At. Reder et al., A REDUCTION IN SERUM GLUCOCORTICOIDS PROVOKES EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS - IMPLICATIONS FOR TREATMENT OF INFLAMMATORY BRAIN DISEASE, Neurology, 44(12), 1994, pp. 2289-2294
Glucocorticoid (GCC) therapy usually inhibits inflammatory diseases, b
ut certain regimens can trigger relapses. Clinical use of steroids is
not uniform and in some instances may be dangerous. In the present stu
dy, GCCs modified the course of experimental allergic encephalomyeliti
s (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 worsen
ed EAE. Sudden withdrawal of DEX also caused severe clinical and histo
logic exacerbations at a time when paired saline-treated animals had c
ompletely 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.