title: Abnormal intrahepatic portal vasculature in native and allograft liver biopsies: a comparative analysis.
abstract: Abnormal portal vessels in small portal tracts can be seen in association with various causes of portal hypertension, such as noncirrhotic portal hypertension (NCPH) and cirrhosis. Very little has been reported about the presence of abnormal portal vessels in livers with normal portal pressure. Little attention has also been given to the presence of abnormal vessels in liver allografts outside the setting of transplant vasculopathy/chronic rejection. This study reports on the portal vasculature abnormalities, many similar to those described in NCPH, encountered in routine native liver biopsies (n = 46) and allograft liver biopsies (n = 48). A classification scheme for the abnormal portal vasculature was adapted from the literature, and the portal vessels were divided into five groups (types 0-IV). Abnormal vessels were present in greater than 25% of the portal tracts in 88% of all the biopsies studied; there was no significant difference between the native and allograft biopsies. In the allograft biopsy group, there were correlations between vascular abnormalities and severity of a concurrent acute cellular rejection episode, the presence of prior rejection episodes, and length of time after transplant. Biopsies from patients with viral hepatitis C infection (HCV) showed more type IV lesions (absent or sclerosed portal vessels) with fragmentation when compared with biopsies obtained for other reasons. The number of portal tracts with abnormal portal veins and fragmented vessels correlated positively with increasing fibrosis. This is the first study to demonstrate the presence of abnormal portal vessels, some of the type seen in NCPH, in a significant number of both native and allograft liver biopsies in patients without evidence of portal hypertension. Abnormal portal vasculature tends to be associated with HCV and increased fibrosis, and, within the transplant group, with the severity of rejection, presence of prior rejection episodes, and increased time posttransplantation.
authors.affiliation: Department of Pathology, Presbyterian Hospital-A610, University of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, PA 15213, USA. krasinskasam@upmc.edu
authors.forename: Alyssa M
authors.initials: AM
authors.lastname: Krasinskas
authors.forename: Jeffrey D
authors.initials: JD
authors.lastname: Goldsmith
authors.forename: Anne
authors.initials: A
authors.lastname: Burke
authors.forename: Emma E
authors.initials: EE
authors.lastname: Furth
mesh_terms: D001706:Biopsy; D006526:Hepatitis C / Q000473:pathology; D006801:Humans; D008099:Liver / Q000473:pathology* / Q000821:virology; D016031:Liver Transplantation / Q000473:pathology*; D008875:Middle Aged; D011168:Portal System / Q000473:pathology*; D014184:Transplantation, Homologous