Search

Background/Aims Familial clustering of hepatitis B virus (HBV) infection is related to perinatal transmission, and is the main cause of familial-type hepatocellular carcinoma (HCC). The route of HBV transmission differs between the children and siblings of patients with HCC. This study examined the differences in HBV carrier rates and HCC-related mortality between two generations in HCC families. Methods From 1992 to 1997, relatives of individuals with HCC were screened prospectively with ultrasonography, alpha-fetoprotein, liver biochemistry tests and viral markers. Total HCC-related deaths during a 9-year period were compared between the generations of index patients and their children. Results The study included a total of 13676 relatives in two generations. More HCC-related deaths occurred in the index patient generation than in the child generation. Furthermore, children of female index patients had higher rates of liver cancer related mortality than children of male index patients. The same was true when the analysis was limited to male HBV carriers. The prevalence of HBsAg in the offspring of HBsAg positive mothers was 66% in the child generation and 72% in the index patient generation. These high prevalences indicated high maternal HBV replication status. Conclusions Perinatal transmission and maternal viral load are important risk factors in hepatocarcinogenesis.

To elucidate the clinicopathological course and the role of hepatitis C virus in posttransfusion and sporadic chronic non-A, non-B hepatitis in Taiwan, we retrospectively studied 85 histologically confirmed patients with long-term follow up. Antibodies against hepatitis C virus (anti-HCV) by a second-generation assay were positive in 81% of the patients: 88% in the posttransfusion group and 76% in the sporadic group. Clinical manifestations were generally mild, and were noted in only half of the patients. During follow up, 33% (28 of 85 patients) had episodes of acute exacerbation of chronic liver disease and 24% (20 of 85) had normalized liver tests. Patients with normalized liver tests were usually anti-HCV negative (55% vs. 8%, p0.001). In 34 patients who had had blood transfusions, initial liver biopsies revealed chronic active hepatitis in 41%, active cirrhosis in 6%, and inactive cirrhosis in 9%. Follow-up biopsies in eight patients in this group showed histological progression in three after an average of 40.6 months. In the 51 sporadically infected patients, initial work-up revealed chronic active hepatitis in 37%, active cirrhosis in 4%, and inactive cirrhosis in 14%. Among the nine who underwent repeated biopsies, only one (11%) had progression. Patients above age 40 displayed more severe histologic activity than those below 40 (p0.005). Three patients, all with cirrhosis, died of hepatocellular carcinoma 7 to 12 years after follow up. Further genotyping study of hepatitis C virus in 28 patients showed that type II virus was most predominant in Taiwan and histologic severity was similar among patients infected with different genotypes.(ABSTRACT TRUNCATED AT 250 WORDS)

The prevalence of antibodies to hepatitis C virus (anti-HCV) in a hepatitis B virus hyperendemic region was evaluated with a second-generation enzyme immunoassay. A general population of 1500 from Northern Taiwan was tested with this immunoassay which includes synthetic peptides from the capsid and non-structural protein region as the solid-phase antigen. A total of 37 subjects out of 1500 (2.5%) were positive, with no significant difference in distribution between hepatitis B antigenemic and non-antigenemic samples. The prevalence of anti-HCV was higher in subjects with abnormal than those with normal liver function tests (8.2% vs. 1.5%). Prevalence increased with age. By polymerase chain reaction, 43% of anti-HCV-positive samples were HCV-RNA-positive. However, only 1 (0.6%) of 150 anti-HCV-negative subjects had HCV-RNA. Comparison of the results with those from a conventional recombinant C100-3-based assay showed that the capsid/non-structural region synthetic antigen system provided more accurate sensitivity and specificity. The more sensitive assay revealed a high prevalence for HCV infection of 2.5% among this general population in Taiwan.

In a follow-up study of 6 months or more of two hundred and ninety-six patients who had received blood transfusion, 37 (12.5%) developed acute posttransfusion hepatitis. Patients with posttransfusion hepatitis had significantly higher donor numbers and transfusion amounts than patients without hepatitis. Frequency was not related to the age, sex or hepatitis B carriage of recipients. There were no cases of fulminant hepatitis. Of 37 patients with hepatitis, 36 were diagnosed as non-A, non-B hepatitis and one as hepatitis B. Twenty-two (59.5%) of the 36 patients with non-A, non-B hepatitis seroconverted to hepatitis C antibody. Two of these were positive for hepatitis C antibody before transfusion and 12 were negative for hepatitis C antibody. Thirty-three of the 36 patients were followed-up for more than 6 months after the onset of hepatitis. While 13 of the 33 patients recovered, the remaining 20 (60.6%) patients still had persistent liver test abnormalities 6 months after the onset of hepatitis. Seventeen (85%) of the 20 patients who developed chronic hepatitis were hepatitis C antibody positive. In contrast, only four (30%) of the 13 patients who recovered after acute hepatitis were positive for the hepatitis C antibody. Chronicity rate was not related to the patient's sex, age, transfusion amount or donor number. Our results suggest a high frequency of posttransfusion hepatitis C in Taiwan and that the infection has a high risk of chronicity.

Background/Aims: To evaluate ultrasound-guided cutting biopsy for hepatocellular carcinoma, we report findings from 10 years of experience. Methods: We performed 455 ultrasound-guided cutting biopsies of hepatic tumors in 420 patients with hepatocellular carcinoma from 1981 to 1990. Results: Liver tissues were adequately sampled for a histological diagnosis of hepatocellular carcinoma in the initial biopsy in 391 sessions. The remaining 64 were proved to have hepatocellular carcinoma after subsequent studies. Ultrasound-guided biopsy changed the initial diagnosis in 9 of the 420 patients: three had been diagnosed with liver abscess, and six with metastatic liver tumors. Complications of the biopsy were rare: the tumor had spread to the chest wall in nine, and internal bleeding was noted in five patients. There was no mortality and no other sequelae. Conclusions: Ultrasound-guided biopsy of hepatic tumors is important in the diagnosis of liver cancer, but this technique should be applied only when the image diagnosis and results of fine needle biopsy are equivocal to minimize possible complications. For patients with small HCCs, who are candidates for surgical resection of hepatocellular carcinoma or liver transplantation, it should not be considered as a first-step invasive procedure.

The serum HBsAg in 4 chronic HBsAg carrier patients with hepatocellular carcinoma (HCC) cleared within 4-38 months after surgical resection of their hepatic tumors. Two patients developed anti-HBs. During the follow-up period from 21 to 28 months after HBsAg clearance, none of the patients regained positive serum HBsAg. Two patients who had had tissue HBsAg present, exclusively in the tumor, showed quick HBsAg clearance after resection. The other 2 patients had a delayed HBsAg clearance. One had tissue HBsAg in both the tumor and nontumoral liver. Only 1 patient had tissue HBsAg in the liver, but not in the tumor. During the same period of observation of 323 chronic HBsAg carriers, who had a variety of histologically-verified chronic liver diseases and were followed for more than 6 months, only 1 cleared the antigen. The spontaneous HBsAg clearance in our HBsAg carriers (1/323) was significantly lower than that (4/64) of HBsAg-positive HCC patients with tumor resection, P less than 0.004. The mechanisms of HBsAg clearance in HCC patients after surgical resection of tumors are discussed.