Objectives: The evaluations of the pathogenetic roles of cell mediated immunity and of the preventive effect for disease progression with interferon(IFN) treatment in patients with chronic active hepatitis-B(CAH-B) are the objectives of this study.
Methods: Thirty-two patients with CAH-B were treated with interferon alpha-2b(IFN alpha-2b) with prednisolone withdrawal and 30 control patients were treated with conventional hepatotonics for 6 months. Peripheral total T cell fractions and T cell subsets of the patients with CAH-B, treated with IFN alpha-2b with prednisolone withdrawal, were examined 1 month before administration of prednisolone, and compared with 12 normal controls for assessing the potential role of cellular immunity in the development of CAH-B. To estimate the effectiveness of IFN therapy for the patients with CAH-B, levels of various liver function tests, HBsAg, anti-HBs, HBeAg, anti-HBe, HBV DNA, anti-HCV and others were assessed for the treatment group and compared with control patients at pre- and post-treatment period each.
Results: The value of CD4 was significantly lower in patients with CAH-B than normal controls (36.3 +/- 7.7% vs 42.1 +/- 5.7%, p < 0.05) and the value of CD8 was significantly higher in patients with CAH-B than normal controls (30.6 +/- 10.3% vs 24.3 +/- 5.2%, p < 0.05) before prednisolone administration. The patients in responder group (n = 26) had significantly lower CD4 cells compared with normal controls, but non-responders (n = 6) did not have. The levels of liver function test(LFT) in the patients with IFN alpha-2b treatment with prednisolone withdrawal were not different from the control patient group at pretreatment, but significantly lower than control patient group's after treatment, regardless of response to IFN alpha-2b treatment with prednisolone withdrawal.
Conclusions: The cellular immunity of the host may have a potential role in the pathogenesis of chronicity of hepatitis B infection. IFN alpha-2b treatment with prednisolone withdrawal may be regarded as one of the effective treatment modalities for the inhibition of disease progression in patients with CAH-B.