Muthuramalingam Avin, Menon Vikas, Rajkumar Ravi Philip, Negi Vir Singh
Department of Psychiatry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
Department of Clinical Immunology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
Indian J Psychol Med. 2016 Mar-Apr;38(2):114-9. doi: 10.4103/0253-7176.178772.
Evidence linking inflammation and depression is marred by several methodological inconsistencies. Further, varying information is present on the role of gender as a potential confounder in this association.
To assess systemic inflammation in drug naοve depression by measuring selected pro-inflammatory (tumor necrosis factor-alpha [TNF-α], interleukin-6 [IL-6]) and anti-inflammatory cytokines (transforming growth factor-beta [TGF-β]) and comparing them with a matched control group. We also aimed at exploring the differences in these markers between genders.
The study was a cross-sectional one carried out a teaching cum Tertiary Care Hospital.
We recruited 55 drug naοve cases diagnosed with major depression and compared them for inflammatory markers with a matched apparently healthy control group (n = 42) at baseline. The inflammatory markers were also compared between the genders. Baseline depression and stress levels were assessed using standard measures.
Mann-Whitney U-test.
In comparison with healthy controls, drug naοve depressed individuals demonstrated significantly raised baseline levels of TNF-α and IL-6 (P < 0.001 for both) but no difference in levels of TGF-β (P = 0.433). Neither the baseline depression nor the stress scores correlated with any of the inflammatory markers (P = 0.955 and 0.816 for TNF-α respectively). Males and females were comparable on the levels of markers studied (P = 0.986, 0.415, and 0.430 for TNF-α, IL-6 and TGF-β respectively).
There is evidence for higher baseline inflammation in depression prior to starting anti-depressant therapy. Gender does not mediate this observed link between inflammation and depression.
将炎症与抑郁症联系起来的证据存在一些方法学上的不一致之处。此外,关于性别作为这种关联中潜在混杂因素的作用,存在不同的信息。
通过测量选定的促炎细胞因子(肿瘤坏死因子-α [TNF-α]、白细胞介素-6 [IL-6])和抗炎细胞因子(转化生长因子-β [TGF-β]),并将其与匹配的对照组进行比较,评估未服用药物的抑郁症患者的全身炎症反应。我们还旨在探讨这些标志物在性别之间的差异。
该研究是在一家教学兼三级护理医院进行的横断面研究。
我们招募了55例被诊断为重度抑郁症的未服用药物患者,并在基线时将他们的炎症标志物与匹配的明显健康对照组(n = 42)进行比较。还比较了不同性别之间的炎症标志物。使用标准测量方法评估基线抑郁和压力水平。
曼-惠特尼U检验。
与健康对照组相比,未服用药物的抑郁症患者的TNF-α和IL-6基线水平显著升高(两者P均<0.001),但TGF-β水平无差异(P = 0.433)。基线抑郁评分和压力评分均与任何炎症标志物无关(TNF-α的P分别为0.955和0.816)。在所研究的标志物水平上,男性和女性相当(TNF-α、IL-6和TGF-β的P分别为0.986、0.415和0.430)。
有证据表明在开始抗抑郁治疗之前,抑郁症患者的基线炎症水平较高。性别并未介导炎症与抑郁症之间的这种观察到的联系。