Necrosis of portal tumor embolus of hepatocellular carcinoma by lipiodol transcatheter chemo-embolization. A case report

We describe a case of hepatocellular carcinoma in which a tumor embolus in the portal vein and 3 of 4 intrahepatic metastases were necrosed completely by Lipiodol transcatheter chemo-embolization (Lipiodol-TCE). Tumor emboli in the portal vein and intrahepatic metastases usually cannot be necrosed by conventional transcatheter chemo-embolization alone, because small nodules such as intrahepatic metastases and tumor emboli in the portal vein are supplied blood from the portal vein. However, in this case, Lipiodol-TCE was effective against tumor emboli in the portal vein and intrahepatic metastases.     

A case of necrosis of hepatocellular carcinoma and tumor thrombus in the portal vein induced by transcatheter arterial lipiodol chemoembolization

A case of hepatocellular carcinoma is reported in which the main tumor, intrahepatic metastases and a tumor thrombus in the portal vein were necrotized completely after Lipiodol chemoembolization. In this case, the tumor thrombus seemed to act as a portal embolus. This phenomenon is interesting because Lipiodol chemoembolization alone usually can not necrotize intra- or extra-capsular invasion, intrahepatic metastasis or tumor thrombus in the portal vein. This case is considered to be suggestive of a possible therapy for hepatocellular carcinoma.     

An Autopsy Case of Metastatic Foci of Hepatocellular Carcinoma in Adenomatous Hyperplasias of the Liver

Adenomatous hyperplasia of the liver is known as a preneoplastic or early developmental stage of hepatocellular carcinoma, in which overt malignant foci occasionally develop. We have recently experienced an autopsy case (a 70-year-old male) of liver cirrhosis with hepatocellular carcinoma and two nodules of adenomatous hyperplasia. The latter two nodules contained several microscopic foci of moderately differentiated hepatocellular carcinoma. There were a number of tumor microemboli in portal vein branches within areas of adenomatous hyperplasia in addition to areas surrounding cirrhotic liver, some of which grew into the parenchyma of adenomatous hyperplasia and cirrhotic regenerative nodules. These findings and the fact that adenomatous hyperplasia contained portal tracts including portal venous branches, suggest that malignant foci in adenomatous hyperplasia of the liver in this case might represent metastases from hepatocellular carcinoma in other parts of the liver via the intrahepatic portal venous system. Acta Pathol Jpn 41: 911 915, 1991.     

An autopsy case of metastatic foci of hepatocellular carcinoma in adenomatous hyperplasias of the liver.

Adenomatous hyperplasia of the liver is known as a preneoplastic or early developmental stage of hepatocellular carcinoma, in which overt malignant foci occasionally develop. We have recently experienced an autopsy case (a 70-year-old male) of liver cirrhosis with hepatocellular carcinoma and two nodules of adenomatous hyperplasia. The latter two nodules contained several microscopic foci of moderately differentiated hepatocellular carcinoma. There were a number of tumor microemboli in portal vein branches within areas of adenomatous hyperplasia in addition to areas surrounding cirrhotic liver, some of which grew into the parenchyma of adenomatous hyperplasia and cirrhotic regenerative nodules. These findings and the fact that adenomatous hyperplasia contained portal tracts including portal venous branches, suggest that malignant foci in adenomatous hyperplasia contained portal tracts including represent metastases from hepatocellular carcinoma in other parts of the liver via the intrahepatic portal venous system.     

