Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Int J Neuropsychopharmacol. 2017 Mar 1;20(3):213-218. doi: 10.1093/ijnp/pyw096.
Brain-derived neurotrophic factors are known to be related to the psychopathology of major depressive disorder. However, studies focusing on drug-naïve first-episode patients are still rare.
Over a 6-year period, we examined the serum brain-derived neurotrophic factors levels in patients with first-episode drug-naïve major depressive disorder and compared them with sex-matched healthy controls. We also investigated the relationships between serum brain-derived neurotrophic factors levels, suicidal behavior, and Hamilton Depression Rating Scale scores before and after a 4-week antidepressant treatment.
The baseline serum brain-derived neurotrophic factors levels of 71 patients were significantly lower than those of the controls (P=.017), and the Hamilton Depression Rating Scale scores in 71 patients did not correlate with brain-derived neurotrophic factor levels. Brain-derived neurotrophic factor levels were significantly lower in 13 suicidal major depressive disorder patients than in 58 nonsuicidal major depressive disorder patients (P=.038). Among 41 followed-up patients, there was no alteration in serum brain-derived neurotrophic factors levels after treatment with antidepressants (P=.126). In receiver operating characteristic curve analysis of using pretreatment brain-derived neurotrophic factors to estimate the response to treatment, the area under the curve was 0.684. The most suitable cut-off point was 6.1 ng/mL (sensitivity=78.6%, specificity = 53.8%).
Our data support the serum brain-derived neurotrophic factor levels in patients with drug-naïve first-episode major depressive disorder were lower than those in the healthy controls, and patients with pretreatment brain-derived neurotrophic factors >6.1 ng/mL were more likely to be responders. Although the relationship of our results to the mechanism of drug action and pathophysiology of depression remains unclear, the measure may have potential use as a predictor of response to treatment. In the future, it needs a large sample to prove these results.
已知脑源性神经营养因子与重性抑郁障碍的精神病理学有关。然而,针对未经药物治疗的首发患者的研究仍然很少。
在 6 年的时间里,我们检测了未经药物治疗的首发重性抑郁障碍患者的血清脑源性神经营养因子水平,并将其与性别匹配的健康对照组进行了比较。我们还研究了血清脑源性神经营养因子水平与自杀行为以及抗抑郁治疗 4 周前后汉密尔顿抑郁量表评分之间的关系。
71 例患者的基线血清脑源性神经营养因子水平明显低于对照组(P=.017),71 例患者的汉密尔顿抑郁量表评分与脑源性神经营养因子水平不相关。13 例有自杀行为的重性抑郁障碍患者的脑源性神经营养因子水平明显低于 58 例无自杀行为的重性抑郁障碍患者(P=.038)。在 41 例随访患者中,抗抑郁治疗后血清脑源性神经营养因子水平没有改变(P=.126)。在使用治疗前脑源性神经营养因子来估计治疗反应的受试者工作特征曲线分析中,曲线下面积为 0.684。最适合的截断点为 6.1ng/ml(灵敏度=78.6%,特异性=53.8%)。
我们的数据支持未经药物治疗的首发重性抑郁障碍患者的血清脑源性神经营养因子水平低于健康对照组,且治疗前脑源性神经营养因子>6.1ng/ml 的患者更有可能是应答者。尽管我们的结果与药物作用机制和抑郁的病理生理学之间的关系尚不清楚,但该指标可能具有作为治疗反应预测因子的潜在用途。未来,需要更大的样本量来证明这些结果。