Treatment-resistant depression and peripheral C-reactive protein.

Treatment-resistant depression and peripheral C-reactive protein.
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DOI:
10.1192/bjp.2018.66
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发表时间:
2019-01
期刊:
The British journal of psychiatry : the journal of mental science
影响因子:
--
通讯作者:
Bullmore ET
Bullmore ET
中科院分区:
其他
文献类型:
--
作者:
Chamberlain SR;Cavanagh J;de Boer P;Mondelli V;Jones DNC;Drevets WC;Cowen PJ;Harrison NA;Pointon L;Pariante CM;Bullmore ET

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C-反应蛋白(CRP)是抑郁症(MDD)的候选生物标志物,但目前尚不清楚外周CRP水平与该疾病的异质性临床表型的关系。探讨CRP与MDD的关系及其与表型的关系。我们招募了102名目前患有抑郁症的治疗抵抗性MDD患者,48名目前未患有抑郁症的治疗反应性MDD患者,48名未接受药物治疗的抑郁症患者和54名健康志愿者。检测外周静脉血超敏C反应蛋白(hsCRP)、体重指数(BMI)及抑郁、焦虑、儿童期创伤问卷。估计CRP的组间差异,偏最小二乘(PLS)分析探讨CRP与特定临床表型之间的关系。与健康志愿者相比,BMI校正的CRP在治疗抵抗组中显著升高(P = 0.007; Cohen's d = 0.47);但在治疗应答组(d = 0.29)和未治疗组(d = 0.18)中无显著性差异。PLS产生了一个最佳的两因素的解决方案,占34.7%的变化,在临床措施和36.0%的变化,CRP。与CRP相关性最强且在第一PLS组分上权重最大的临床表型是植物性抑郁症状、BMI、状态焦虑和儿童时感觉不被爱或希望有不同的童年。CRP在MDD患者中升高,在治疗抵抗患者中更是如此。与CRP升高相关的其他表型包括童年逆境和特定的抑郁和焦虑症状。我们认为,MDD患者分层的促炎生物标志物,如CRP,有一个独特的临床资料,可能是响应二线治疗抗炎药物。S.R.C.剑桥认知和夏尔咨询;他在这个项目中的投入是由威康信托临床奖学金(110049/Z/15/Z)资助的。E.T. B在剑桥大学和葛兰素史克公司各工作了一半时间;他持有葛兰素史克公司的股票。在过去的三年里,P.J.C.曾在Lundbeck的顾问委员会任职不适用葛兰素史克的顾问警察局D.N.C.J.和W.C.D.是杨森研发有限责任公司的员工,持有约翰逊和约翰逊的股份,并持有约翰逊和约翰逊的股票。其他作者没有报告财务披露或潜在的利益冲突。
C-reactive protein (CRP) is a candidate biomarker for major depressive disorder (MDD), but it is unclear how peripheral CRP levels relate to the heterogeneous clinical phenotypes of the disorder. To explore CRP in MDD and its phenotypic associations. We recruited 102 treatment-resistant patients with MDD currently experiencing depression, 48 treatment-responsive patients with MDD not currently experiencing depression, 48 patients with depression who were not receiving medication and 54 healthy volunteers. High-sensitivity CRP in peripheral venous blood, body mass index (BMI) and questionnaire assessments of depression, anxiety and childhood trauma were measured. Group differences in CRP were estimated, and partial least squares (PLS) analysis explored the relationships between CRP and specific clinical phenotypes. Compared with healthy volunteers, BMI-corrected CRP was significantly elevated in the treatment-resistant group (P = 0.007; Cohen's d = 0.47); but not significantly so in the treatment-responsive (d = 0.29) and untreated (d = 0.18) groups. PLS yielded an optimal two-factor solution that accounted for 34.7% of variation in clinical measures and for 36.0% of variation in CRP. Clinical phenotypes most strongly associated with CRP and heavily weighted on the first PLS component were vegetative depressive symptoms, BMI, state anxiety and feeling unloved as a child or wishing for a different childhood. CRP was elevated in patients with MDD, and more so in treatment-resistant patients. Other phenotypes associated with elevated CRP included childhood adversity and specific depressive and anxious symptoms. We suggest that patients with MDD stratified for proinflammatory biomarkers, like CRP, have a distinctive clinical profile that might be responsive to second-line treatment with anti-inflammatory drugs. S.R.C. consults for Cambridge Cognition and Shire; and his input in this project was funded by a Wellcome Trust Clinical Fellowship (110049/Z/15/Z). E.T.B. is employed half time by the University of Cambridge and half time by GlaxoSmithKline; he holds stock in GlaxoSmithKline. In the past 3 years, P.J.C. has served on an advisory board for Lundbeck. N.A.H. consults for GlaxoSmithKline. P.d.B., D.N.C.J. and W.C.D. are employees of Janssen Research & Development, LLC., of Johnson & Johnson, and hold stock in Johnson & Johnson. The other authors report no financial disclosures or potential conflicts of interest.
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