Background/Purpose: Cognitive dysfunction (CD) affects 15 – 60% of SLE patients; nevertheless, its pathogenesis and predisposing factors are unknown. Objective: To identify factors associated with CD in SLE, focusing on clinical manifestations, neuropsychiatric syndromes (NPSLE), disease activity, inflammation, treatment, and co-morbidities.

Methods: Patients and methods: A random sample of 100 ambulatory patients from a prospective cohort of SLE of recent-onset (<12 months) at enrollment, participated. At entry into the cohort, patients have a standardized medical history with emphasis in atherosclerosis and NPSLE, physical examination, and laboratory tests (chemical analyses, lipids, homocystein, hsCRP, autoantibodies, complement, etc.).  Every 3-6 months, patients are seen for medical care, and disease activity (SLEDAI-2K), medications use/dose are assessed. Every year, information is up-dated; including damage accrual (SLICC-DI), co-morbidities, cardiovascular risk-factors, NPSLE, and a blood sample is drawn. Clinical information is stored in a database containing demographic, anthropometric, lifestyle habits, medical family history, obstetric variables, and lupus information. Two rheumatologists perform all assessments.

At screening for CD, participants were assessed using: Trail Making test, Digit Span, California Verbal Learning test, Rey-Osterrieth complex figure test, the Stroop Color-Word test, WAIS III letter-number sequencing, Animal naming test, Controlled Oral Word association, WAIS-R/III digit symbol substitution test, Grooved pegboard test, and WAIS-R/III similarities. Tests were grouped in 7 cognitive domains: memory, attention/executive function, visuospatial, motor, psycho-motor speed, language, and problem solving. An expert neuropsychologist applied and graded the cognitive tests. Cognitive Dysfunction was defined as at least -2 SD in 2 or more cognitive domains. A nested analysis of autoantibodies, cytokines and chemokines in serum and cerebrospinal fluid (CSF) was conducted among 10 patients with moderate/severe CD and 30 patients without CD.

Results: At enrolment into the cohort, mean age of patients was 25.9 (8.2) years, and SLE duration 5.3 (3.7) months. At screening for CD, mean age was 32.6 years, 93% females, SLE duration 6.2 years. CD was diagnosed in 16 (16%) patients, since age 24 years and from 1.2 years of diagnosis. Patients with CD had lower education 9 vs.12 years (p=0.006), higher BMI 26.7 vs. 24.3 (p=0.03), tested positive of IgG aCL antibodies (50% vs. 18%, p=0.009), and were older (35 vs. 31 years, p=0.09). They had had other NPSLE more often (50% vs. 27%, p=n.s.) and their median number was higher ( 2.5 vs. 1, p=0.04). No difference was observed in other variables including disease activity, anti-dsDNA antibodies, C3, C4, or treatment.

No difference in autoantibodies, cytokines and chemokines was observed in serum and CSF in the nested analysis, except for higher levels of MCP-1 in CSF (886.1 vs. 515.8, pg/mL, p=0.04) among patients with CD.

Conclusion: Cognitive dysfunction is a non-inflammatory NPSLE syndrome. Lower education, higher BMI, presence of IgG aCL antibodies, and previous NPSLE syndromes influence its onset.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/cognitive-dysfunction-a-non-inflammatory-neuropsychiatric-syndrome-in-systemic-lypus-erythematosus/