The Effect of Antidepressant Medication Treatment on Serum Levels of Inflammatory Cytokines: A Meta-Analysis

The Effect of Antidepressant Medication Treatment on Serum Levels of Inflammatory Cytokines: A Meta-Analysis
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DOI:
10.1038/npp.2011.132
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发表时间:
2011-11-01
影响因子:
7.6
通讯作者:
Bloch, Michael
Bloch, Michael
中科院分区:
医学1区
文献类型:
--
作者:
Hannestad, Jonas;DellaGioia, Nicole;Bloch, Michael

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血清炎症因子水平,如肿瘤坏死因子α (TNF α)、白细胞介素6 (IL-6)和IL-1 β (1L-1 β),在重度抑郁症(MDD)患者中升高。发生这种情况的原因尚不清楚。炎症细胞因子水平升高可能是重度抑郁症患者脑功能障碍的结果。炎症细胞因子也可能导致重度抑郁症的抑郁症状。如果第一个假设是正确的,人们会期望治疗后抑郁发作的缓解会使水平正常化。一些研究测量了抗抑郁治疗期间细胞因子水平的变化;然而,结果各不相同。本研究的目的是收集抗抑郁治疗期间血清TNF α、IL-6和IL-1 β水平变化的所有可用数据,以确定这些水平是否发生变化。如果研究使用了经批准的药物治疗抑郁症,患者被诊断为重度抑郁症,并且在治疗前后测量血清中TNF α、IL-6和/或IL-1 β的水平,则纳入研究。22项研究符合这些标准。这些研究的荟萃分析显示,总的来说,虽然药物抗抑郁治疗减轻了抑郁症状,但它并没有降低血清TNF - α水平。另一方面,抗抑郁治疗确实降低了IL-1 β的水平,也可能降低了IL-6的水平。按抗抑郁药类别分层亚组分析表明,血清素再摄取抑制剂可降低IL-6和TNF - α水平。其他抗抑郁药虽然对抑郁症状有效,但似乎并没有降低细胞因子水平。这些结果反驳了抑郁发作的缓解与循环炎性细胞因子水平正常化相关的观点;然而,研究结果与炎症细胞因子导致抑郁症状的可能性是一致的,抗抑郁药阻断了炎症细胞因子对大脑的影响。神经精神药理学(2011)36,2452-2459;doi: 10.1038 / npp.2011.132;2011年7月27日在线发布
Serum levels of inflammatory cytokines, for example, tumor necrosis factor alpha (TNF alpha), interleukin-6 (IL-6), and IL-1 beta (1L-1 beta), are elevated in subjects with major depressive disorder (MDD). The reason why this occurs is unclear. Elevated levels of inflammatory cytokines could be a result of brain dysfunction in MDD. It is also possible that inflammatory cytokines contribute to depressive symptoms in MDD. If the first assumption is correct, one would expect levels to normalize with resolution of the depressive episode after treatment. Several studies have measured changes in cytokine levels during antidepressant treatment; however, the results vary. The purpose of this study was to pool all available data on changes in serum levels of TNF alpha, IL-6, and IL-1 beta during antidepressant treatment to determine whether these levels change. Studies were included if they used an approved pharmacological treatment for depression, patients had a diagnosis of MDD, and serum levels of TNF alpha, IL-6, and/or IL-1 beta were measured before and after treatment. Twenty-two studies fulfilled these criteria. Meta-analysis of these studies showed that, overall, while pharmacological antidepressant treatment reduced depressive symptoms, it did not reduce serum levels of TNF alpha. On the other hand, antidepressant treatment did reduce levels of IL-1 beta and possibly those of IL-6. Stratified subgroup analysis by class of antidepressant indicated that serotonin reuptake inhibitors may reduce levels of IL-6 and TNF alpha. Other antidepressants, while efficacious for depressive symptoms, did not appear to reduce cytokine levels. These results argue against the notion that resolution of a depressive episode is associated with normalization of levels of circulating inflammatory cytokines; however, the results are consistent with the possibility that inflammatory cytokines contribute to depressive symptoms and that antidepressants block the effects of inflammatory cytokines on the brain. Neuropsychopharmacology (2011) 36, 2452-2459; doi: 10.1038/npp.2011.132; published online 27 July 2011