BACKGROUND/AIMS: The aim of this study was to understand the changes in the proportion of hepatitis B virus precore stop mutant during the course of prednisolone primed interferon (IFN) therapy. METHODS:Three groups of patients were included: patients receivingprednisolone-primed IFN treatment (Group I, n=31), IFN treatment only (Group II, n=29), and placebo (Group III, n=25). The proportion of precore stop mutant was measured by a quantitative amplification-created restriction site method. RESULTS: Distinct patterns of the progression of the proportion of mutant were found among these three groups. A steady increase in the proportion of mutant was observed only in Group III patients. In Group II patients, the presence of a higher percentage of mutant (> 25%) immediately before IFN treatment was predictive for the subsequent clearance of hepatitis B e antigen (HBeAg) (p<0.01), but not for complete anti-viral response (p>0.05). Prednisolone pretreatment resulted in an increase in the proportion of mutant in patients with initially low percentages (< or = 25%) of mutant. During the period of IFN treatment, both the relative and absolute amount of the precore stop mutant decreased significantly in Group I patients who cleared HBeAg. The presence of such a decrease in this group of patients was predictive for both HBeAg clearance and complete anti-viral response. CONCLUSIONS: Our data suggest that prednisolone serves as a modulator to enhance elimination of precore stop mutant by IFN, which advocates the benefit of corticosteroid pretreatment in an area where the precore mutants are prevalent.
RCT Entities:
BACKGROUND/AIMS: The aim of this study was to understand the changes in the proportion of hepatitis B virus precore stop mutant during the course of prednisolone primed interferon (IFN) therapy. METHODS: Three groups of patients were included: patients receiving prednisolone-primed IFN treatment (Group I, n=31), IFN treatment only (Group II, n=29), and placebo (Group III, n=25). The proportion of precore stop mutant was measured by a quantitative amplification-created restriction site method. RESULTS: Distinct patterns of the progression of the proportion of mutant were found among these three groups. A steady increase in the proportion of mutant was observed only in Group III patients. In Group II patients, the presence of a higher percentage of mutant (> 25%) immediately before IFN treatment was predictive for the subsequent clearance of hepatitis B e antigen (HBeAg) (p<0.01), but not for complete anti-viral response (p>0.05). Prednisolone pretreatment resulted in an increase in the proportion of mutant in patients with initially low percentages (< or = 25%) of mutant. During the period of IFN treatment, both the relative and absolute amount of the precore stop mutant decreased significantly in Group I patients who cleared HBeAg. The presence of such a decrease in this group of patients was predictive for both HBeAg clearance and complete anti-viral response. CONCLUSIONS: Our data suggest that prednisolone serves as a modulator to enhance elimination of precore stop mutant by IFN, which advocates the benefit of corticosteroid pretreatment in an area where the precore mutants are prevalent.