A CLINICOPATHOLOGICAL STUDY OF ADENOMATOUS HYPERPLASIA OF THE LIVER IN 209 CONSECUTIVE CIRRHOTIC LIVERS EXAMINED BY AUTOPSY

Citation
T. Terada et al., A CLINICOPATHOLOGICAL STUDY OF ADENOMATOUS HYPERPLASIA OF THE LIVER IN 209 CONSECUTIVE CIRRHOTIC LIVERS EXAMINED BY AUTOPSY, Cancer, 72(5), 1993, pp. 1551-1556
Citations number
20
Categorie Soggetti
Oncology
Journal title
CancerACNP
ISSN journal
0008543X
Volume
72
Issue
5
Year of publication
1993
Pages
1551 - 1556
Database
ISI
SICI code
0008-543X(1993)72:5<1551:ACSOAH>2.0.ZU;2-5
Abstract
Background. Adenomatous hyperplasia (AH), also called macroregenerativ e nodule, of the cirrhotic liver is currently considered to be a prene oplastic or early neoplastic lesion in human hepatocellular carcinogen esis. Methods. The authors surveyed 209 consecutive cirrhotic livers f rom patients who had undergone autopsy at our laboratory during the la st 18 years (1974-1991), and examined the prevalence and clinicopathol ogic characteristics of cirrhotic livers with AH. AH was classified in to two types: ordinary and atypical. Ordinary AH (OAH) is devoid of he patocellular atypia, whereas atypical AH (AAH) consists of atypical he patocytes equivocal as to benignity and malignancy and occasionally co ntains overt malignant foci. Results. A total of 123 AH were found in 45 (21.5%) of the 209 cirrhotic livers; 38 AAH were found in 12 cirrho tic livers (5.7%), and 85 OAH was found in 41 cirrhotic liver (19.6%). Nineteen AAH contained overt malignant hepatocellular foci. Comparing the first 9 years (1974-1982) with the latter 9 years (1983-1991), 4 (3.8%) of 104 cirrhotic livers harbored AAH in the first period, and 8 (7.4%) of 105 cirrhotic livers contained AAH in the latter period. Si xteen (15.4%) of 104 cirrhotic livers harbored OAH in the first period , and 25 (23.8%) of 105 cirrhotic livers contained OAH in the latter p eriod. Etiology of the 12 cirrhotic livers with AAH was as follows: 1 was hepatitis B virus, 10 were non-A non-B hepatitis virus, and 1 was primary biliary cirrhosis. Etiology of 41 cirrhotic livers with OAH wa s as follows: 16 were hepatitis B virus, 18 were non-A non-B hepatitis virus, and 7 were other causes. AAH occurred commonly in mixed nodula r cirrhosis, whereas OAH occurred usually in macronodular or mixed nod ular cirrhosis. All 12 cirrhotic livers with AAH were associated with hepatocellular carcinoma (HCC), particularly HCC of nodular type, wher eas 17 cirrhotic livers with OAH were associated with HCC and the rema ining 24 cirrhotic livers with OAH were not associated with HCC. Concl usions. These results suggest that the number of cirrhotic livers with AH is increasing gradually, and that cirrhotic livers with AAH are ch aracterized by the association with non-A non-B hepatitis virus as wel l as simultaneous occurrence of HCC. Thus, AAH may be an important pre neoplastic lesion in cirrhotic livers associated with non-A non-B hepa titis virus (probably hepatitis C virus).