Rush Gavin, O'Donovan Aoife, Nagle Laura, Conway Catherine, McCrohan AnnMaria, O'Farrelly Cliona, Lucey James V, Malone Kevin M
St. Patrick's University Hospital, Dublin, Ireland.
School of Medicine and Medical Sciences, University College Dublin, Dublin, Ireland; Department of Psychiatry, Psychotherapy and Mental Health Research, St. Vincent's University Hospital, Dublin, Ireland; Stress and Health Research Program, San Francisco Veteran's Affairs Medical Center, San Francisco, CA, United States; Department of Psychiatry, University of California, San Francisco, CA, United States.
J Affect Disord. 2016 Nov 15;205:60-68. doi: 10.1016/j.jad.2016.06.035. Epub 2016 Jun 17.
Immune system dysfunction is implicated in the pathophysiology of major depression, and is hypothesized to normalize with successful treatment. We aimed to investigate immune dysfunction in melancholic depression and its response to ECT.
55 melancholic depressed patients and 26 controls participated. 33 patients (60%) were referred for ECT. Blood samples were taken at baseline, one hour after the first ECT session, and 48h after ECT series completion.
At baseline, melancholic depressed patients had significantly higher levels of the pro-inflammatory cytokine IL-6, and lower levels of the regulatory cytokine TGF-β than controls. A significant surge in IL-6 levels was observed one hour after the first ECT session, but neither IL-6 nor TGF-β levels normalized after completion of ECT series. Seventy per cent (n=23) of ECT recipients showed clinical response and 42% (n=10) reached remission. Neither IL-6 nor TGF-β changes correlated with clinical improvement following ECT. No significant changes in IL-10, TNF-α and CRP levels were found in relation to melancholia or response to ECT.
As a naturalistic study, some potential confounders could not be eliminated or controlled, including medication use.
Melancholic depressed patients demonstrated a peripheral increase in IL-6 and reduction in TGF-β, which did not normalize despite clinical response to ECT. These findings may be consistent with emerging hypotheses of the role of inflammation in mediating neurotrophin expression. The implications of chronic inflammation in the melancholic depressed population for future medical health, particularly cardiovascular risk, are largely unknown and warrant further investigation.
免疫系统功能障碍与重度抑郁症的病理生理学有关,并且据推测成功治疗后可恢复正常。我们旨在研究 melancholic 抑郁症中的免疫功能障碍及其对ECT的反应。
55名 melancholic 抑郁症患者和26名对照参与研究。33名患者(60%)被转诊接受ECT治疗。在基线、首次ECT治疗后1小时以及ECT系列治疗完成后48小时采集血样。
在基线时,melancholic 抑郁症患者的促炎细胞因子IL-6水平显著高于对照组,而调节性细胞因子TGF-β水平低于对照组。首次ECT治疗后1小时观察到IL-6水平显著升高,但ECT系列治疗完成后IL-6和TGF-β水平均未恢复正常。70%(n = 23)的ECT接受者显示出临床反应,42%(n = 10)达到缓解。ECT治疗后IL-6和TGF-β的变化均与临床改善无关。未发现与 melancholia 或ECT反应相关的IL-10、TNF-α和CRP水平有显著变化。
作为一项自然主义研究,一些潜在的混杂因素无法消除或控制,包括药物使用。
melancholic 抑郁症患者表现出外周IL-6升高和TGF-β降低,尽管对ECT有临床反应,但这些指标并未恢复正常。这些发现可能与炎症在介导神经营养因子表达中的作用的新假说是一致的。melancholic 抑郁症患者慢性炎症对未来医疗健康,特别是心血管风险的影响在很大程度上尚不清楚,值得进一步研究。