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 prednisone-treated 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.

Among infants born to women in whom sera are positive for both the hepatitis B surface antigen and the e antigen, 85% to 90% are infected with hepatitis B virus and become chronic hepatitis B surface antigen carriers. In a study to assess the effectiveness of passive-active prophylaxis (hepatitis B immune globulin and hepatitis B vaccine) of such infants, we screened 18,842 pregnant Asian-American women: 8.7% were positive for hepatitis B surface antigen and 3.0% were also positive for hepatitis B e antigen. Thus far, 113 infants have received hepatitis B immune globulin (0.5 mL at birth) and hepatitis B vaccine (three 20-micrograms doses beginning at birth or at 1 month) and have been followed up for nine to 18 months. Among these infants, 16 have become chronic carriers, an incidence of only 14.2%. All of the uninfected infants have retained high levels of antibody to surface antigen, suggesting that they have had an active immune response to the vaccine and should have long-term protection against hepatitis B virus.

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Five patients with hepatitis B surface antigen (HBsAg) positive chronic hepatitis and histologically confirmed primary hepatocellular carcinoma (PHC) were treated with 3 X 10(6) units/day of partially purified human leukocyte interferon intramuscularly for 2 consecutive months. During interferon therapy, one patient had stable disease, while the remaining four patients had progressive disease. Following interferon therapy no changes were noted in the hepatitis B viral markers or in serum alphafetoprotein levels. Data on the effects of human leukocyte interferon on lymphocyte subpopulations and on the cytotoxic activity of peripheral blood mononuclear cells against a hepatitis B surface antigen expressing primary hepatocellular carcinoma cell line are presented.

In vitro synthesis of the anti-HBc, anti-HBs and polyclonal IgG and IgM classes of antibodies were determined from supernatants of peripheral blood mono-nuclear cells cultured in the presence of pokeweed mitogen. Thirty-seven patients with chronic hepatitis B and 10 healthy control subjects whose sera were positive for anti-HBs formed the study group. Twenty-four of 37 patients showed histologic evidence of chronic active hepatitis B while the remaining 13 patients had chronic persistent hepatitis B. Lymphocytes from chronic persistent hepatitis B, chronic active hepatitis B and healthy controls secreted similar levels of IgM. However, IgG synthesis was markedly impaired (p less than 0.002) in the chronic persistent hepatitis B group as compared with healthy controls or chronic active hepatitis B patients. In vitro anti-HBc production and serum anti-HBc titers correlated directly with hepatocellular inflammation and inversely with serum hepatitis B virus DNA. Anti-HBc synthesis was significantly higher in chronic active hepatitis B patients who exhibited a more pronounced hepatocellular damage when compared to chronic persistent hepatitis B patients who had little or no liver cell injury.