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山东大学学报 (医学版) ›› 2018, Vol. 56 ›› Issue (6): 51-57.doi: 10.6040/j.issn.1671-7554.0.2017.261

• 医学心理学 • 上一篇    下一篇

抑郁症患者血清hs-CRP水平变化及其对抗抑郁药疗效的预测作用

王丹1,杨晓华2,郑云哨2,阚伟京1,寻广磊2   

  1. 1.山东大学齐鲁医学院, 山东 济南 250012;2.山东省精神卫生中心精神科, 山东 济南 250014
  • 发布日期:2022-09-27
  • 通讯作者: 寻广磊. E-mail:xungl@163.com

Serum level of hs-CRP in patients with depression and its predictive role for the efficiency of antidepressants

WANG Dan1, YANG Xiaohua2, ZHENG Yunshao2, KAN Weijing1, XUN Guanglei2   

  1. 1. Cheeloo College of Medicine, Shandong University, Jinan 250012, Shandong, China;
    2. Department of Psychiatry, Shandong Mental Health Center, Jinan 250014, Shandong, China
  • Published:2022-09-27

摘要: 目的 探讨抑郁症患者血清超敏C反应蛋白(hs-CRP)水平在治疗前后的变化,以及基线hs-CRP水平对抗抑郁药疗效的预测作用。 方法 61例抑郁症患者(研究组)随机分为舍曲林治疗亚组(30例)和度洛西汀治疗亚组(31例),疗程8周,于基线及8周末测hs-CRP水平,并评定HAMD量表。32例健康受试者(对照组)在入组及8周后测hs-CRP水平。 结果 研究组基线hs-CRP水平高于对照组,抗抑郁治疗后显著下降,但仍高于同期对照组(P<0.05),研究组治疗前、后hs-CRP水平与HAMD评分均呈正相关(P<0.05)。度洛西汀亚组基线hs-CRP≥3 mg/L者的有效率及HAMD-17减分率显著高于<3 mg/L者;在基线hs-CRP≥3 mg/L的患者中,度洛西汀的有效率显著高于舍曲林。二元Logistic回归分析显示,基线hs-CRP水平、亚组组别×基线hs-CRP水平进入疗效的回归方程,析因设计的方差分析结果显示药物和基线hs-CRP水平的交互作用对疗效有一定的影响(P<0.05)。 结论 炎症反应参与了抑郁症的病理机制,血清hs-CRP水平可能在一定程度上反映抑郁严重程度;度洛西汀对基线hs-CRP水平较高的抑郁症患者可能有更好疗效,但尚需更大样本量的研究进行验证。

关键词: 抑郁症, 超敏C反应蛋白, 炎症, 度洛西汀, 舍曲林

Abstract: Objective To explore the changes of high sensitivity C reactive protein(hs-CRP)level before and after antidepressant treatment, as well as the predictive role of hs-CRP level at baseline for the efficiency of antidepressants. Methods A total of 61 patients with depression(study group)were randomized into the sertraline subgroup(n=30)and duloxetine subgroup(n=31). At baseline and the end of 8-week treatment, the serum level of hs-CRP was measured, and Hamilton Depression Scale-17 items(HAMD-17)were evaluated. Additionally, serum hs-CRP level was measured in 32 well-matched healthy controls(control group)and re-measured 8 weeks later. Results At baseline, the serum level of hs-CRP was higher in the study group than in control group, and it decreased significantly after 8-week treatment but was still significantly higher than that in the control group at the endpoint(P<0.05). Serum hs-CRP level in the study group was positively correlated with HAMD-17 score at baseline and endpoint(P<0.05). In the duloxetine subgroup, the effective rate and reduction rate of HAMD-17 in patients with higher level of baseline hs-CRP(≥3 mg/L)were significantly higher than those in patients with lower baseline hs-CRP(<3 mg/L)(P<0.05). Moreover, in patients with higher baseline hs-CRP level, the effective rate of duloxetine was significantly higher than that of sertraline(P<0.05). Binary Logistic regression analysis indicated that baseline hs-CRP level and subgroup × baseline hs-CRP level 山 东 大 学 学 报 (医 学 版)56卷6期 -王丹,等.抑郁症患者血清hs-CRP水平变化及其对抗抑郁药疗效的预测作用 \=-entered the regression equation of efficacy. Factorial design ANOVA illustrated that interaction between antidepressant and baseline hs-CRP level had certain effects on the efficacy of treatment(P<0.05). Conclusion Elevated inflammatory response is involved in the pathophysiology of depression. Serum hs-CRP level may partly reflect the severity of depression. Depressive patients with high baseline hs-CRP level are more likely to respond to duloxetine. Validation in a larger sample is warranted.

