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© 1993 British Society for Rheumatology

other

COGNITIVE IMPAIRMENT AND AUTOANTLBODIES IN SYSTEMIC LUPUS ERYTHEMATOSUS

J. G. HANLY*,, N. M. WALSH{dagger}, J. D. FISK{ddagger}, B. EASTWOOD§, C. HONG*, G. SHERWOOD*, J. V. JONES*, E. JONES* and K. ELKON{dagger}{dagger}

*The Division of Rheumatology, Department of Medicine Halifax, Nova Scotia, Canada
{dagger}Department of Pathology Victoria General Hospital and Dalhousie University Halifax, Nova Scotia, Canada
{ddagger}Department of Psychology, Camp Hill Medical Centre Halifax, Nova Scotia, Canada
{dagger}{dagger}The Hospital for Special Surgery and Cornell University New York, NX USA
§Community Health and Epidemiology, Dalhousie University Halifax, Nova Scotia, Canada

Correspondence to: Correspondence to J. G. Hanly, Rheumatic Disease Unit, Halifax Civic Building, 5938 University Avenue, Halifax, Nova Scotia, B3H 1V9, Canada

Nervous system involvement in systemic lupus erythematosus (SLE) includes a wide array of manifestations some of which have been associated with specific autoantibodies. These include reactivity to surface neuronal and lymphocyte antigens, ribosomal P and cardiolipin. The aim of the present study was to examine the association between cognitive abnormalities and these autoantibodies in an unselected female population of SLE patients. Using a battery of standardized neuropsychological tests, cognitive impairment was identified in 15/70 (21%) SLE patients compared to 1/25 (4%) patients with rheumatoid arthritis and 1/23 (4%) healthy subjects (P=0.04). Circulating antineuronal antibodies were measured by indirect immunofluorescence using human neuroblastoma cell lines IMR-6 and SK-N-SH. Lyrnphocytotoxic antibodies were measured by microcytotoxicity. Antibodies to ribosomal P and cardiolipin were measured by ELISA. Antineuronal antibodies were detected in 34%, lymphocytotoxic antibodies in 47%, anti-P antibodies in 17% and anticardiolipin antibodies in 24% of patients. In the cognitively impaired and unimpaired SLE patients there was no significant difference in the prevalence of antineuronal antibodies (33 vs 35%), lymphocytotoxic antibodies (40 vs 50%), anti-P antibodies (20 vs 17%) or anticardiolipin antibodies (7 vs 29%). The titre and isotype of autoantibodies were also similar in both groups. These results suggest that autoantibodies which have previously been associated with nervous system manifestations of SLE are not likely to be directly involved in the pathogenesis of cognitive dysfunction.

KEY WORDS: Cognitive impairment, Autoantibodies, Lupus


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