Cerebral atrophy related to corticotherapy in systemic lupus erythematosus(SLE)

The aim of this study was to evaluate the frequency and intensity of cerebr al atrophy using CT scanning and the possible relation to corticosteroid th erapy or disease in systemic lupus erythematosus (SLE) and to analyse the r elationships between cerebral atrophy and activity disease and neuropsychia tric manifestations in lupus patients. We studied 107 consecutive SLE patie nts (American Rheumatology Association 1982 criteria) who were taking stero id drugs at the time and not selected for any particular manifestation (gro up 1). A complete clinical, neurological and laboratory evaluation was perf ormed. The American College of Rheumatology's classification for neuropsych iatric manifestations and SLE disease activity index for activity were empl oyed. Group 2 comprised 39 non-SLE patients with oral chronic steroid use ( I mg/k/day for more than 3 consecutive months); 50 normal individuals were the controls (group 3). There were no demographic differences between the g roups. Brain CT was performed in all individuals and the frequency and the intensity (minimal, moderate and severe) of atrophy analysed, through well- defined measures and indices, by two neuroradiologists. Cerebral atrophy wa s significantly more frequent in groups I and 2 than in group 3, but with n o significant difference between groups I and 2. The severity of cerebral a trophy was significantly higher in SLE patients (p <0.05), independent of s teroid dose or duration of disease. In both groups no patient presented sev ere atrophy. Lupus patients with and without cerebral atrophy presented neu ropsychiatric manifestations and activity disease in a similar proportion. The more frequent neuropsychiatric manifestation in lupus patients with cer ebral atrophy was seizures (p <0.05). Chronic glucocorticoid therapy was re sponsible for cerebral atrophy, with a comparable incidence in both lupus a nd non-lupus patients compared to age and gender-matched normal subjects un treated with glucocorticoids. The disease activity was not related to cereb ral atrophy in group I and seizures were the neurologic manifestation relat ed to cerebral atrophy. The severity of the cerebral atrophy was independen t of steroid dose, or duration of treatment. Moreover, the disease itself c ontributes to the severity of this process, but not to the development of c erebral atrophy.