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Abstract Number: 300

Prevalence and Clinical Significance of Hippocampal Atrophy in Childhood-Onset Systemic Lupus Erythematosus

Aline T. Lapa1, Renata Brabosa2, Mariana Postal1, Nailu A. Sinicato1, Roberto Marini3, Fernando Cendes4 and Simone Appenzeller5, 1Medicine, State University of Campinas, Campinas, Brazil, 2Medicine, Faculdade de Ciencias Medicas, Universidade Estadual de Campinas, Campinas, Germany, 3State University of Campinas, Campinas, Brazil, 4Neurology, State University of Campinas, Campinas, Brazil, 5Medicine, Faculty of Medical Science, State University of Campinas Unicamp, São Paulo, Brazil

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Cognitive dysfunction and systemic lupus erythematosus (SLE)

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Session Information

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

Session Type: Abstract Submissions (ACR)

Background/Purpose: Hippocampal atrophy is associated with corticosteroid use and may be related to cognitive impairment in systemic lupus erythematosus (SLE).Objectives: To determine the prevalence of hippocampal atrophy in childhood-onset SLE (cSLE) using manual magnetic resonance imaging (MRI) volumetric measurements. To determine the possible relationship between hippocampal atrophy and disease duration, corticosteroid therapy, central nervous system (CNS) manifestations and the presence of antiphospholipid antibodies. 

Methods:

A total of 21 cSLE patients (21 female; mean age 17.28; SD=3.63) and 21 healthy age and sex matched volunteers (21 female; 20.57; SD=5.39) were enrolled in this study. A complete clinical, laboratory and neurological evaluation was performed. Neurological manifestations were analyzed according to the ACR classification 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. Mood disorders were determined through Becks Depression and Becks Anxiety Inventory in all participants. 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.  The cumulative dose of corticosteroids used was calculated by the sum of daily dosages versus time (days) of treatment. MRI scans were performed in a 3T Phillips scanner using a standardized protocol. Volumetric 1mm T1 weighted images were used for manual volumetric measurements. Volumes smaller 2 standard deviation from the means of controls were considered abnormal. Non-parametric tests and correlation were used for statistical analysis.

Results: Right (mean volume=3.65cm3; SD=0.49) and left (mean volume=3.64cm3; SD=0.41) hippocampal volumes were significantly smaller in cSLE  compared to healthy volunteers (right mean hippocampal volume=4.59cm3; SD=0.0.44; p<0.001; and left mean hippocampal volume=3.94cm3; SD=1.5; p<0.001). Hippocampal atrophy was observed in 13 (62%) cSLE patients and none of the controls. Hippocampal atrophy was associated with the presence of positive ANA (p=0.048), anticardiolipine antibodies (p=0.02), total corticosteroid dose (p=0.029), low complement (p=0.029) and vasculitis (p=0.03). Cognitive impairment was more frequently observed in patients with hippocampal atrophy (p=0.002). No relationships between hippocampal atrophy and age, disease duration, SLEDAI and SDI was observed. 

Conclusion: Hippocampal atrophy is frequently observed in cSLE and associated with the presence of cognitive impairment. Immunological and clinical features and total dose of corticosteroids are associated with hippocampal atrophy.


Disclosure:

A. T. Lapa,
None;

R. Brabosa,
None;

M. Postal,
None;

N. A. Sinicato,
None;

R. Marini,
None;

F. Cendes,
None;

S. Appenzeller,

FAPESP and CNPq,

2.

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