• chronic hepatitis B;
  • HBsAg;
  • HBV-DNA;
  • luteinizing hormone;
  • releasing hormone;
  • testosterone

ABSTRACT—Aims/Background: There is epidemiological evidence that progression of hepatitis B virus (HBV)-induced liver disease is adversely influenced by male gender. Furthermore, in male transgenic mice, HBsAg levels increase after puberty, resulting in 4- to 10-fold higher HBsAg levels than in female transgenic mice. Castration reduces HBsAg levels by 90–95%, while substitution of testosterone to castrated animals rapidly increases HBsAg concentrations. We hypothesized that suppression of endogenous testosterone levels may have similar effects on HBsAg serum levels in men, as observed in male mice. Methods: To test our hypothesis, we studied the influence of reversible testosterone suppression by the LHRH-analog triptorelin on serum concentrations of HBsAg and HBV-DNA. Eight male patients, who were chronically infected with HBV, were studied in a prospective interventional study. Results: Triptorelin decreased serum testosterone levels to castration levels for several weeks. However, this reversible testosterone suppression had no effect on HBsAg or HBV-DNA serum concentrations (p>0.05). Conclusions: Suppression of endogenous testosterone levels had no effect on HBsAg levels in men, which points to a different regulation of HBsAg expression in men compared with transgenic mice.