Early hepatocellular carcinoma macroscopically resembling adenomatous hyperplasia: Pathological resemblance to carcinoma-in-situ

The pathological features of 11 nodules of early hepatocellular carcinoma (EHCC) were studled. Their macroscopic features resembled those of adenomatous hyperplasia and differed from those of advanced hepatocellular carcinomas (AHCC). The EHCC extended along the hepatic lobular structure and lacked expansive growth. The endothelial cells in the dnusoids of EHCC did not react to Ulex europeeus aggiutinin 1 (UEA1) like adenomatous hyperplasla or other liver parenchyma, whereas the endothelial celis in the AHCC did react to UEA1. immunohistochemically, CD68-positlve Kupffer cells were noted in the alnusolds of EHCC, whereas in the AHCC Kupfter cails were not seen. Tumor emboli in the portal vein and intrahepatic metastases were not Identified In EHCC. which seemed to be carcinoma-in-situ or a microinvasive stage of hepatocareinogenesis.     

Intrahepatic metastases in hepatocellular carcinoma: the role of the portal vein as an efferent vessel

The mechanism and pathogenesis of the high frequency of intrahepatic metastasis in hepatocellular carcinoma (HCC) has not yet been elucidated. Two hundred and thirty one tumors ( 5 cm in diameter) of resected specimens of HCC were examined for the relationship between mode of tumor spread and tumor size. Efferent vessels in HCC were identified by direct injection of radiopaque material into the tumor in 23 resected liver specimens selected at random from the 231 tumors. The most frequent site for tumor spread in HCC was capsular invasion followed by extracapsular invasion, vascular invasion, and finally intrahepatic metastasis. There was a strong statistical correlation between the presence of intrahepatic metastasis and the frequency of vascular invasion (correlation coefficient = 0.998). Radiopaque material injected directly into 23 resected tumors entered only the portal vein in 17 tumors and into both the portal and hepatic veins in six tumors. In all eight patients with unresectable lesions, radiopaque media injected percutaneously into tumor nodules flowed only into the portal vein. These findings suggest that tumor spread in HCC progresses from capsular invasion to intrahepatic invasion and that the portal vein may act as an efferent tumor vessel.     

结直肠癌原发灶、门静脉血和肝转移灶K-ras基因突变的研究

目的:观察结直肠癌患者门静脉血液、原发肿瘤组织及相应肝转移灶K-ras基因突变情况,分析三者的一致性,探讨结直肠癌患者门静脉血K-ras基因突变与肝转移关系。方法:实时荧光定量PCR技术和基因测序技术检测59例结直肠癌患者门静脉血液、原发肿瘤组织及15例肝转移灶K-ras基因突变,结合其临床资料分析。结果:59例结直肠癌组织中20例(33.9%)发现K-ras基因突变,18例(30.5%)结直肠癌患者的门静脉血中也发现K-ras基因突变,15例肝转移灶中8例(53.3%)发现K-ras基因突变,与原发癌组织的基因突变率差异不明显(P0.05)。18例门静脉血存在K-ras基因突变者,其相应的肿瘤组织中均发现K-ras突变。结直肠癌组织中无K-ras基因突变者,患者门静脉血未发现基因突变。8例肝转移灶发现K-ras基因突变者门静脉血亦均有K-ras基因突变,7例肝转移灶无K-ras突变者门静脉血也无K-ras突变。原发肿瘤组织、相应门静脉血和5例同时性、2例异时性肝转移灶的K-ras基因突变类型基本一致(即K-ras基因12密码子GGT突变为GAT或GTT),1例异时性肝转移灶K-ras基因突变类型为13密码子GGC突变为GAC。原发癌组织与门静脉血K-ras基因突变一致率为96.6%(57/59),肝转移灶与门静脉血K-ras基因突变情况基本一致,但突变类型有不同。结论:结直肠癌的原发灶、门静脉血及肝转移灶的K-ras基因突变较为一致,原发癌组织和门静脉血均有K-ras基因的突变,预示着肿瘤可能通过血行转移至肝脏。     

Hepatocellular carcinoma with extension to the diaphragm, falciform ligament, rectus abdominis and paraumbilical vein

Hepatocellular carcinoma is the most common primary tumour of the liver. The most common extrahepatic metastatic sites are the lung, lymph nodes, bones and adrenal glands. All forms of HCC demonstrate a tendency for vascular invasion, producing extensive intrahepatic metastases and, occasionally, portal vein or inferior vena cava extension with spread into the right atrium in extreme cases. Tumour spread of abdominal diseases via hepatic ligaments has also been previously reported. We report a rare case of hepatocellular carcinoma with extension into the falciform ligament, overlying rectus sheath and adjacent diaphragm with concomitant infiltration into the recanalised paraumbilical vein.     

