No abstract available.
Carcinoma, Hepatocellular*

The identification of serum HBV DNA is very important for the assessment of the disease activity in persistent infection, for the evaluation of the infectivity of an individuals blood. The dot blot, however, has limited sensitivity and sometimes inconsistent with other serological markers and clinical settings. Using the most important recent advance in molecular biology, the polymerase chain reaction(PCR), specific DNA sequences can be amplified more than a million-fold in a few hours and with this technique the detection of the extreme low level of DNA is possible. This study was to determine sensitivity of the PCR for the detection of serum HBV DNA in comparison with dot blot analysis and to investigate the serum HBV DNA status and clinical significance of PCR in patients with chronic HBsAg positive liver disease. The subjects of this study were 17 patients with asymptomatic HBsAg carriers(9 HBeAg positive patients, 8 anti-HBe positive patients), 91 chronic hepatitis B(50 HBeAg positive patients, 41 anti-HBe positive patients), 57 liver cirrhosis(21 HBeAg positive patients, 36 anti-HBe positive patients), 27 hepatocellular carcinoma(10 HBeAg positive patients, 17 anti-HBe positive patients). The results were summerized as following; The detection rates of HBV DNA by dot blot, PCR were 58.9%, 72.2% in HBeAg positive patients, 34.3%, 53.9% in anti-HBe positive patients. The detection rates of HBV DNA by PCR in HBeAg negative patients were 25.0% in asymptomatic HBsAg carriers, 61.0% in chronic hepatitis B, 52.8% in liver cirrhosis, 52.9% in hepatocellular carcinoma. The positive rate for HBV DNA is a significant difference between HBeAg positive and negative asymptomatic HBsAg carriers, but not significantly difference in other groups. In conclusions, this study confirmed that the PCR is much more sensitive than the dot blot analysis in detecting the HBV DNA in the sera of patients with chronic liver disease. The presence of HBV DNA in the serum was detected by PCR with higher sensitivity and it suggested that active viral replication is still going on in most patients with chronic HBsAg positive liver disease irrespective of HBeAg/anti-HBe status, and PCR may be used as a prognostic factor in asymptomatic HBsAg carriers.
Carcinoma, Hepatocellular

To evaluate the tissue expression rate and pattenr of HBsAg and HBcAg in tumors and peritumoral livers, an immunohistochemical study was undertaken on 47 surgically resected hepatocellular carcinomas(HCCs). The results are as follows. 1. Patient's sera were positive for HBsAg in 40 cases(85.1%). In the remaining 7 cases, the tumor and peritumoral liver expressed neither HBcAg nor HbSaG, suggesting that they were caused by other etiologies than hepatitis B virus. 2. The peritumoral liver had HBsAg and HBcAg in 95.0% and 27.5% among the 40 cases, respectively. But the tumor expressed HBsAg in 50.0% and HBcAg in none. 3. The expression of HBsAg within the tumor and both HBsAg and HBcAg in the peritumoral liver tended to be more frequent in the pretreated cases before surgery. 4. Edmondson-Steiner grade IV tumors revealed a lower expression rate of HBsAg than the low grade tumors(p<0.05). Incases with cirrhosis at peritumoral tissues, HBcAg was less frequently found than in those without cirrhosis. The majority of tissue HBsAg and HBcAg was represented as groups of positive cells. These results suggest that, during the development and progression of HCCs, the HBcAg containing cells are repeatedly removed and the HBcAg negative cells are selected, because cellular expression of HBcAg is the target of host immune response.
Carcinoma, Hepatocellular

Pelioid hepatocellular carcinoma (HCC), a type of atypical HCC, is a rare histologic type of HCC. The radiologic findings of the pelioid HCC is differ from the typical type of HCC. To our knowledge, this case report is the second literature to show the enhancing features of a pelioid HCC on dynamic computed tomography (CT). Here we describe the dynamic CT findings in a case of surgically confirmed pelioid HCC.
Carcinoma, Hepatocellular

