Jha Manish K, Minhajuddin Abu, Gadad Bharathi S, Greer Tracy, Grannemann Bruce, Soyombo Abigail, Mayes Taryn L, Rush A John, Trivedi Madhukar H
Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Psychoneuroendocrinology. 2017 Apr;78:105-113. doi: 10.1016/j.psyneuen.2017.01.023. Epub 2017 Jan 24.
Currently, no valid measures inform treatment selection for depressed patients. Whether C-reactive protein (CRP) in particular and two other acute phase reactants (inflammatory markers) could differentiate between patients responding to either of two treatments with different mechanisms of action was assessed.
Subjects included Combining Medications to Enhance Depression Outcomes (CO-MED) trial participants randomly assigned to either escitalopram plus placebo (SSRI monotherapy, n=51) or bupropion plus escitalopram combination (bupropion-SSRI combination, n=55) with baseline plasma samples. CRP, serum amyloid P component, and alpha-2-macroglobulin were measured using the Bioplex Pro™ human acute-phase 4-plex panel. We conducted mixed model analyses of depressive symptom (Quick Inventory of Depressive Symptomatology Self-Report) and side-effect burden (Frequency, Intensity, and Burden of Side-Effects Rating Scale) obtained weekly or every other week over the 12-week acute-phase of CO-MED trial to evaluate the relationship between these outcomes and baseline CRP and other acute-phase reactants.
The treatment arms did not differ in depressive symptom or side effect outcomes. Most participants (69.8%, 74/106) had baseline CRP levels greater than 1mg/L (indicative of systemic inflammatory activity). Higher baseline CRP levels were associated lower depression severity (correlation coefficient=-0.63) with bupropion-SSRI combination but not with SSRI monotherapy (correlation coefficient=0.40). The overall remission rate was 41.5%. The estimated remission rate with CRP threshold based assignment (SSRI monotherapy for <1mg/L and Bupropion-SSRI for ≥1mg/L) was 53.1%, with a number needed to treat of 8.6. Side effect burden was unrelated to any baseline inflammatory marker.
Baseline CRP levels relate differentially to antidepressant treatment outcomes in persons with major depressive disorder. Clinicaltrials.gov identifier: NCT00590863.
目前,尚无有效的措施为抑郁症患者的治疗选择提供依据。我们评估了C反应蛋白(CRP)以及其他两种急性期反应物(炎症标志物)能否区分对两种作用机制不同的治疗有反应的患者。
研究对象包括联合用药改善抑郁转归(CO-MED)试验的参与者,他们被随机分配接受艾司西酞普兰加安慰剂(SSRI单药治疗,n = 51)或安非他酮加艾司西酞普兰联合治疗(安非他酮-SSRI联合治疗,n = 55),并采集了基线血浆样本。使用Bioplex Pro™人急性期4联检试剂盒检测CRP、血清淀粉样蛋白P成分和α-2-巨球蛋白。我们对CO-MED试验12周急性期每周或每两周获得的抑郁症状(抑郁症状快速自评量表)和副作用负担(副作用频率、强度和负担评定量表)进行混合模型分析,以评估这些结果与基线CRP及其他急性期反应物之间的关系。
治疗组在抑郁症状或副作用结果方面没有差异。大多数参与者(69.8%,74/106)的基线CRP水平高于1mg/L(表明存在全身炎症活动)。较高的基线CRP水平与安非他酮-SSRI联合治疗组较低的抑郁严重程度相关(相关系数=-0.63),但与SSRI单药治疗组无关(相关系数=0.40)。总体缓解率为41.5%。基于CRP阈值分配的估计缓解率(CRP<1mg/L时采用SSRI单药治疗,CRP≥1mg/L时采用安非他酮-SSRI联合治疗)为53.1%,治疗所需人数为8.6。副作用负担与任何基线炎症标志物均无关。
在重度抑郁症患者中,基线CRP水平与抗抑郁治疗结果的关系存在差异。Clinicaltrials.gov标识符:NCT00590863。