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Abstract Number: 2661

Serum Neuronal Biomarkers and Brain Atrophy in Childhood-Onset Systemic Lupus Erythematosus

Aline T. Lapa1, Mariana Postal1, Nailu A. Sinicato1, Renata Barbosa2, Fernando Cendes3, Roberto Marini4 and Simone Appenzeller5, 1Medicine, State University of Campinas, Campinas, Brazil, 2Medicine, Faculdade de Ciencias Medicas, Universidade Estadual de Campinas, Campinas, Germany, 3Neurology, State University of Campinas, Campinas, Brazil, 4Departament of Pediatrics, State University of Campinas, Campinas, Brazil, 5Medicine, Faculty of Medical Science, State University of Campinas Unicamp, São Paulo, Brazil

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Magnetic resonance imaging (MRI), Nervous system lupus, Neuroimaging and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment: Epidemiology, Women's Health, Cardiovascular and CNS

Session Type: Abstract Submissions (ACR)

Background/Purpose We aimedto investigate the association of serum biomarkers and regional and diffuse brain atrophy in cSLE.

Methods We included consecutive cSLE patients (disease-onset before the age of 18) followed in a cohort at the Pediatric Rheumatology Unit at the State University of Campinas and age and sex matched healthy controls.A complete clinical, laboratory and neurological evaluation was performed in all subjects. Neurological manifestations were analyzed according to the ACR classification criteria. Disease activity was measured by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and cumulative SLE-related damage was determined using the Systemic Lupus International Collaborating Clinics (SLICC)/ACR Damage Index (SDI). Magnetic resonance imaging (MRI) scans were obtained through a standardized protocol (3Tessla Philips) and normalized volumetric 1mm Tl weighted images were used for manual volumetric measurements. Volumes ≤2 standard deviation from the means of controls were considered abnormal. Serum biomarkers (S100β, NF-H and antiribossomal P (Anti-P) and anticardiolipin antibodies levels were measured by enzyme-linked immunosorbent assay using commercial kits from BioVendor, Inc(Czech Republic).Anti-double stranded DNA (dsDNA) antibodies were determined by indirect immunofluorescenceusingCrithidia as substrate and considered positive if ≥ 1:20.Precipitating antibodies to extractable nuclear antigens (ENAs),including Ro (SSA), La (SSB), and Sm were detected by a standardizedELISA method, and considered positive if higher than 1:40.Anticardiolipin antibodies (aCL) of theIgG and IgMisotypes were measured by an ELISA method. Thelupus anticoagulant (LA) activity was detected by coagulation assaysin platelet-free plasma obtained by double centrifugation. Non-parametric-tests and correlation were used for statistical analysis.

Results We included 76 cSLE patients (69 women; median age 16 years; range 9-30), with median disease duration was 3 years (range 0-13 years). Neuropsychiatric manifestations were observed in 32 (42.1%). Structural brain abnormalities were identified in 51 (67%) cSLE patients and in in none of the controls (p<0.001). Cerebral atrophy was identified in 18 (23.7%), corpus callosum atrophy in 20 (26.3%) and hippocampal atrophy in 46 (60.5%). We did not observe an association between structural brain abnormalities and S100β, NF-H and anti-P protein.The presence of cerebral atrophy was associated with cumulative corticosteroid dose (p=0.026), active disease (SLEDAI≥3) (p=0.044), aCL (p=0.024), anti-dsDNA (p=0.022) and anti-Smith (p=0.049) antibodies.The presence of corpus callosum atrophy was associated with low complement levels (p=0.011). Hippocampal atrophy was associated with low complement levels (p=0.014) and LA (p=0.019).

Conclusion

Regional and diffuse brain atrophy is frequently observed in cSLE patients. We did not observe an association with neuronal biomarkers, however aPL, LA, low complement levels and cumulative corticosteroid dose were associated with atrophy in this cohort.


Disclosure:

A. T. Lapa,
None;

M. Postal,
None;

N. A. Sinicato,
None;

R. Barbosa,
None;

F. Cendes,
None;

R. Marini,
None;

S. Appenzeller,
None.

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