Zincir Serkan, Öztürk Pelin, Bilgen Ali Emrah, İzci Filiz, Yükselir Cihad
Department of Psychiatry, Gölcük Military Hospital, Kocaeli, Turkey.
Psychiatry Clinic, Erenkoy Training and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey.
Neuropsychiatr Dis Treat. 2016 Jun 15;12:1389-96. doi: 10.2147/NDT.S106652. eCollection 2016.
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.
近年来的研究表明,神经免疫事件和免疫激活可能在抑郁症的病因中占有一席之地。数据显示,免疫系统激活与促炎细胞因子(如白细胞介素1(IL-1)、IL-6和肿瘤坏死因子-α(TNF-α))的过度释放与抑郁症的病因之间存在因果关系。尽管电休克疗法(ECT)的作用机制尚不清楚,但有证据表明它可以减少细胞因子和免疫系统的变化。在我们的研究中,我们旨在确定ECT对重度抑郁症患者血清免疫调节剂水平的影响。本研究对50例难治性重度抑郁症患者进行。将患者的数据与30名具有相似人口统计学特征的健康个体进行比较。患者出现临床反应,并在治疗结束时测量IL-1、IL-6、TNF-α、IL-10、IL-4和干扰素-γ水平。用17项汉密尔顿抑郁量表评估疾病严重程度。使用SPSS 15版进行数据分析。重度抑郁症患者与对照组在基础血清IL-1、IL-6、TNF-α、IL-10、IL-4和干扰素-γ水平方面存在显著差异。ECT治疗显示可减少这些差异。ECT可能会引起免疫系统活性的显著变化。考虑免疫-内分泌-神经递质系统之间的关系可能有助于提出关于抗抑郁治疗机制和抑郁症生物学的新理论。