Hirai N, Shimizu M, Morioka T, Hinoue Y, Tanaka N, Kobayashi K, Hattori N, Hashimoto T
First Department of Internal Medicine, School of Medicine, Kanazawa University, Ishikawa, Japan.
Liver. 1988 Jun;8(3):138-45. doi: 10.1111/j.1600-0676.1988.tb00982.x.
Changes in the host interferon system during short-term steroid hormone (prednisolone) withdrawal therapy in seven patients with HBeAg-positive chronic hepatitis B were investigated by estimating the in vitro interferon-alpha production in peripheral blood lymphocytes and 2-5 oligoadenylate synthetase activity in the serum. The interferon-alpha production induced by the Sendai virus and estimated in lymphocyte cultures was rapidly and significantly (p less than 0.01) reduced by prednisolone administration and subsequently followed by a recovery corresponding to its withdrawal. The serum 2-5 oligoadenylate synthetase activity showed a similar tendency to diminish under prednisolone administration and to revive during its withdrawal. In all four patients who developed an acute and transient post-prednisolone withdrawal exacerbation a significant initial increase in serum HBV-DNA levels was noted in accordance with the reduction in the host interferon system activity. The results suggest that the changes in the host interferon system activity, i.e. an initial fall and subsequent recovery as caused by a short-term steroid administration with gradual withdrawal, appear to promote viral replication in the early phase and the development of acute and transient exacerbation of hepatitis in the post-steroid withdrawal phase, which may lead to HBeAg/anti-HBe seroconversion in HBeAg-positive chronic hepatitis B patients.
通过评估外周血淋巴细胞中体外α干扰素的产生以及血清中2-5寡腺苷酸合成酶的活性,对7例HBeAg阳性慢性乙型肝炎患者在短期停用类固醇激素(泼尼松龙)治疗期间宿主干扰素系统的变化进行了研究。在淋巴细胞培养物中,由仙台病毒诱导产生并评估的α干扰素产量在给予泼尼松龙后迅速且显著降低(p<0.01),随后随着药物停用而恢复。血清2-5寡腺苷酸合成酶活性在给予泼尼松龙时呈现类似的降低趋势,并在停药期间恢复。在所有4例出现急性短暂的泼尼松龙停药后病情加重的患者中,随着宿主干扰素系统活性降低,血清HBV-DNA水平显著升高。结果表明,宿主干扰素系统活性的变化,即短期给予类固醇激素并逐渐停药所导致的最初下降和随后恢复,似乎在早期促进病毒复制,并在类固醇停药后阶段导致肝炎急性短暂加重,这可能导致HBeAg阳性慢性乙型肝炎患者发生HBeAg/抗-HBe血清学转换。