials: M
authors.lastname: Jacobsen
authors.forename: P
authors.initials: P
authors.lastname: Rowland
authors.forename: K
authors.initials: K
authors.lastname: Simpson
mesh_terms: D000818:Animals; D002371:Cat Diseases / Q000235:genetics / Q000382:microbiology / Q000473:pathology*; D002415:Cats; D002761:Cholangitis / Q000235:genetics / Q000473:pathology / Q000662:veterinary*; D005260:Female; D020022:Genetic Predisposition to Disease; D006520:Hepatitis, Animal / Q000235:genetics / Q000473:pathology*; D007150:Immunohistochemistry / Q000662:veterinary; D016130:Immunophenotyping / Q000662:veterinary*; D008099:Liver / Q000473:pathology; D008297:Male; D016133:Polymerase Chain Reaction; D012189:Retrospective Studies