Background: Overweight and hepatic steatosis have been increasingly recognized recently. This study aimed to test whether substantial amount of fatty infiltration in liver, which may interfere with cytoplasmic distribution of hepatitis B surface antigen (HBsAg), can contribute to HBsAg seroclearance in HBsAg carriers. Methods: Clinical and laboratory data including ultrasound grading of hepatic steatosis were studied in 54 HBsAg carriers with HBsAg seroclearance, and the results were compared with 108 age-and sex-matched carriers with HBsAg persistence. Results: Body mass index and ultrasound grading of hepatic steatosis were significantly higher in HBsAg carriers with HBsAg seroclearance than in those with HBsAg persistence. The degrees of hepatic steatosis correlated significantly with body mass index (Po0.001). The prevalence of mild hepatic steatosis showed no significant difference (33% (18/54) vs 31% (33/108), P ¼ 0.72), but moderate-severe hepatic steatosis was significantly more prevalent in patients with HBsAg seroclearance (33% (18/54) vs 13% (17/108), P ¼ 0.01). HBsAg carriers with moderate and severe hepatic steatosis were associated with a 3.2-fold (95% confidence interval: 1.2-8.4, P ¼ 0.02) and 3.9-fold (95% confidence interval: 1.1-14.2, P ¼ 0.04), respectively, increased odds of HBsAg seroclearance compared to those without hepatic steatosis. Conclusion: Moderate-severe hepatic steatosis may contribute to HBsAg seroclearance in HBsAg carriers.
Patients with dual infection with hepatitis B virus (HBV) and delta virus (HDV) responded poorly to interferon (IFN) therapy. Little is known about the effect of IFN therapy in patients with HBV and hepatitis C virus (HCV) dual infection. The patients in two randomized controlled trials with chronic HBV infection were retrospectively assayed for HCV markers. The HBV responses to IFN therapy in patients with and without HCV markers were compared. An open trial was conducted in 4 patients who had lost their serum HBV surface antigen (HBsAg) but had continuing HCV viremia and hepatitis. Of the 15 patients seropositive for HCV marker(s), only 1 (6.7%) responded with seroclearance of HBV DNA and HBV e antigen, as compared with 46 (28%) of 164 HCV-negative patients (p = 0.058). Icteric hepatitis developed in 1 patient on emergence of serum HCV RNA in association with seroclearance of HBV DNA. In contrast, good response was demonstrated in 3 of the 4 patients who had lost serum HBsAg before therapy. The results suggest that IFN therapy is not only of limited value in patients with dual infection with HBV and HCV but also has a potential risk of severe hepatitis if the clearance of one virus removes its suppressive effect on and facilitates the emergence of the other. However, patients with continuing HCV hepatitis after termination of the chronic HBsAg carrier state responded well to IFN therapy.
Background:As most cases of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) have concurrent cirrhosis, viral factors identified to be associated with HCC might be related to cirrhosis rather than HCC.Methods:Hepatitis B virus DNA levels, genotypes and precore/basal core promoter (BCP) mutants were compared between cirrhotic HCC and non-cirrhotic HCC patients. Age- and sex-matched case–control studies were performed to identify the risk factors.Results:Hepatitis B virus DNA levels showed no significant difference betwen non-cirrhotic HCC patients (n=20) and cirrhotic HCC patients (n=140) or 1 : 3 age- and sex-matched cirrhotic HCC patients (n=60), but genotype C and BCP mutant were significantly more prevalent in the latter than in the former. In multiple logistic regression, BCP mutant but not genoype C correlated significantly with the presence of cirrhosis in HCC patients. Compared with inactive carriers (n=60), non-cirrhotic HCC patients (n=20) had significantly higher HBV DNA levels but no difference in HBV genotypes and precore/BCP mutants. Furthermore, HBV DNA levels, the distribution of HBV genotypes and the prevalence of precore/BCP mutants all failed to show any significant difference between cirrhotic HCC patients (n=60) and cirrhotic patients without HCC (n=60).Conclusion:Basal core promoter mutant is associated with progression to cirrhosis rather than HCC in chronic HBV infection.
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