Department of Medical Psychology, CoRPS-Center of Research on Psychology in Somatic Diseases, Tilburg University, Tilburg, The Netherlands.
J Psychosom Res. 2011 Jul;71(1):13-7. doi: 10.1016/j.jpsychores.2010.11.006. Epub 2011 Jan 15.
Treatment-resistant depression has recently emerged as a marker of increased risk for morbidity and mortality in patients with coronary heart disease (CHD). Studies in depressed patients without CHD suggest that elevated markers of inflammation predict poor response to treatment. This may help to explain the increased risk of cardiac events associated with depression. We therefore studied the relationship between pretreatment markers of inflammation and treatment response in patients with CHD and major depression.
This was a planned, secondary analysis of a clinical trial in which 122 patients with CHD and comorbid major depression were randomly assigned to 50 mg of sertraline plus 2 g/day omega-3 fatty acids or to 50 mg of sertraline plus 2 g/day corn oil placebo capsules for ten weeks. Depressive symptoms were assessed with the Beck Depression Inventory-II (BDI-II). Blood samples were collected at baseline to determine levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α). The primary outcome was the post-treatment BDI-II depression score.
Baseline levels of hs-CRP, IL-6, and TNF-α were not associated with the 10-week post-treatment depression score (P=.89, P=.88, and P=.31, respectively). Treatment responders (>50% reduction from baseline BDI-II score) did not differ from non-responders in either baseline hs-CRP, IL-6, or TNF-α (P=.83, P=.93, and P=.24, respectively). Similarly, depression remitters (BDI-II ≤8 at post-treatment) did not differ from non-remitters on the three baseline inflammation markers.
These findings do not support the hypothesis that elevated baseline inflammatory markers predict poor response to sertraline in patients with CHD and major depression. The explanation for the increased risk of cardiac events associated with poor response to depression treatment remains unclear.
近期有研究显示，治疗抵抗性抑郁症是冠心病（CHD）患者发病率和死亡率升高的一个标志。在无 CHD 的抑郁患者中进行的研究表明，炎症标志物升高预示着对治疗的反应不佳。这可能有助于解释与抑郁相关的心脏事件风险增加的原因。因此，我们研究了 CHD 合并重度抑郁症患者治疗前炎症标志物与治疗反应之间的关系。
这是一项临床试验的计划二次分析，122 例 CHD 合并重度抑郁症患者被随机分为两组，分别接受舍曲林 50mg 联合 ω-3 脂肪酸 2g/天或舍曲林 50mg 联合玉米油安慰剂胶囊治疗，疗程 10 周。采用贝克抑郁自评量表（BDI-II）评估抑郁症状。基线时采集血样以测定高敏 C 反应蛋白（hs-CRP）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平。主要结局为治疗后 10 周的 BDI-II 抑郁评分。
基线 hs-CRP、IL-6 和 TNF-α 水平与 10 周治疗后抑郁评分无关（P 值分别为 0.89、0.88 和 0.31）。治疗反应者（BDI-II 评分较基线降低≥50%）与无反应者在基线 hs-CRP、IL-6 或 TNF-α水平上无差异（P 值分别为 0.83、0.93 和 0.24）。同样，BDI-II 评分≤8 的抑郁缓解者与未缓解者在三个基线炎症标志物上也无差异。
这些发现不支持炎症标志物基线升高预示 CHD 合并重度抑郁症患者对舍曲林治疗反应不佳的假设。与抑郁治疗反应不佳相关的心脏事件风险增加的原因仍不清楚。
