Session Type: ACR Poster Session B
Session Time: 9:00AM-11:00AM
Background/Purpose: The pathophysiology of brain damage SLE is complex. The aim of this study was to determine brain atrophy progression and the association with Th1 and Th2 in systemic lupus erythemathosus (SLE) patients.
Methods: Consecutive SLE patients followed at the Rheumatology unit of the State University of Campinas were enrolled in this follow-up study. Healthy volunteers, matched by age and sex, were included as control group. A complete clinical, laboratory and neurological evaluation was performed in all subjects. 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 therapy. MRIs were repeated in all individuals after a mean follow-up time of a minimum of 12 months. Sagittal T1-weighted images were used for volumetric measurements (Neuroline®). Volumes smaller 2 standard deviation from the means of controls were considered abnormal. Sera cytokines Th1 (TNF-α, IFN-γ, IL-12) and Th2 (IL-4, IL-6, IL-10) were performed by enzyme linked immunosorbent assay (ELISA) at the end of the study. 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. Data were compared by non-parametric tests.
Results: Eighty-five SLE patients (81 women; mean age of 41.14±11.08 years; range 24-73) and 59 (52 women; mean age of 40.14±13.42 years; range 18-69) healthy controls were included. At the first MRI, 38 patients had active disease (mean SLEDAI scores of 3.71± 4.24; range 0-16). 60 (70.5%) had SDI≥1. Neuropsychiatric manifestations were observed in 31 (36.4%). aCL were positive in 35.5%. Mean total dose of corticosteroid dose was 41.95± 34.09g (0-13.58). Mean cerebral (1056.45± 86.75cm3 and corpus callosum volume 11.57±2.1cm3) were significant smaller at baseline when compared to controls (cerebral 1086.37± 165.77cm3; corpus callosum 14.67±14.33 cm3 volume; p<0.01). We observed a significant greater progressive loss of cerebral (2.3±1.08%), and corpus callosum volume (5.83%±4.97%) in SLE patients when compared to controls (cerebral volume change=0.32±1.73%; p=0.028 and corpus callosum volume change=0.03±0.19%; p<0.001). There was an association between IL-12 and progressive brain atrophy (p=0.008) and a direct correlation between sera IL-12 levels and percentage loss of brain volume (rs=0.3; p=0.015). We did not observe an association between brain or corpus callosum atrophy and aCL (p=0.688; p=0.094), total dose of corticosteroids (p=0.479; p=0.647, respectively), or other cytokines, clinical, laboratory manifestations and treatment.
Conclusion: IL-12 was associated with progressive loss of brain volume in SLE, suggesting immunological basis for global atrophy in SLE. Cytokines act as crucial mediators in the bidirectional signaling between the immune system and the brain and may be considered biomarkers for brain damage in SLE.
To cite this abstract in AMA style:Postal M, Lapa AT, Peliçari KO, Sinicato NA, Peres FA, Ferreira WG, Costallat LT, Cendes F, Appenzeller S. Analysis of Progressive Brain and Corpus Callosum Atrophy and Association with Th1 and Th2 Cytokines in Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/analysis-of-progressive-brain-and-corpus-callosum-atrophy-and-association-with-th1-and-th2-cytokines-in-systemic-lupus-erythematosus/. Accessed May 12, 2021.
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