Key words: Depression, High sensitivity C reactive protein, Inflammation, Duloxetine, Sertraline

中图分类号: 

  • R749.4
[1] Dowlati Y, Herrmann N, Swardfager W, et al. A meta-analysis of cytokines in major depression[J]. Biol Psychiatry, 2010, 67(5): 446-457.
[2] Liu Y, Ho RC, Mak A. Interleukin(IL)-6, tumour necrosis factor alpha(TNF-α)and soluble interleukin-2 receptors(sIL-2R)are elevated in patients with major depressive disorder: a meta-analysis and meta-regression[J]. J Affect Disord, 2012, 139(3): 230-239.
[3] Papakostas GI, Shelton RC, Kinrys G, et al. Assessment of a multi-assay, serum-based biological diagnostic test for major depressive disorder: a pilot and replication study[J]. Mol Psychiatry, 2013, 18(3): 332-339.
[4] 张明园, 何燕玲. 精神科评定量表手册[M]. 2版. 长沙: 湖南科学技术出版社, 2015: 142-148.
[5] Maes M. Evidence for an immune response in major depression: a review and hypothesis[J]. Prog Neuropsychopharmacol Biol Psychiatry, 1995, 19(1): 11-38.
[6] Vreeburg SA, Hoogendijk WJ, van Pelt J, et al. Major depressive disorder and hypothalamic-pituitary-adrenal axis activity: results from a large cohort study[J]. Arch Gen Psychiatry, 2009, 66(6): 617-626.
[7] Licht CM, de Geus EJ, Zitman FG,et al. Association between major depressive disorder and heart rate variability in the Netherlands Study of Depression and Anxiety(NESDA)[J]. Arch Gen Psychiatry, 2008, 65(12): 1358-1367.
[8] Marsland AL, Gianaros PJ, Abramowitch SM, et al. Interleukin-6 covaries inversely with hippocampal grey matter volume in middle-aged adults[J]. Biol Psychiatry, 2008, 64(6): 484-490.
[9] Blank T, Detje CN, Spieß A, et al. Brain endothelial- and epithelial-specific interferon receptor chain 1 drives virus-induced sickness behavior and cognitive impairment[J]. Immunity, 2016, 44(4): 901-912.
[10] Khairova RA, Machado-Vieira R, Du J, et al. A potential role for pro-inflammatory cytokines in regulating synaptic plasticity in major depressive disorder[J]. Int J Neuropsychopharmacology, 2009, 12(4): 561.
[11] Dantzer R, O’Connor JC, Freund GG, et al. From inflammation to sickness and depression: when the immune system subjugates the brain[J]. Nat Rev Neurosci, 2008, 9(1): 46-56.
[12] Shelton RC, Claiborne J, Sidoryk-Wegrzynowicz M, et al. Altered expression of genes involved in inflammation and apoptosis in frontal cortex in major depression[J]. Mol Psychiatry, 2011, 16(7): 751-762.
[13] Valkanova V, Ebmeier KP, Allan CL. CRP, IL-6 and depression: a systematic review and meta-analysis of longitudinal studies[J]. J Affect Disord, 2013, 150(3): 736-744.
[14] Wium-Andersen MK, Ørsted DD, Nielsen SF, et al. Elevated C-reactive protein levels, psychological distress, and depression in 73131 individuals[J]. JAMA Psychiatry, 2013, 70(2): 176-184.
[15] Lopresti AL, Maker GL, Hood SD, et al. A review of peripheral biomarkers in major depression: the potential of inflammatory and oxidative stress biomarkers[J]. Prog Neuropsychopharmacol Biol Psychiatry, 2014, 48(1433): 102-111.
[16] Vogelzangs N, Duivis HE, Beekman AT, et al. Association of depressive disorders, depression characteristics and antidepressant medication with inflammation[J]. Transl Psychiatry, 2012, 2(2): e79. doi: 10.1038/tp.2012.8.
[17] Copeland WE, Shanahan L, Worthman C, et al. Cumulative depression episodes predict later C-reactive protein levels: a prospective analysis[J]. Biol Psychiatry, 2012, 71(1): 15-21.
[18] Zalli A, Jovanova O, Hoogendijk WJ, et al. Low-grade inflammation predicts persistence of depressive symptoms[J]. Psychopharmacology(Berl), 2016, 233(9): 1669-1678.
[19] Almeida OP, Norman PE, Allcock R, et al. Polymorphisms of the CRP gene inhibit inflammatory response and increase susceptibility to depression: the Health in Men Study[J]. Int J Epidemiol, 2009, 38(4): 1049-1059.
[20] Dieperink E, Willenbring M, Ho SB. Neuropsychiatric symptoms associated with hepatitis C and interferon alpha: a review[J]. Am J Psychiatry, 2000, 157(6): 867-876.
[21] Raison CL, Rutherford RE, Woolwine BJ, et al. A randomized controlled trail of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers[J]. JAMA Psychiatry, 2013, 70(1): 31-41.
[22] Miller AH, Maletic V, Raison CL. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression[J]. Biol Psychiatry, 2009, 65(9): 732-741.
[23] Chavda N, Kantharia ND, Jaykaran. Effects of fluoxetine and escitalopram on C-reactive protein in patients of depression[J]. J Pharmacol Pharmacother, 2011, 2(1): 11-16.
[24] Felger JC, Li Z, Haroon E, et al. Inflammation is associated with decreased functional connectivity within corticostriatal reward circuitry in depression[J]. Mol Psychiatry, 2016, 21(10): 1358-1365.
[25] Mowla A, Dastgheib SA, Razeghian Jahromi L. Comparing the effects of sertraline with duloxetine for depression severity and symptoms: a double-blind, randomized controlled trial[J]. Clin Drug Investig, 2016, 36(7): 539-543.
[26] Uher R, Tansey KE, Dew T, et al. An inflammatory biomarker as a differential predictor of outcome of depression treatment with escitalopram and nortriptyline[J]. Am J Psychiatry, 2014, 171(12): 1278- 1286.
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