Related Experiment Videos
Vascular supply in adenomatous hyperplasia of the liver and hepatocellular carcinoma: a morphometric study
1Second Department of Pathology, Kanazawa University School of Medicine, Japan.
Insights
Vascular changes in the liver progress from ordinary adenomatous hyperplasia (AH) to atypical AH and finally to hepatocellular carcinoma (HCC). These changes show a stepwise increase in abnormal arteries, indicating evolving hemodynamic states during cancer development.
Area of Science:
- Hepatology
- Vascular Biology
- Oncology
Background:
- Adenomatous hyperplasia (AH) is a preneoplastic lesion of hepatocellular carcinoma (HCC).
- Understanding the vascular differences between AH and HCC is crucial for early detection and treatment.
Purpose of the Study:
- To morphometrically examine and compare the vascular supply of ordinary AH, atypical AH, and HCC.
- To identify sequential vascular changes during hepatocarcinogenesis.
Main Methods:
- Morphometric analysis of vascular supply in 73 AH nodules (43 ordinary, 30 atypical) and HCC nodules.
- Comparison of arterial and portal vein characteristics between lesions and surrounding liver tissue.
Main Results:
- Both ordinary and atypical AH showed slight increases in arteries and decreases in portal veins compared to normal liver.
- A significant increase in the number and cumulative luminal area of arteries, and a decrease in portal veins, was observed in HCC.
- The proportion of abnormal arteries increased progressively from ordinary AH (20.7%) to atypical AH (46.8%) and HCC (93.6%).
Conclusions:
- Vascular supply differs significantly across ordinary AH, atypical AH, and HCC.
- These vascular differences likely reflect sequential hemodynamic alterations during the progression to liver cancer.
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.