Levels of serum immunomodulators and alterations with electroconvulsive therapy in treatment-resistant major depression

Abstract

Studies in recent years have indicated that neuroimmunological events and immune activation may have a place in the etiology of depression. It has been suggested from data that there is a causal relationship between activation of the immune system and excessive release of proinflammatory cytokines, such as interleukin 1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-alpha), and the etiology of depression. Although the mechanism of action of electroconvulsive therapy (ECT) is unclear, there is evidence that it can reduce cytokines and immune system changes. In our study, we aimed to determine how levels of serum immunomodulators were affected by ECT in major depression patients. This study was conducted on 50 patients with treatment-resistant major depression. The data of the patients were compared with 30 healthy individuals with similar demographic characteristics. A clinical response occurred in the patients and at the end of therapy, IL-1, IL-6, TNF-alpha, IL-10, IL-4, and interferon-gamma levels were measured. The disease severity was assessed with the 17-item Hamilton Depression Rating Scale. Data analysis was performed using SPSS Version 15. Significant differences were determined between the patients with major depression and control group with respect to basal serum IL-1, IL-6, TNF-alpha, IL-10, IL-4, and interferon-gamma levels. ECT treatment was shown to reduce these differences. ECT may cause significant changes in the activity of the immune system. The consideration of the relationship between the immune endocrine neurotransmitter systems could contribute to new theories regarding the mechanism of antidepressant treatment and biology of depression.

Low tumor necrosis factor‐α levels predict symptom reduction during electroconvulsive therapy in major depressive disorder

“…No similar correlations were found during subsequent sessions. No findings suggesting associations between a low TNFα level and symptom reduction during ECT have been reported in previous studies (First et al., 1996; Fluitman et al., 2011; Hestad et al., 2003; Rotter et al., 2013; Rush et al., 2016; Zincir et al., 2016). If replicated in the future studies, this finding supports the role of TNFα in the pathogenesis of MDD and in the mechanism of action of ECT; it may also guide the selection of treatment modalities for patients with severe MDD.…”

“…The effect of ECT on the TNFα level appears to be transitory because the TNFα level returned to the basic level before next ECT session. This finding differs from some previous reports in which the TNFα level either increased, did not change, or decreased by ECT (First et al., 1996; Fluitman et al., 2011; Hestad et al., 2003; Rotter et al., 2013; Rush et al., 2016; Zincir et al., 2016). The design of the study by Hestad et al.…”

“…The TNFα levels in these two latter studies were serum (not plasma) levels, making comparison with the present results difficult. Moreover, three studies found no change in the serum/plasma/plasma (respectively) TNFα level during and after the ECT series (First et al., 1996; Hestad et al., 2003; Zincir et al., 2016). However, in these studies, the timing of the blood samplings and procedures were somewhat different, hampering comparison with the present results (First et al., 1996; Hestad et al., 2003; Zincir et al., 2016).…”

“…Some studies have addressed the association between TNFα and ECT (First, Spitzer, Gibbon, & Williams, 1996; Fluitman et al., 2011; Hestad et al., 2003; Rotter et al., 2013; Rush et al., 2016; Zincir, Ozturk, Bilgen, Izci, & Yukselir, 2016). In 2003, Hestad et al.…”

“…(Fluitman et al., 2011) reported a decrease in the TNFα level in patients with MDD along with clinical improvement during and after an ECT series, whereas another study revealed a rapid increase in the TNFα level after a single ECT session but no long‐term change during the ECT series (Rotter et al., 2013). Other studies have found no change in the TNFα level during or after the ECT series (First et al., 1996; Hestad et al., 2003; Zincir et al., 2016). A recent study revealed a decrease in the TNFα level during and after an ECT series, although the baseline TNFα level before ECT was lower in patients than in controls (Rush et al., 2016).…”