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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that may affect multiple organ systems, including the central nervous system (CNS). Psychiatric symptoms are present in the majority of patients with SLE, among which major depression is the most common psychiatric manifestations. The tumor necrosis factor alpha (TNF-α) is a pleiotropic cytokine that produces different stimuli in various physiological and pathological condition. TNF-α may underlie the mechanism of depression by an activation of the hypothalamo-pituitary-adrenocortical (HPA) axis, an activation of neuronal serotonin transporters and the stimulation of the indoleamine 2, 3-dioxygenase which leads to tryptophan depletion.
The aim of this study was to measure the level of tumor necrosis factor alpha in patients with SLE, and assess its possible association with depressive symptoms among these patients.
The present study is a case control study conducted on 90 individuals selected from Immunology Outpatient Clinic and Internal Medicine Department Inpatients, Ain Shams University Hospitals.
Patients were subjected to full clinical examination, disease activity scoring using SLEDAI score and laboratory investigation including TNF-α and psychiatric interview. The patients were further divided into three groups of 30 each: group I (SLE patients with active disease: SLEDAI score >6), group II (SLE patients with inactive disease: SLEDAI sore <6) and group III (healthy individuals serving as a control group).
Our study showed that there is a higher prevalence of depression among active SLE group which demonstrated that depression is strongly associated with SLE. In addition, SLE patients exhibited high levels of serum TNF-α. Moreover, TNF-α values were significantly elevated in active SLE patients. Also, TNF-α was increased significantly among SLE patients with depression and TNF-α was the only independent predictor of depression. These findings suggest a potential role of TNF-α on depressive symptoms in SLE patients.
It is important to consider some limitations of the study analyzing depression mediated by TNF-α, such as the small number of the study groups, the short follow-up period and that the survey was limited to one medical center. Longitudinal studies are necessary to determine the causal relationship between TNF-α and depression in SLE patients regardless of the disease activity.