二氧化碳肝动脉造影在显示肝癌门脉癌栓中的作用

目的:探索二氧化碳肝动脉造影造影在显示肝癌患者门脉癌栓中的作用。材料与方法:120例肝癌患者二氧化碳和碘造影剂肝动脉造影,比较两组门静脉显示情况以及门脉癌栓的显示率。结果:二氧化碳造影显示门静脉41例,碘造影剂显示19例,该19例门脉均被二氧化碳造影所发现,两组有显著性差异(χ2=43.497,P=0.000)。二氧化碳显示门脉癌栓者27例,而碘造影剂显示13例,两组有显著差异(χ2=5.880,P=0.015)。结论:二氧化碳肝动脉在显示HCC患者门静脉及其癌栓方面优于碘造影剂。     

Segmentation and reconstruction of hepatic veins and intrahepatic portal vein based on the coronal sectional anatomic dataset

Three-dimensional (3D) reconstruction of intrahepatic vessels is very useful in visualizing the complex anatomy of hepatic veins and intrahepatic portal vein. It also provides a 3D anatomic basis for diagnostic imaging and surgical operation on the liver. In the present study, we built a 3D digitized model of hepatic veins and intrahepatic portal vein based on the coronal sectional anatomic dataset of the liver. The dataset was obtained using the digital freezing milling technique. The pre-reconstructed structures were identified and extracted, and then were segmented by the method of manual intervention. The digitized model of hepatic veins and intrahepatic portal vein was established using 3D medical visualization software. This model facilitated a continuous and dynamic displaying of the hepatic veins and intrahepatic portal vein at different orientations, which demonstrated the complicated relationship of adjacent hepatic veins and intrahepatic portal vein realistically in the 3D space. This study indicated that high-quality 2D images, precise data segmentation, and suitable 3D reconstruction methods ensured the reality and accuracy of the digital visualized model of hepatic veins and intrahepatic portal vein.     

COMBINED HEPATOCELLULAR AND CHOLANGIOCARCINOMA ARISING IN A CIRRHOTIC LIVER: Report of an Autopsy Case

A rare case of combined hepatocellular and cholangiocarcinoma arising in a 56–year-old female is reported. The autopsy disclosed the presence of two different kinds of tumors in the right lobe of the liver, which showed advanced cirrhosis; a massive rubbery, ill-defined and whitish-yellow cholangiocarcinoma and a nodular soft, encapsulated and dark green hepatocellular carcinoma. They were adjacent to each other, but showed no intermingling. Only the massive cholangiocarcinoma had invaded the portal vein and showed several intrahepatic metastatic foci and hepatic, pancreaticoduodenal and perigastric lymph node metastases. Immunohistochemically, carbohydrate antigen 19–9 was strongly positive only for the cholangiocarcinoma component, explaining the high titer of this antigen in the serum on admission. On the basis of these findings, the possible morphogenesis of the tumor observed in the cirrhotic liver is discussed.     

Combined hepatocellular and cholangiocarcinoma arising in a cirrhotic liver. Report of an autopsy case

A rare case of combined hepatocellular and cholangiocarcinoma arising in a 56-year-old female is reported. The autopsy disclosed the presence of two different kinds of tumors in the right lobe of the liver, which showed advanced cirrhosis; a massive rubbery, ill-defined and whitish-yellow cholangiocarcinoma and a nodular soft, encapsulated and dark green hepatocellular carcinoma. They were adjacent to each other, but showed no intermingling. Only the massive cholangiocarcinoma had invaded the portal vein and showed several intrahepatic metastatic foci and hepatic, pancreaticoduodenal and perigastric lymph node metastases. Immunohistochemically, carbohydrate antigen 19-9 was strongly positive only for the cholangiocarcinoma component, explaining the high titer of this antigen in the serum on admission. On the basis of these findings, the possible morphogenesis of the tumor observed in the cirrhotic liver is discussed.     