Massive hydrothorax is uncommon but well recognized complication of peritoneal dialysis. Possible mechanisms include a disorder of lymphatic drainage, pleuro-peritoneal pressure gradient, and congenital diaphragmatic defects. Hydrothorax in a CAPD patient caused by infiltrative disease or malignancy is very rare. Recently, two cases of hydrothorax in CAPD patients caused by systemic amyloidosis involving diaphragm were reported. However, no case of pleuro-peritoneal communication secondary to HCC infiltrating diaphragm was reported. This case was of a hydrothorax due to HCC in a CAPD patient. We performed video-assited thoracoscopic resection of diaphragmatic mass, diaphragmatic repair and thoracoscopic talc pleurodesis. This case showed that malignancy might be considered as a cause of a hydrothorax in a CAPD patient.
Carcinoma, Hepatocellular

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

Tumor suppressive effect of dehydroepiandrosterone (DHEA) on the experimentally induced hepatocellular carcinoma was investigated, especially focusing on glutatione transferase and transglutaminase with aptosis in the carcinogenesis. The chemical hepatocarcinogenic procedure of Solt-Farber method was used on Sprague-Dawley rats. Experimental groups were divided into AA group treated by the standard Solt-Farber regimen of diethylnitrosamine (DEN) and 2-acetamidofluorene (AAF) and AD group treated with DHEA simultaneously with AAF and the AAD group treated by DHEA after treatment with AAF. Each group was divided by time sequence further into four subgroups, GI (8wk), G2 (16wk), G3 (28wk), and G4 (36wk). For neoplastic lesion, the immuno histochemical study with anti GSTP antibody was carried out, while the activity and expression of TGase was compared at the same time. The results were summarized as follows; GST-P positive foci detected in AD groups were significantly more suppressed by DHEA treatment than AA groups (P<0.05). AD groups. AD group showed higher activities of TGase than AA groups (P<0.05), which was confirmed by Western and Northern blot analysis. But the number of apoptotic bodies was not correlated with activity and expression of TGase in the nodule. These results suggest that the suppressive effect of DHEA on the murine hepatocellular carcinogenesis might be operating on the promotion process of carcinogenesis rather than regression process of transformed hyperplastic nodules.
Carcinoma, Hepatocellular

Necleolar organizer regions(NORs) ARE LOOPS OF DNA which transcribe to ribosomal RNA by RNA polymerase I. Since NOR-associated proteins are argyrophilic, silver staining method has been used for demonstration of AgNORs. The numbers and/or configurations of NORs may reflect the activities of cells in hyperplastic and neoplastic conditions. To evaluated the applicability of AgNORs in the diagnosis of hepatocellular carcinoma, the author had performed silver staining on the routinely processed, formalin-fixed, paraffin-embedded sections of 14 cases of normal liver(control), 23 cirrhotic liver, and 21 hepatocellular carcinoma. The results are summarized as follows: 1) The mean number of AgNORs per nucleus(mAgNOR) of normal liver, cirrhotic liver and hepatocellular carcinoma was 1.45+/-0.07, 2.53+/-0.38 and 5.52+/-1.63, respectively. The difference of mAgNOR between normal and cirrhotic liver, and between cirrhotic liver and hepatocellular carcinoma was statistically significant, respectively(p<0.01). 2) The percentage of nuclei showing five or more AgNORs per nucleus(pAgNOR) was 0.07% in normal liver, 7.59% in cirrhotic liver, and 60.49% in hepatocellular carcinoma. 3) AgNORs in hepatocellular carcinoma were large, pleomorphic and irregularly clumped, in addition to increase of mAgNOR and high pAgNOR. In conclusion, the increase of mAgNOR, high pAgNOR and large, irregular AgNORs are regarded as an additional helpful finding for the histopathological diagnosis of hepatocellular carcinoma.
Carcinoma, Hepatocellular