Background/Purpose: About 16-95% of SLE patients have vitamin D insufficiency. Vitamin D levels, especially vitamin D deficiency, are associated with cognitive performance in adults. We aimed to analyze the association of vitamin D levels, cognitive impairment and cerebral structures in childhood-onset Systemic Lupus Erythematosus (cSLE).

Methods: We screened consecutive cSLE patients, disease-onset before the age of 18 years followed in the pediatric rheumatology unit at the State University of Campinas.  Controls were matched for age, sex and demographic background. Levels of 25-hydroxyvitamin D3 were measured in serum samples, using a commercial enzyme-linked immunosorbent assay; vitamin D levels were considered deficient (<10pg/mL), insufficient (10-29pg/mL), sufficient (30-100pg/mL) and toxic (>100pg/mL). cSLE patients were assessed for disease activity by Systemic Lupus Erythematosus disease activity index (SLEDAI) and damage [Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)]. Cognitive evaluation was performed in all participants using Wechsler Intelligence Scale, according to age and validated in Portuguese. Cognitive dysfunction was defined when scores were ≤-2 standard deviations (SD) from controls in 1 or more subtests. Magnetic resonance imaging scans were performed using a standardized protocol and volumetric 1mm T1 weighted images were used for analysis. Volumes ≤ 2 SD from the means of controls were considered abnormal. White matter (WM) lesions were analyzed in T2-weighted images using a semiautomatic computer program (Neuroline®). Non-parametric tests were used for statistical analysis.

Results:

We included 100 cSLE patients (mean age 16.8 years (SD±4.4) and 37 controls (mean age 18.7 years (SD±4.8). The mean vitamin D level was 32.4±18.7pg/ml in cSLE and 36.5±19.8pg/ml in controls (p=0.22). Cognitive impairment was observed in 27 (47%) cSLE patients and 6 (25%) controls (p=0.001). No association between vitamin D levels and cognitive impairment (p=0.219), SLEDAI (p=0.469), SDI (p=0.915) and corticosteroid use (p=0.486) was observed.

Forty-seven (47%) cSLE patients and 13 (35%) controls had vitamin D insufficiency (p=0.08). Vitamin D insufficiency was not associated with cognitive impairment (p=0.24). When analyzing individual cognitive tests, we observed that vitamin D levels were associated with forward digits span (p=0.04) and correlated indirectly with cubes (r=-0.265;p=0.05) in cSLE patients. No association with structural abnormalities [hippocampal (p=0.466), cerebral (p=0.610) and cerebellum (p=0.475) atrophy] and WM lesion (p=0.601) was observed.

Conclusion: Vitamin D insufficiency was frequent in both cSLE and controls. Although vitamin D levels were not associated with cognitive impairment and cerebral structural abnormalities, we observed an association of vitamin D insufficiency and cognitive subtests associated with retention of immediate memory, analytical skills, visual-motor-spatial coordination, perceptual speed and organization in cSLE patients. Therefore vitamin D levels may contribute to cognitive dysfunction in cSLE and should be followed closely and corrected when indicated.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/vitamin-d-cognition-and-cerebral-structural-abnormalities-in-childhood-onset-systemic-lupus-erythematosus/