OBJECTIVE: The purpose of this study was to describe the CT findings of hepatic hypereosinophilic syndrome in which hepatic lobes or segments were involved. MATERIALS AND METHODS: Seven patients with hypereosinophilic syndrome with hepatic lobar or segmental involvement were included in our study. In all seven, diagnosis was based on liver biopsy and the results of corticosteroid treatment. CT findings were retrospectively reviewed by three radiologists, who reached a consensus. Biopsy specimens were examined, with special reference to portal and periportal inflammation. RESULTS: CT demonstrated well-defined, homogeneous or heterogeneous low attenuation with a straight margin limited to a hepatic lobe (n = 2), segments (n = 3), or subsegments (n = 2), particularly during the portal phase. Where there was subsegmental involvement, lesions were multiple, ovoid or wedge-shaped, and showed low attenuation. In two patients with lobar or segmental involvement, segmental portal vein narrowing was observed. Histopathologic examination dis-closed eosinophilic infiltration in the periportal area, sinusoids and central veins, as well as portal phlebitis. CONCLUSION: Hypereosinophilic syndrome may involve the presence of hepatic lobar, segmental, or subsegmental low-attenuated lesions, as seen on CT images. Their presence may be related to damage of the liver parenchyma and to portal phlebitis.
Adult ; Female ; Human ; Hypereosinophilic Syndrome/pathology/*radiography ; Liver/pathology ; Liver Diseases/pathology/*radiography ; Male ; *Tomography, X-Ray Computed

OBJECTIVE: The purpose of this study was to describe the CT findings of hepatic hypereosinophilic syndrome in which hepatic lobes or segments were involved. MATERIALS AND METHODS: Seven patients with hypereosinophilic syndrome with hepatic lobar or segmental involvement were included in our study. In all seven, diagnosis was based on liver biopsy and the results of corticosteroid treatment. CT findings were retrospectively reviewed by three radiologists, who reached a consensus. Biopsy specimens were examined, with special reference to portal and periportal inflammation. RESULTS: CT demonstrated well-defined, homogeneous or heterogeneous low attenuation with a straight margin limited to a hepatic lobe (n = 2), segments (n = 3), or subsegments (n = 2), particularly during the portal phase. Where there was subsegmental involvement, lesions were multiple, ovoid or wedge-shaped, and showed low attenuation. In two patients with lobar or segmental involvement, segmental portal vein narrowing was observed. Histopathologic examination dis-closed eosinophilic infiltration in the periportal area, sinusoids and central veins, as well as portal phlebitis. CONCLUSION: Hypereosinophilic syndrome may involve the presence of hepatic lobar, segmental, or subsegmental low-attenuated lesions, as seen on CT images. Their presence may be related to damage of the liver parenchyma and to portal phlebitis.
Adult ; Female ; Human ; Hypereosinophilic Syndrome/pathology/*radiography ; Liver/pathology ; Liver Diseases/pathology/*radiography ; Male ; *Tomography, X-Ray Computed

There is accumulating evidence that cancer stem cells (CSCs) play an integral role in the initiation of hepatocarcinogenesis and the maintaining of tumor growth. Liver CSCs derived from hepatic stem/progenitor cells have the potential to differentiate into either hepatocytes or cholangiocytes. Primary liver cancers originating from CSCs constitute a heterogeneous histopathologic spectrum, including hepatocellular carcinoma, combined hepatocellular-cholangiocarcinoma, and intrahepatic cholangiocarcinoma with various radiologic manifestations. In this article, we reviewed the recent concepts of CSCs in the development of primary liver cancers, focusing on their pathological and radiological findings. Awareness of the pathological concepts and imaging findings of primary liver cancers with features of CSCs is critical for accurate diagnosis, prediction of outcome, and appropriate treatment options for patients.
Bile Duct Neoplasms/pathology/radiography ; Bile Ducts, Intrahepatic/pathology/radiography ; Carcinoma, Hepatocellular/pathology/radiography ; Cholangiocarcinoma/pathology/radiography ; Humans ; Liver Neoplasms/*pathology/radiography ; Magnetic Resonance Imaging ; Neoplastic Stem Cells/*pathology/radiography ; Tomography, X-Ray Computed

BACKGROUNDDuring scanning of the right hypochondrium and right intercostal regions with an ultrasonic transducer, several ultrasonic images of oblique sections are obtained. It is still a challenge for ultrasonography to divide these non-conventional sections into an accurate hepatic segmentation pattern. The aim of this research was to investigate the value of the virtual hepatic segment model (VHSM) in assisting the ultrasonic localization of space-occupying hepatic lesions.

