Since the institution of Taiwan's program of universal hepatitis B vaccination, the incidence of hepatocellular carcinoma in children has declined.

No abstract

No abstract

We are researchers who have published analyses of nucleic acid sequence variation of hepatitis C virus (HCV) and associated virological and clinical significance. We are concerned that our investigations are hampered by the lack of a consensus nomenclature for variants of HCV and that this leads to confusion when results from different laboratories are compared. Furthermore, because there are no consistently applied criteria by which new genotypes are defined, investigators assign new type descriptions to novel sequence variants on an ad hoc basis without agreement from

No abstract

To assess the contribution of hepatitis C virus (HCV) in liver disease in Taiwan, antibody to HCV (anti-HCV) was studied by radioimmunoassay in 392 patients with chronic liver disease and in 440 healthy adults and 444 subjects at risk. The anti-HCV prevalence was 0.95% in 420 volunteer blood donors, 90% in 100 hemophiliacs, and 81% in 58 parenteral drug abusers. Anti-HCV was present in 6 (7.7%) of 78 hepatitis B surface antigen (HBsAg)-positive and 28 (65%) of 43 HBsAg-negative patients with chronic hepatitis, 3 (10%) of 31 HBsAg-positive and 13 (43%) of 30 HBsAg-negative cirrhotics, and 7 (17%) of 42 HBsAg-positive and 15 (63%) of 24 HBsAg-negative patients with hepatocellular carcinoma (HCC). An outbreak of non-A, non-B hepatitis revealed 18% of 57 patients to be positive for anti-HCV, and in 29 patients with posttransfusion hepatitis prospectively followed, 7 (24%) developed anti-HCV. Thus, HCV infection appears to play a relatively minor role in HBsAg-positive liver disease in Taiwan but is strongly associated with HBsAg-negative chronic liver disease and HCC. The infection is extremely common in hemophiliacs and parenteral drug abusers.

No abstract

Loss of hepatitis B surface antigen (HBsAg) usually indicates the cure of hepatitis B virus (HBV) infection. In spontaneous hepatitis B e antigen (HBeAg) seroconverters, lower serum HBsAg and HBV DNA levels have been shown to be associated with HBsAg loss over time. However, little is known about their impacts on HBsAg loss in HBeAg-negative patients with limited viral replication. A total of 688 HBeAg-negative patients with baseline serum HBV DNA levels <2000 IU/mL were enrolled in Taiwan. The relationships of HBsAg and HBV DNA levels with subsequent HBsAg loss were investigated. In a mean follow-up of 11.6 years, the average annual rate of HBsAg loss was 1.6%. Baseline HBsAg and HBV DNA levels were inversely associated with subsequent HBsAg loss. When compared to patients who had HBsAg levels >1000 IU/mL, the rates of HBsAg loss were significantly higher in patients with HBsAg levels of 100-999, 10-99, and <10 IU/mL, with hazard ratios of 2.5 (95% confidence interval [CI], 1.6-4.0), 2.8 (95% CI, 1.6-5.0), and 13.2 (95% CI, 8.1-21.5), respectively. Multivariate analysis showed that HBsAg level, but not HBV DNA, remained as an independent factor. The adjusted hazard ratio of HBsAg loss was 13.2 (95% CI, 7.8-22.1) for HBsAg level <10 versus !1000 IU/mL. When compared to HBV DNA level by receiver operating characteristic curve analysis, HBsAg level served as a better predictor of both 5-year and 10-year HBsAg loss. Conclusion: In HBeAgnegative patients with HBV genotype B or C infection who have HBV DNA level <2000 IU/mL, HBsAg level <10 IU/mL is the strongest predictor of HBsAg loss. (HEPATOLOGY 2012;55:68-76) H epatitis B virus (HBV) infection is a global health problem, resulting in more than one million deaths per year. 1 Patients with chronic HBV infection are at increased risk of developing cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC). [1][2][3] It is estimated that in HBV carriers who acquire the virus early in life, the lifetime risk of developing these complications is 25%-40%. 3,4 The REVEAL-HBV (Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer HBV) Study has indicated that in patients with chronic HBV infection, HBV DNA level is a major driver of disease progression. 5,6 Of particular note is that patients with serum HBV DNA levels !2000 IU/mL start to have an increased risk of developing adverse outcomes, including hepatitis, cirrhosis, HCC, and liver-related death. [5][6][7][8] In contrast, those individuals with HBV DNA levels <2000 IU/mL have a higher likelihood of becoming inactive carriers, and some clear hepatitis B surface antigen (HBsAg) during the follow-up, 9,10