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Vascular supply in adenomatous hyperplasia of the liver and hepatocellular carcinoma: a morphometric study.

作者信息

Ueda K, Terada T, Nakanuma Y, Matsui O

机构信息

Second Department of Pathology, Kanazawa University School of Medicine, Japan.

出版信息

Hum Pathol. 1992 Jun;23(6):619-26. doi: 10.1016/0046-8177(92)90316-u.

DOI:10.1016/0046-8177(92)90316-u
PMID:1317345
Abstract

Vascular supply of adenomatous hyperplasia (AH) of the liver, a preneoplastic or early neoplastic lesion of hepatocellular carcinoma (HCC), and that of HCC were morphometrically examined. Seventy-three nodules of AH were divided into 43 ordinary and 30 atypical AHs. The latter showed a variety of hepatocellular atypias that were, however, insufficient to make a diagnosis of HCC, while the former lacked such atypias. Arteries were slightly more numerous and portal veins were slightly less frequent in both ordinary and atypical AHs compared with the surrounding liver. In ordinary AHs, cumulative areas of arterial lumen and portovenous lumen were almost equal to or less than those in the surrounding liver in two thirds of our cases. The cumulative area of arterial lumen was equal to, and that of portovenous lumen was less than, the cumulative area in the surrounding liver in the remaining one third of our cases. In a majority of atypical AHs, the cumulative area of arterial lumen was equal to, and that of portovenous lumen was less than, the cumulative area in the surrounding liver. In most HCC nodules, the number and cumulative luminal area of arteries were much more, and those of portal veins were much less, than the number and cumulative area in the surrounding liver. The relative number and cumulative luminal area of abnormal arteries compared with all arteries showed a stepwise increase in the following order: ordinary AH (20.7% and 17.5%), atypical AH (46.8% and 52.5%), and HCC (93.6% and 92.0%). These data suggest that ordinary AH, atypical AH, and HCC are different in vascular supply, and that these differences may reflect sequential changes in the hemodynamic state during hepatocarcinogenesis.

摘要

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