METHODSVHSM was constructed via 3D reconstruction according to the first Chinese visible human dataset. Preoperative ultrasonography, contrast-enhanced CT scan and VHSM techniques were performed in 100 patients with space-occupying focal lesions in the liver parenchyma for segmental localization. The results of these three techniques were compared with the operative findings.

RESULTSVHSM was successfully detected on 2D sectional images by 3D reconstruction through surface rendering and volume rendering. The model could simulate ultrasonic directions to conduct a virtual dissection on any section plane, and fine liver segmentation could be displayed in any virtual plane. In 100 patients, there were 112 liver space-occupying focal lesions distributed in 148 liver segmentations. Regarding the positioning accuracies for lesions of different sizes and the lesion segmental distribution accuracies estimated using the three methods mentioned above, ultrasonography exhibited a significantly lower accuracy than VHSM for the segmental localization of lesions (P < 0.05), and contrast-enhanced CT was not significantly different from ultrasonography plus VHSM (P > 0.05).

CONCLUSIONVHSM increased the accuracy of ultrasonic localization of space-occupying hepatic lesions, particularly in hepatic hypovascular regions.

No abstract available.
Female ; Humans ; Liver Cirrhosis, Biliary/*diagnosis/pathology/radiography ; Middle Aged

No abstract available.
Colonic Neoplasms/*pathology/radiography ; Female ; Human ; Liver Neoplasms/radiography/*secondary ; Middle Aged ; Tomography, X-Ray Computed

This paper presents an unusual solid mesenchymal hamartoma of the liver (MHL) in adult. A well defined solid mass in the left lobe of the liver was found in a 57-year-old female. Preoperative radiologic examinations demonstrated solid mass with multifocal calcifications abutting the gallbladder. By light microscopy, the lesion was composed of dense fibrous stroma with hyalinization, bile ducts and thick-walled vessels without hepatocytes. The solid and hyalinized mesenchymal component would suggest an unusual degenerative change representing a burnt-out MHL.
Case Report ; Female ; Hamartoma/surgery ; Hamartoma/radiography ; Hamartoma/pathology* ; Human ; Liver Neoplasms/surgery ; Liver Neoplasms/radiography ; Liver Neoplasms/pathology* ; Mesoderm/pathology ; Middle Age ; Tomography, X-Ray Computed

No abstract available.
Aged ; Carcinoma, Hepatocellular/radiography/*secondary ; Gallbladder Neoplasms/radiography/*secondary ; Humans ; Liver Neoplasms/*pathology/radiography ; Male ; Tomography, X-Ray Computed

No abstract available.
Gastroscopy ; Glomus Tumor/pathology/*radiography/ultrasonography ; Hemangioma/radiography ; Humans ; Liver Neoplasms/radiography ; Male ; Middle Aged ; Stomach Neoplasms/pathology/*radiography/ultrasonography ; Tomography, X-Ray Computed

Budd-Chiari syndrome (BCS) is a disorder caused by occlusion of the hepatic vein or inferior vena cava. The clinical presentation include abdominal pain, hepatomegaly, ascites, leg edema, collateral venous dilatation of the body trunk, and portal hypertension. In addition, BCS can cause hepatocellular carcinoma (HCC) in some patients, although its pathogenesis is not yet completely understood. The average reported time lag from diagnosis of BCS to full-blown HCC ranges from several years to several decades. Hepatic carcinogenesis in patients with BCS perhaps reflects a prolonged and persistent liver injury in that it occurs in the primary inferior vena cava obstruction rather than the primary hepatic vein thrombosis. Among patients with BCS, membranous obstruction of the vena cava (MOVC) usually presents an insidious and chronic illness, whereas primary hepatic vein thrombosis presents an acute or subacute illness. We experienced a case of a patient with BCS, which progressed rapidly that HCC developed only nine months after the diagnosis of BCS. The factors causing this rapid progression are still unclear and remain to be investigated.
Adult ; Carcinoma, Hepatocellular/*etiology/pathology/radiography ; Disease Progression ; Fatal Outcome ; Female ; Hepatic Vein Thrombosis/*complications/pathology/radiography ; Human ; Liver/*pathology/radiography ; Liver Neoplasms/*etiology/pathology/radiography ; Tomography, X-Ray Computed