Anti-inflammatory treatment for major depressive disorder: implications for patients with an elevated immune profile and non-responders to standard antidepressant therapy.
Anti-inflammatory treatment for major depressive disorder: implications for patients with an elevated immune profile and non-responders to standard antidepressant therapy.
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DOI：
10.1177/0269881117711708
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发表时间：
2017-09
期刊：
影响因子：
--
通讯作者：
de Vries EF
中科院分区：
文献类型：
--
作者：
Kopschina Feltes P;Doorduin J;Klein HC;Juárez-Orozco LE;Dierckx RA;Moriguchi-Jeckel CM;de Vries EF
重度抑郁症（MDD）是一种流行的致残性精神疾病，对抗抑郁药无反应的比率为30- 50%。从历史上看，单胺耗竭假说主导了抑郁症的病理生理学观点。然而，对抗抑郁药缺乏反应和治疗抵抗表明，其他机制可能发挥作用。有证据表明，抑郁症患者的一个亚组可能存在潜在的免疫失调，这可以解释抗抑郁药缺乏治疗益处。炎症和感染等刺激可以触发小胶质细胞的激活以释放促炎细胞因子，作用于两个主要途径：（1）下丘脑-垂体肾上腺轴的激活，产生肾上腺素能和去甲肾上腺素能回路的不平衡;（2）吲哚胺-2，3-双加氧酶的活性增加，导致血清素水平的消耗和喹啉酸的产生。如果这一假设被证明是正确的，MDD患者亚组的促炎细胞因子水平升高，主要是IL-6，TNF-α和IL-1β，可能会受益于抗炎干预。在这里，我们讨论了临床前和临床研究，提供了支持与非甾体类抗炎药治疗抑郁症患者的炎症合并症或免疫功能升高，以及标准抗抑郁药的抗炎特性的证据。
Major depressive disorder (MDD) is a prevalent and disabling psychiatric disease with rates of non-responsiveness to antidepressants ranging from 30–50%. Historically, the monoamine depletion hypothesis has dominated the view on the pathophysiology of depression. However, the lack of responsiveness to antidepressants and treatment resistance suggests that additional mechanisms might play a role. Evidence has shown that a subgroup of depressive patients may have an underlying immune deregulation that could explain the lack of therapeutic benefit from antidepressants. Stimuli like inflammation and infection can trigger the activation of microglia to release pro-inflammatory cytokines, acting on two main pathways: (1) activation of the hypothalamic–pituitary adrenal axis, generating an imbalance in the serotonergic and noradrenergic circuits; (2) increased activity of the enzyme indoleamine-2,3-dioxygenase, resulting in depletion of serotonin levels and the production of quinolinic acid. If this hypothesis is proven true, the subgroup of MDD patients with increased levels of pro-inflammatory cytokines, mainly IL-6, TNF-α and IL-1β, might benefit from an anti-inflammatory intervention. Here, we discuss the pre-clinical and clinical studies that have provided support for treatment with non-steroidal anti-inflammatory drugs in depressed patients with inflammatory comorbidities or an elevated immune profile, as well as evidences for anti-inflammatory properties of standard antidepressants.
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