The pathology of the atrophy/hypertrophy complex (AHC) of the liver. A light microscopic and immunohistochemical study Academic Article uri icon

Overview

MeSH Major

  • Liver

abstract

  • The term, atrophy/hypertrophy complex (AHC) of the liver, denotes a distinct combination of hepatic atrophy and hypertrophy occurring in situations of significant impairment of bile flow and/or portal or hepatic venous blood flow. In the lobes or segments concerned atrophy ensues, whereas areas not or less involved develop compensatory hypertrophy, resulting in a characteristic gross deformity of the organ and, in some instances, in rotation of the liver around a virtual hilar axis. As recognition and early detection of AHC have a strong implication on the treatment of several hepatobiliary diseases, adequate combined clinical, radiological and histopathological strategies have to be used in order to arrive at a correct diagnosis. The present investigation was designed to analyze the morphology of AHC in detail and to define lesion patterns having the highest predictive value. For atrophy, the following features were highly characteristic: 1) Advanced septal fibrosis with or without nodular change of parenchyma; 2) Biliary piecemeal necrosis with formation of vascular structures; 3) Ductular proliferations, frequently extending into septa and involving the parenchyma; 4) Capillarization of sinusoids with type IV collagen deposition in Disse's space; 5) Factor VIII-associated antigen expression by sinusoidal endothelia; 6) a seemingly paradoxical increase of proliferative activity of hepatocytes as based on PCNA staining. The severity of lesions in atrophy was related to the type of underlying disease, in that the changes were clearly more expressed in situations of longstanding obstruction due to benign disease. Using a set of well-defined morphological parameters, atrophy can be reproducibly distinguished from hypertrophy in biopsy material from AHC.

publication date

  • January 1994

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed ID

  • 7981501

Additional Document Info

start page

  • 541

end page

  • 54

volume

  • 9

number

  • 3