We investigated the efficacy of a short course of prednisone therapy in 20 patients with histologic evidence of chronic active hepatitis B. Sixteen of 20 prednisonetreated patients who were initially serum hepatitis B virus DNA-positive had a transient elevation of their serum ALT activity on withdrawal of prednisone. Subsequently, 14 of these 16 patients (87.5%) became persistently negative for serum hepatitis B virus DNA, and 10 also lost their HBeAg. In addition, there was a significant fall in serum ALT levels and HBsAg titers up to 12 months of follow-up in the prednisone-treated group. Five of 20 (25%) prednisone-treated patients experienced a transient episode of hepatic decompensation coinciding with the peak of enzyme elevation. To contrast, only 3 of 15 (20%) initially hepatitis B virus DNA-positive matched untreated patients followed during the same time period became negative for serum hepatitis B virus DNA, and no significant changes in serum ALT values or HBsAg titers were noted over the 12-month study period. Thus, patients with chronic active hepatitis B appear to be responsive to immunologic manipulation with prednisone as indicated by a pronounced rebound immune response and clearance of hepatitis B virus DNA with improvement in liver disease activity.
Chronic active hepatitis B (CAH-B) virus infection is a serious form of liver disease which frequently progresses to cirrhosis and primary hepatocellular carcinoma (1-10). No effective therapy exists for this condition. It has been postulated that CAH-B is the result of a continual host immune response against viral antigens and/or liver-specific membrane antigens (1 1-15). Active viral replication appears to be an important determinant for ongoing hepatocellular necrosis as well as for prolongation of viral infectivity. Spontaneous disappearance of markers for hepatitis B virus (HBV) replication, e.g., HBeAg, HBV-specific DNA polymerase and HBV DNA, have been shown to correlate with a remission in the clinical and biochemical parameters of active liver disease (16-21).