T cell subsets in chronic hepatitis B and the effect of prednisolone withdrawal and interferon alpha-2b

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 α-2b(IFN α-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 IFNα-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 α-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 α-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 α-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.