Session Title: Systemic Lupus Erythematosus: Clinical Aspects
Session Type: Abstract Submissions (ACR)
Elevated serum levels of tumor necrosis factor alpha (TNF-α) have been reported in patients with major depressive disorder and in patients with depression in multiple sclerosis. However, the association between activation of the immune system, levels of proinflammatory cytokines and mood disorders is still unknown in systemic lupus erythematosus (SLE).
Objective: To determine if increased serum levels of TNF-α are associated with mood disorders in SLE.
We included 153 SLE patients (women 148; mean age 32.16±14.49; range 10-67) and 41 healthy (women 32; mean age 31±12.04; range 12-59) age and sex matched controls. Mood disorders were determined through Becks Depression and Becks Anxiety Inventory in all participants. The total score ranges from 0 to 63 for BDI and BAI. The cutoffs used for the BDI were: 0–13: no/minimal depression; 14–19: mild depression; 20–28: moderate depression; and 29–63: severe depression and for the BAI: 0-7: no/minimal level of anxiety; 8-15: mild anxiety; 16-25: moderate anxiety; 26-63: severe anxiety. 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. Serum samples were obtained from all participants in the absence of infections. TNF-α levels were measured by enzyme-linked immunosorbent assay using commercial kits from R&D Systems. Mann-Whitney Test was used to compare TNF-α concentrations between groups. Multivariate analysis was performed including sex, age, SLE duration, disease activity, and cumulative damage, severity of depression and anxiety and current drug exposures.
Depression was identified in 70 (45.7%) SLE and in 10 (25%) controls (p<0.001). Anxiety was identified in 93 (60.7%) SLE and in 17 controls (41.5%) (p<0.001). Serum TNF-α levels were increased in individuals with depression (p<0.001) and with anxiety (p=0.037). A direct correlation between the severity of depression and serum TNF-α levels (r=0.15; p=0.023) was observed. TNF-α levels were significantly increased in patients with active disease (SLEDAI≥3) (p=0.007) and with current prednisone dosage (p<0.001). In addition, we observed a correlation between serum TNF-α levels and SLEDAI (r=0.23, p=0.004) and with current prednisone dosage (r=0.18; p=0.031). No association between TNF-α levels and other clinical, laboratory variable and SDI scores was observed. No difference in TNF-α levels was observed between patients with and without hydroxicloroquine or other immunosuppressants. In the multivariate analysis, serum TNF-α levels were independently associated with depression (OR=3.1; 95%CI 1.8-5.6) and with disease activity (OR=4.4; 95%CI 1.3-7.1).
Serum TNF-α levels are elevated in individuals with mood disorders. In SLE, serum TNF-α levels were independently associated with depression and with disease activity. The etiology of mood disorders is still debated in SLE, but our findings suggest the presence of immunological basis for depression in SLE.
A. T. Lapa,
N. A. Sinicato,
FAPESP and CNPq,
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