三维动态对比增强磁共振肝门静脉造影成像效果及解剖学分析

目的：探讨三维动态对比增强磁共振肝门静脉造影(3DDCEMRP)的成像质量并观测肝内肝门静脉的解剖和变异。方法：共进行61例门静脉3DDCEMRP检查，通过对MPV、LPV、RPV，SV及SMV显示情况和对门脉右支显示能力的分析，评价3DDCEMRP的成像质量。测量门脉系统各主要干支的径线并对门静脉的解剖和变异做分型，计算各型的构成比。结果：所有病例均完整显示门静脉主干及肝内4级以上分支。61次成像中，4例(6．6％)显示门脉主干呈三叉状，3例(4．9％)门脉主干先发出右后支，继续上行分为左支和右前支，2例(3．3％)门脉右前支起自左支，l例(1．6％)门脉右支缺如，其余5l例(83．6％)显示正常门脉分支。结论：肝内门脉变异并不少见，3D DCE MRP是一种有效、微创技术。能方便而清楚地显示肝内门脉的解剖和蛮异。     

基于冠状面数据的肝静脉和肝内门静脉的三维重建

目的:构建基于肝连续薄层冠状断面数据集的肝静脉和肝内门静脉的三维数字化可视模型。方法:应用数控冷冻铣削技术获取1例肝的连续薄层冠状断面数据集;采用体绘制和面绘制的方法,通过人工干预对数据集中肝内管道系统进行人工识别提取和图像数据分割;运用3D医学可视化软件实现三维重建,构建肝静脉和肝内门静脉的三维可视化模型。结果:肝静脉和肝内门静脉的可视化模型可清晰显示门静脉及其分支和肝静脉及其属支的空间构形,真实地再现了肝门静脉和肝静脉之间复杂的空间毗邻关系。模型中的肝静脉和肝门静脉可单独或总体显示,可在三维空间位置上绕任意轴旋转任意角度,并能从不同的角度对某一血管分支进行多角度、多方位的观察。结论:高质量的二维图像、精确的数据分割和合适的三维重建方法保证了三维数字化可视模型的真实性和准确性。     

Diffuse Hepatic Intravascular Carcinomatous Embolization Resulting in Fatal Liver Failure: A Clinicopathologic Study of 4 Cases

The authors report four cases in which patients died of acute or fulminant hepatic failure resulting from massive intravascular metastatic carcinomatous embolization, a rarely reported manifestation of metastatic disease. Neoplasms were high grade carcinomas. Tumor emboli were present within portal branches ranging 0.12-2.9 mm in diameter and were free floating or attached to the vascular wall, with or without varying degrees of superimposed organization. In one case, intravascular tumor necrosis was prominent and appeared as granular casts with superimposed dystrophic calcification and/or entrapped foamy histiocytes. There were associated geographical areas of parenchymal (4 cases) and tumor (1 case) ischemic necrosis with a multifocal and regional topographic distribution. An associated predominant pattern of intrasinusoidal tumor infiltration (with or without fibrosis) was present in 3 cases, whereas the fourth case had underlying micronodular cirrhosis, providing ancillary evidence for preexisting altered intrahepatic microcirculation. The literature on fatal hepatic failure resulting from neoplasia is reviewed with a reassessment of its pathobiological significance.     

