title: Histopathological study of intrahepatic aberrant vessels in cases of noncirrhotic portal hypertension.
abstract: Aberrant vessels, which are defined as dilated blood vessels immediately adjacent to the peripheral portal tract, appear under conditions of extrahepatic portal obstruction and nodular regenerative hyperplasia as well as idiopathic portal hypertension. Our study was undertaken to compare their morphological aspects in these three disease cases. Aberrant vessels were found in 84% of cases of idiopathic portal hypertension, 67% of cases of extrahepatic portal obstruction infantile type, 78% of cases of extrahepatic portal obstruction adult type and 83% of cases of nodular regenerative hyperplasia. They were divided into three types: type I--no communication with the portal vein, the lumen of which is normally open; type II--communication with the portal vein; and type III--no communication with the portal vein, which is occluded. The most common types of aberrant vessel were type III in idiopathic portal hypertension (51%), type I in extrahepatic portal obstruction infantile type (46%), type II in extrahepatic portal obstruction adult type (43%) and type III in nodular regenerative hyperplasia (45%). Serial sections revealed transition between types I, II and III, at frequencies between types II and III, types I and II, and types I and III of 35.7%, 33.7% and 30.6%, respectively. Aberrant vessels demonstrated the same immunoreactivity as portal veins for collagen type IV, laminin, factor VIII and ulex europaeus agglutinin-I. They were concluded to arise from the vasa septalis or inlet venules, which would be used as intrahepatic shunts draining portal blood flow blocked by stenosed portal veins. Increased portal pressure would be expected to enhance development of aberrant vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pathology, Kitasato University School of Medicine, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ohbu
authors.forename: M
authors.initials: M
authors.lastname: Okudaira
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Takai
mesh_terms: D001808:Blood Vessels / Q000737:chemistry / Q000473:pathology; D003094:Collagen / Q000032:analysis; D003251:Constriction, Pathologic / Q000473:pathology; D004108:Dilatation, Pathologic / Q000473:pathology; D005169:Factor VIII / Q000032:analysis; D006801:Humans; D006965:Hyperplasia; D006975:Hypertension, Portal / Q000473:pathology*; D007150:Immunohistochemistry; D007797:Laminin / Q000032:analysis; D037102:Lectins / Q000032:analysis; D008099:Liver / Q000098:blood supply* / Q000473:pathology; D037121:Plant Lectins; D011169:Portal Vein / Q000473:pathology
chemical_list: D007797:Laminin; D037102:Lectins; D037121:Plant Lectins; C036850:Ulex europaeus lectins; D005169:Factor VIII; D003094:Collagen