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Abstract Number: 1260

Serum S100β Is Associated With Neuropsychiatric Manifestations In Childhood-Onset Systemic Lupus Erythematosus

Aline T. Lapa1, Mariana Postal1, Nailu A. Sinicato1, Bruna Bellini1, Paula T Fernandes2, Roberto Marini3 and Simone Appenzeller4, 1Medicine, State University of Campinas, Campinas, Brazil, 2Faculty of Physical Education, State University of Campinas, Campinas, Brazil, 3State University of Campinas, Campinas, Brazil, 4Medicine, Faculty of Medical Science, State University of Campinas Unicamp, São Paulo, Brazil

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Cognitive dysfunction, neuropsychiatric disorders and systemic lupus erythematosus (SLE)

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Session Information

Title: Pediatric Rheumatology - Clinical and Therapeutic Aspects II: Pediatric Systemic Lupus Erythematosus, Pediatric Vasculitis and Pediatric Myositis

Session Type: Abstract Submissions (ACR)

Background/Purpose: Involvement of the central nervous system (CNS) in systemic lupus erythematosus (SLE) is an important source of morbidity and mortality.  S100β has been considered a potential biomarker that could indicate damage or dysfunction of the CNS in adult SLE patients. However there are no studies in childhood-onset SLE patients (cSLE). Objective:To investigate serum S100β protein levels in cSLE and to elucidate their association with disease activity and NP manifestations. 

Methods: We included 72 SLE patients (women=67; mean age 18.21±4.75; range 9-37) and 53 healthy (women =45; mean age 19.72±6.10; range 6-31) age and sex matched controls. Neuropsychiatric manifestations were analyzed according to the American College of Rheumatology criteria. Cognitive evaluation was performed in all participants using Wechsler Intelligence Scale for children (WISC-III) and Wechsler Intelligence Scale for adults (WAIS), according to age and validated in Portuguese. Scores lower than 2 standard deviations were considered abnormal. Mood disorders were determined through Becks Depression and Anxiety Inventory. SLE patients were further assessed for clinical and laboratory SLE manifestations, disease activity [SLE Disease Activity Index (SLEDAI)], damage [Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)] and current drug exposures. Total dose of corticosteroids and other immunosuppressant medications used since the onset of disease were calculated by data obtained by careful review of the medical charts. Sera samples were obtained from all participants in the absence of infections at the day of clinical evaluation. S100β protein levels were measured by enzyme-linked immunosorbent assay using commercial kits from BioVendor, Inc (Czech Republic) and compared by non-parametric tests. Multivariate analysis was performed including S100β protein levels, total corticosteroid dose, disease duration, antiphospholipid antibodies, anxiety and depression.

Results: The mean S100β protein levels was significantly higher in cSLE patients [143.98 pg/mL (SD± 99.34)]  when compared to controls [56.63 pg/mL (SD±44.07); p<0.001)].  NP manifestations were observed in 53 (73.6%) cSLE. S100β protein levels was significantly higher in NPcSLE patients (N=53; mean=161.98; SD=106.8) when compared to non-NPcSLE patients (N=19; mean=95.11; SD=52.1; p<0.001). Among individual NP manifestations,  serum concentrations of S100β protein were significantly higher in cSLE patients with cognitive impairment (N=28; mean=186.76; SD=1022.61) when compared to cSLE patients without cognitive impairment (N=44; mean=115.37; SD=85.0; p<0.001). No difference of S100β levels were observed in cSLE patients with other NP manifestations, disease activity or damage. In the multivariate analysis cognitive impairment was independently associated with serum S100β levels (OR=2.69; 95%CI=1.25-5.78). 

Conclusion: Serum S100β levels are significantly increased in cSLE patients with NP involvement, especially cognitive impairment, independently of otherdisease feature. S100β protein may be considered a potential biomarker for cognitive impairment in cSLE.


Disclosure:

A. T. Lapa,

FAPESP,

9;

M. Postal,

FAPESP,

9;

N. A. Sinicato,

FAPESP,

9;

B. Bellini,

FAPESP,

2;

P. T. Fernandes,
None;

R. Marini,
None;

S. Appenzeller,

FAPESP and CNPq,

2.

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