Reder A T, Thapar M, Jensen M A
Department of Neurology, University of Chicago, IL 60637.
Neurology. 1994 Dec;44(12):2289-94. doi: 10.1212/wnl.44.12.2289.
Glucocorticoid (GCC) therapy usually inhibits inflammatory diseases, but certain regimens can trigger relapses. Clinical use of steroids is not uniform and in some instances may be dangerous. In the present study, GCCs modified the course of experimental allergic encephalomyelitis (EAE) in Lewis rats, a model of inflammatory CNS disease. Continuous treatment with dexamethasone (DEX) completely blocked EAE. RU 486, a GCC antagonist, counteracted the effects of endogenous GCCs and worsened EAE. Sudden withdrawal of DEX also caused severe clinical and histologic exacerbations at a time when paired saline-treated animals had completely recovered. In rats that had complete clinical recovery from EAE, and would not have relapsed without this acute steroid deficit, a short pulse of DEX was followed by severe exacerbations. In contrast, a slow steroid taper prevented exacerbations. Abrupt discontinuation of GCCs provokes inflammatory brain disease.
糖皮质激素（GCC）疗法通常可抑制炎症性疾病，但某些治疗方案可能引发病情复发。类固醇的临床应用并不统一，在某些情况下可能存在危险。在本研究中，GCC改变了Lewis大鼠实验性变态反应性脑脊髓炎（EAE）的病程，EAE是一种炎症性中枢神经系统疾病模型。地塞米松（DEX）持续治疗可完全阻断EAE。GCC拮抗剂RU 486可抵消内源性GCC的作用并使EAE恶化。突然停用DEX也会在配对的生理盐水处理动物已完全恢复时导致严重的临床和组织学恶化。在已从EAE实现完全临床恢复且若无这种急性类固醇缺乏就不会复发的大鼠中，短疗程DEX脉冲治疗后会出现严重恶化。相比之下，缓慢减少类固醇剂量可预防病情恶化。突然停用GCC会引发炎症性脑病。
