No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract availalbe.
Carcinoma, Hepatocellular*

To pursue a desirable format for the pathological diagnosis of liver cirrhosis, the authors attempted to classify 369 biopsy-proven cirrhosis on the basis of etiology and made effort to find out the morphological characteristics of each category. About 735 of total cases were HBsAg seropositive postnecrotic cirrhosis. Alcholic cirrhosis ws the second most frequent type, although accounted only 6.8%. In about 15%, the etiology was not known. Excluding the congenital biliary atresia, chronic biliary obstruction appeared to be a rare cause of cirrhosis among these biopsied cases. Of the HBsAg positive postnecrotic cirrhosis, the eAg seropositive cases tended to be micronodular and to show a higher necroinflammatory activity, in contrast to eAg seronegative cases and those complicated by hepatocellular carcinoma (HCC), suggesting that the loss of eAg is followed by a decrease of the destructive activity, active regeneration of hepatocytes and finally the development of HCC. alcoholic cirrhosis was micronodular in 64% and revealed histologic evidences of alcoholic liver disease in most cases. The results indicate that etiological diagnosis can be made in most cases of cirrhosis by the morphological characteristics and the precise clinical informations, including those on the NANB virus and the inborn error of metabolism, and that the pathological diagnosis should be more comprehensive, implicating the etiology, the nodular size and the necroinflammatory activity.
Carcinoma, Hepatocellular

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

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

No abstract available.
Carcinoma, Hepatocellular*