Antidepressant treatment resistance is associated with increased inflammatory markers in patients with major depressive disorder.

Antidepressant treatment resistance is associated with increased inflammatory markers in patients with major depressive disorder.
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DOI:
10.1016/j.psyneuen.2018.05.026
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发表时间:
2018-09
影响因子:
3.7
通讯作者:
Miller AH
Miller AH
中科院分区:
医学2区
文献类型:
--
作者:
Haroon E;Daguanno AW;Woolwine BJ;Goldsmith DR;Baer WM;Wommack EC;Felger JC;Miller AH

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三分之一的重度抑郁症(MDD)患者对目前可用的抗抑郁药物没有反应。炎症可能通过影响与抗抑郁疗效相关的神经递质系统而导致治疗无应答。在事后分析中,治疗前炎性标志物浓度升高可预测抗抑郁反应不良。然而,有限的数据存在是否抑郁症患者与多个失败的治疗试验,在他们目前的抑郁症发作表现出炎症增加。通过马萨诸塞州综合医院抗抑郁治疗反应问卷,在未用药、病情稳定的MDD患者(n = 98)和不同数量的适当抗抑郁治疗试验中测量炎症标志物的血浆浓度。协变量包括年龄、性别、种族、教育、体重指数(BMI)和抑郁症的严重程度,如有说明,纳入统计模型。治疗失败的次数与肿瘤坏死因子(TNF)、可溶性TNF受体2(sTNF-R2)和白细胞介素(IL)-6之间存在显著相关性(多变量分析中所有p < 0.05)。多重检验校正后的事后成对比较显示,与0或1次试验的个体相比,在当前发作中有3次或3次以上试验失败的患者的血浆TNF、sTNF-R2和IL-6显著更高(所有p < 0.05)。高敏C反应蛋白也与更多的治疗失败相关,但仅在排除BMI的模型中。测量炎症标志物和靶向炎症或其下游介质可能与当前抑郁发作中多次抗抑郁药治疗试验失败的抑郁症患者相关。
One third of patients with major depressive disorder (MDD) fail to respond to currently available antidepressant medications. Inflammation may contribute to treatment non-response through effects on neurotransmitter systems relevant to antidepressant efficacy. In post-hoc analyses, increased concentrations of inflammatory markers prior to treatment predict poor antidepressant response. However, limited data exists on whether depressed patients with multiple failed treatment trials in their current episode of depression exhibit increased inflammation. Plasma concentrations of inflammatory markers were measured in unmedicated, medically stable patients with MDD (n = 98) and varying numbers of adequate antidepressant treatment trials in the current depressive episode as measured by the Massachusetts General Hospital Antidepressant Treatment Response Questionnaire. Covariates including age, sex, race, education, body mass index (BMI) and severity of depression were included in statistical models where indicated. A significant relationship was found between number of failed treatment trials and tumor necrosis factor (TNF), soluble TNF receptor 2 (sTNF-R2) and interleukin (IL)-6 (all p < 0.05 in multivariate analyses). Post hoc pairwise comparisons with correction for multiple testing revealed that patients with 3 or more failed trials in the current episode had significantly higher plasma TNF, sTNF-R2 and IL-6 compared to individuals with 0 or 1 trial (all p < 0.05). High sensitivity c-reactive protein was also associated with a greater number of treatment failures, but only in models with BMI excluded. Measuring inflammatory markers and targeting inflammation or its downstream mediators may be relevant for depressed patients with multiple failed antidepressant treatment trials in their current depressive episode.
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