Hepatocarcinogenesis: Multistep Changes of Drainage Vessels at CT during Arterial Portography and Hepatic Arteriography—Radiologic-Pathologic Correlation

Abstract

To clarify the changes that occur in drainage vessels of dysplastic nodules and hepatocellular carcinoma (HCC) during hepatocarcinogenesis by using computed tomography (CT) during arterial portography (CTAP) and CT during hepatic arteriography (CTHA), with histologic findings as the reference standard. Institutional ethics committee approval and informed consent were obtained. According to the findings at CTAP and CTHA, 46 surgically resected hepatocellular nodules were classified into three types: type A (n = 18) (equivalent or decreased portal perfusion compared with background liver at CTAP, decreased arterial perfusion, and no corona enhancement [perinodular contrast material drainage] at CTHA), type B (n = 13) (no portal perfusion, increased arterial perfusion, and thin (< or = 2-mm) corona enhancement), or type C (n = 15) (no portal perfusion, increased arterial perfusion, and thick (> 2-mm) corona enhancement). We compared the histopathologic features and microangioarchitecture between the types. Type A nodules histologically consisted of dysplastic nodules and well-differentiated HCC; type B and C nodules were moderately differentiated HCC. Replacing growth was commonly observed in type A nodules, whereas compressing growth was more frequently seen in types B and C. Sixty percent of type C nodules had a fibrous capsule. There were significantly fewer intranodular hepatic veins in types B and C. Serial pathologic slices demonstrated continuity from intranodular capillarized sinusoids to hepatic veins in type A nodules and to surrounding hepatic sinusoids in type B nodules. In type C nodules, intranodular capillarized sinusoids were connected to extranodular portal veins either directly or through portal venules within the fibrous capsule. Drainage vessels of HCC change from hepatic veins to hepatic sinusoids and then to portal veins during multistep hepatocarcinogenesis.