Unidad Gestión Clínica de Salud Mental, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga/Universidad de Málaga, Málaga, Spain.
Addiction Research Group, Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
PLoS One. 2019 Mar 14;14(3):e0213791. doi: 10.1371/journal.pone.0213791. eCollection 2019.
Major depressive disorder (MDD) is the most prevalent comorbid mental disorder among people with substance use disorders. The MDD can be both primary and substance-induced and its accurate diagnosis represents a challenge for clinical practice and treatment response. Recent studies reported alterations in the circulating expression of inflammatory mediators in patients with psychiatric disorders, including those related to substance use. The aim of the study was to explore TNF-α, IL-1β, CXCL12, CCL2, CCL11 (eotaxin-1) and CX3CL1 (fractalkine) as potential biomarkers to identify comorbid MDD and to distinguish primary MDD from substance-induced MDD in patients with substance disorders. Patients diagnosed with cocaine (CUD, n = 64) or alcohol (AUD, n = 65) use disorders with/without MDD were recruited from outpatient treatment programs [CUD/non-MDD (n = 31); CUD/primary MDD (n = 18); CUD/cocaine-induced MDD (N = 15); AUD/non-MDD (n = 27); AUD/primary MDD (n = 16) and AUD/alcohol-induced MDD (n = 22)]. Sixty-two healthy subjects were also recruited as control group. Substance and mental disorders were assessed according to "Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision" (DSM-IV-TR) and a blood sample was collected for determinations in the plasma. The cocaine group showed lower TNF-α (p<0.05) and CCL11 (p<0.05), and higher IL-1β (p<0.01) concentrations than the control group. In contrast, the alcohol group showed higher IL-1β (p<0.01) and lower CXCL12 (p<0.01) concentrations than the control group. Regarding MDD, we only observed alterations in the cocaine group. Thus, CUD/MDD patients showed lower IL-1β (p<0.05), CXCL12 (p<0.05) and CCL11 (p<0.05), and higher CXC3CL1 (p<0.05) concentrations than CUD/non-MDD patients. Moreover, while CUD/primary MDD patients showed higher CCL11 (p<0.01) concentrations than both CUD/non-MDD and CUD/cocaine-induced MDD patients, CUD/cocaine-induced MDD patients showed lower CXCL12 (p<0.05) concentrations than CUD/non-MDD patients. Finally, a logistic regression model in the cocaine group identified CXCL12, CCL11 and sex to distinguish primary MDD from cocaine-induced MDD providing a high discriminatory power. The present data suggest an association between changes in inflammatory mediators and the diagnosis of primary and substance-induced MDD, namely in CUD patients.
重度抑郁症(MDD)是物质使用障碍患者中最常见的合并精神障碍。MDD 既可以是原发性的,也可以是物质诱发的,其准确诊断对临床实践和治疗反应构成挑战。最近的研究报告称,精神障碍患者的循环炎症介质表达发生改变,包括与物质使用相关的改变。本研究旨在探索 TNF-α、IL-1β、CXCL12、CCL2、CCL11(嗜酸性粒细胞趋化因子 1)和 CX3CL1( fractalkine)作为潜在的生物标志物,以识别物质使用障碍患者的合并 MDD,并区分原发性 MDD 和物质诱发的 MDD。从门诊治疗计划中招募了被诊断为可卡因(CUD,n = 64)或酒精(AUD,n = 65)使用障碍且/或伴 MDD 的患者 [CUD/非 MDD(n = 31);CUD/原发性 MDD(n = 18);CUD/可卡因诱发的 MDD(n = 15);AUD/非 MDD(n = 27);AUD/原发性 MDD(n = 16)和 AUD/酒精诱发的 MDD(n = 22)]。还招募了 62 名健康受试者作为对照组。根据“精神障碍诊断与统计手册,第 4 版,文本修订版”(DSM-IV-TR)评估物质和精神障碍,并采集血液样本进行血浆测定。与对照组相比,可卡因组 TNF-α(p<0.05)和 CCL11(p<0.05)浓度较低,IL-1β(p<0.01)浓度较高。相反,与对照组相比,酒精组 IL-1β(p<0.01)和 CXCL12(p<0.01)浓度较高。关于 MDD,我们仅观察到可卡因组的变化。因此,CUD/MDD 患者的 IL-1β(p<0.05)、CXCL12(p<0.05)和 CCL11(p<0.05)浓度较低,CXC3CL1(p<0.05)浓度较高,而 CUD/非 MDD 患者。此外,CUD/原发性 MDD 患者的 CCL11(p<0.01)浓度高于 CUD/非 MDD 和 CUD/可卡因诱发的 MDD 患者,而 CUD/可卡因诱发的 MDD 患者的 CXCL12(p<0.05)浓度低于 CUD/非 MDD 患者。最后,在可卡因组中,一个逻辑回归模型确定了 CXCL12、CCL11 和性别来区分原发性 MDD 和可卡因诱发的 MDD,提供了较高的鉴别能力。本研究数据表明,炎症介质的变化与原发性和物质诱发的 MDD 的诊断有关,尤其是在 CUD 患者中。