Alteration of immune markers in a group of melancholic depressed patients and their response to electroconvulsive therapy.
Alteration of immune markers in a group of melancholic depressed patients and their response to electroconvulsive therapy.
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DOI：
10.1016/j.jad.2016.06.035
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发表时间：
2016-11-15
影响因子：
6.6
通讯作者：
Malone KM
中科院分区：
文献类型：
--
作者：
Rush G;O'Donovan A;Nagle L;Conway C;McCrohan A;O'Farrelly C;Lucey JV;Malone KM
免疫系统功能障碍与抑郁症的病理生理机制有关，治疗成功后，免疫系统功能障碍有望恢复正常。我们的目的是调查抑郁症患者的免疫功能障碍及其对电疗的反应。55例抑郁症患者和26例对照组参与研究。33例患者(60%)转诊为ECT。分别在首次ECT治疗结束后1小时和ECT治疗结束后48小时采集血样。在基线水平，抑郁症患者的促炎细胞因子IL-6水平显著高于对照组，而调节性细胞因子转化生长因子β水平显著低于对照组。IL-6水平在第一次电休克治疗后1小时显著升高，但在电休克治疗结束后，IL-6和转化生长因子-β水平均未恢复正常。接受ECT治疗的患者中，70%(n=23)有临床反应，42%(n=10)达到缓解。IL-6和转化生长因子-β的变化与电休克治疗后的临床改善无关。IL-10、肿瘤坏死因子-α和C反应蛋白水平与抑郁症或电休克治疗反应无明显关系。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。抑郁症患者表现出外周IL-6的升高和转化生长因子-β的降低，尽管电休克治疗有临床反应，但这些变化并未恢复正常。这些发现可能与炎症在调节神经促性腺激素表达中的作用的新兴假说一致。忧郁抑郁人群中的慢性炎症对未来医疗健康的影响，特别是心血管风险，在很大程度上是未知的，值得进一步研究。
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 48 hours 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 neurotropin 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.