门静脉的解剖与变异

目的：利用经动脉性门静脉造影CT重建门静脉、肝静脉三维结构，观察生理状态下的门静脉的解剖与变异。方法：150例病人，导管置入于肠系膜上动脉内，注入造影剂后门静脉期和肝静脉期连续扫描肝脏。三维重建门静脉及肝静脉，分析门静脉的解剖与变异。结果：150次成像中门静脉变异25例，12例（8．0％）显示门静脉呈三分叉状，10例（6，7％）门静脉先分出右后支，然后上行分为左支和右前支，1例（0．7％）门静脉左支水平段缺如，门静脉右支缺如2例（1．3％），余下125例（83．3％）显示正常左右门静脉分支。结论：门静脉的三维图像重建及类型分析对术前手术方式的确定有一定的临床意义。     

Intrahepatic termination of the left gastric vein (vena gastrica sinistra): a new case of this unusual anatomic variation

The intrahepatic termination of the left gastric vein is an unusual anatomic variation. A new case studied after dissection is described. The left gastric vein is divided in 2 terminal branches which enter the left liver lobe after flowing through the pars condensa of the lesser omentum. One is a terminal branch which contributes to the portal irrigation of the superior lateral subsegment. The other anastomoses to the ramus cranialis of the left branch of the portal vein. The diameter of the left gastric vein, portal vein and splenic vein obtained after morphometric study can be considered normal. The existence of portal hypertension prior to death is discarded.     

多层螺旋CT肝门静脉成像及其临床应用价值

目的：探讨多层螺旋CT肝门静脉成像(MScTP)技术在显示肝内肝门静脉解剖及其在占位性病变定位中的应用价值。方法：对170例疑有肝脏疾病患者行增强后肝门静脉期扫描，对每一例均行三维重建后处理．对二维及三维图像进行对比分析。结果：MSCTP对肝内门静脉第5级以上分支的显示率为94．5％；170例肝内门静脉可分为3种类型；二维及三维图像对病变定位不相符合率为36．8％。结论：MSCTP可以用来准确评价肝内门静脉解剖并对肝脏病灶进行准确定位：     

Meal induced changes in hepatic and splanchnic circulation: a noninvasive Doppler study in normal humans

Summary The haemodynamic effects of a meal on the splanchnic and hepatic circulation were evaluated in 30 healthy volunteers, using Doppler ultrasonography. The resistance index (RI) of the superior mesenteric artery and of the left and right intrahepatic arteries, the portal vein blood flow as well as the ratio between maximal velocity in the left and right intrahepatic arteries and the adjacent portal vein were measured initially, then 15, 30, 45, and 60 min after the ingestion of a standard balanced liquid meal. Postprandial haemodynamic changes were maximal 30 min after the meal; at that time, mesenteric artery RI decreased significantly [mean –11% (SEM 14%)] whereas portal vein blood flow increased markedly [mean +79% (SEM 14%)]; a significant increase in hepatic artery RI was observed in both liver lobes. The ratio between maximal velocities of the intrahepatic artery and the intrahepatic portal vein was reduced significantly; this ratio decreased more markedly in the right lobe of the liver. These findings would suggest that there was an adaptation of hepatic artery to portal vein blood flow after a meal. The subsequent increase in intrahepatic portal vein flow velocity was found to be greater in the right lobe of the liver.     

Partial nodular transformation of liver in an adult with persistent ductus venosus. Review with hypothesis on pathogenesis

Partial nodular transformation of the liver (PNT) is a rare condition of unknown pathogenesis in which nodules composed of hepatocytes replace portions of the parenchyma. There is usually evidence of portal hypertension and portal vein thrombosis. We present a case of PNT in a man with persistent ductus venosus and hypoplasia of the major intrahepatic portal veins but without evidence of portal hypertension or portal vein thrombosis. Portal venules were largely absent between nodules, as documented by morphometry. We suggest the pathogenesis of PNT is similar to that previously proposed for nodular regenerative hyperplasia, that is, atrophy occurs in parenchyma with insufficient blood supply and nodules arise by hyperplasia in areas with adequate supply. Partial nodular transformation and nodular regenerative hyperplasia differ mainly in the cause and distribution of the portal vein obliteration.