THE PATHOLOGY OF THE ATROPHY HYPERTROPHY COMPLEX (AHC) OF THE LIVER -A LIGHT-MICROSCOPIC AND IMMUNOHISTOCHEMICAL STUDY

Citation
J. Lory et al., THE PATHOLOGY OF THE ATROPHY HYPERTROPHY COMPLEX (AHC) OF THE LIVER -A LIGHT-MICROSCOPIC AND IMMUNOHISTOCHEMICAL STUDY, Histology and histopathology, 9(3), 1994, pp. 541-554
Citations number
84
Categorie Soggetti
Cytology & Histology
ISSN journal
02133911
Volume
9
Issue
3
Year of publication
1994
Pages
541 - 554
Database
ISI
SICI code
0213-3911(1994)9:3<541:TPOTAH>2.0.ZU;2-9
Abstract
The term, atrophy/hypertrophy complex (AHC) of the liver, denotes a di stinct combination of hepatic atrophy and hypertrophy occurring in sit uations of significant impairment of bile flow and/or portal or hepati c 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 so me instances, in rotation of the liver around a virtual hilar axis. As recognition and early detection of AHC have a strong implication on t he treatment of several hepatobiliary diseases, adequate combined clin ical, 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 les ion patterns having the highest predictive value. For atrophy, the fol lowing features were highly characteristic: 1) Advanced septal fibrosi s with or without nodular change of parenchyma; 2) Biliary piecemeal n ecrosis with formation of vascular structures; 3) Ductular proliferati ons, 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 e ndothelia; 6) a seemingly paradoxical increase of proliferative activi ty of hepatocytes as based on PCNA staining. The severity of lesions i n atrophy was related to the type of underlying disease, in that the c hanges were clearly more expressed in situations of longstanding obstr uction due to benign disease. Using a set of well-defined morphologica l parameters, atrophy can be reproducibly distinguished from hypertrop hy in biopsy material from AHC.