Longitudinal analysis of white and gray matter structural abnormalities in juvenil systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease that presents a broad spectrum of signs and symptoms. The occurrence of structural and functional damage in patient's brain is independent of the occurrence of NP manifestations. The aim of this study was to analyze, during a period of 22,5±17,2 months, the structural changes in childhood-onset SLE (cSLE) and to determine whether sera S100? and NF-H levels were associated to structural abnormalities. Eighty-six cSLE patients were included [77 (89.5%) women; mean age of 15.6±4.1 years]. The control group consisted of 95 healthy volunteers [75 (78.9%) women; mean age of 16.4 ± 3.4 years]. Disease activity was determined by [SLE Disease Activity Index (SLEDAI)] and the cumulative damage by [Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)]. All patients underwent two magnetic resonance imaging (MRI) exams during the follow-up period. Cerebral, corpus callosum and ventricles volumes were determined by the semiautomatic program Neuroline®. The cortical thickness was determined by the FreeSurfer® automatic program. All patients completed the Montreal cognitive assessment (MoCA), the Beck Depression Inventory (BDI) and the Beck Anxiety Inventory (BAI). Sera S100? and NF-H protein levels were performed by Enzyme Linked Immunosorbent Assay (ELISA). Statistical analysis was performed through non-parametric tests. The mean progression of cerebral volume loss in patients with SLE was 1.67 ± 2.71% and observed in 44 (51.16%) patients. Twenty-three (26.7%) SLE patients presented reduction of 2.31 ± 5.48% of the corpus callosum volume. The mean progression of ventricular enlargement was 5.03 ± 9.81% and observed in 33 (38.37%) patients with SLE. In the control group we observed loss of cerebral volume progress of 0.85 ± 2.00% (p <0.001) which were identified in 24 (25.35%, p <0.001) controls. Eleven (11.5%; p = 0.013) controls had a reduction of 1.07 ± 0.73% (p = 0.013). Seventeen (17.9%; p = 0.003) of the controls presented increase of ventricular volume with media of 1.11 ± 3.21% (p = 0.003). On visual analysis of white matter hyperintensities (WMH) 37 (43%) patients presented WMH at study entry and 21 (24.4%) patients presented WMH at follow-up (p=0.001). Three (3.15%) controls presented WMH at the study entry and follow-up of the study. Higher numbers of WMH were associated with serum NF-H levels (p = 0.004). We observed a reduction of cortical volume at study entry. We observed that, at the study entry the left superior frontal gyrus presented a significantly lower volume in patients with NP manifestations (p = 0.034). In conclusion, we observed progression of cerebral atrophy and corpus callosum in SLE patients. NP manifestations, corticosteroid dose, disease damage and serum levels of S100? were associated with this progression. Patients with SLE often have WMH; the number and volume decreased, probably by controlling the activity of the disease. Cortical thickness reduction was associated with signs of disease activity and damage in SLE (AU)