J Psychiatr Res：初诊抑郁症与动脉粥样硬化相关

　　近期发表于《精神病学研究杂志》（J Psychiatr Res）上的一项研究表明，相比健康对照组，初诊抑郁症患者体内的血小板CD62P（P-选择素）、动脉粥样硬化标志物（CD40，CD40L）、血清血小板因子4（PF4）和β-血小板球蛋白（β-TG）水平会有所升高，说明抑郁症与血栓和炎症状态相关，而这可能会加速动脉粥样硬化。

　　炎症在动脉粥样硬化疾病中扮演重要角色。目前只有有限证据表明抑郁患者心血管并发症的发病机制。本研究的目的是评估初诊抑郁患者的血小板活化程度以及动脉粥样硬化性疾病的血小板源性标志物。

　　研究采用全血血小板聚集、流式细胞仪和ELISA法检测了46例受试者的P-选择素表达以及动脉粥样硬化标志物（CD40，CD40L）、PF4和β-TG水平。初诊且未接受药物治疗的患者（n=21）被用于和健康对照组相比较。

　　结果发现抑郁症患者体内的血小板活化标志物CD62p水平显著较高（2.62%抑郁症 对 1.27%对照组；P=0.006）。此外，研究发现，抑郁症患者体内的基底CD40（6.7% 对 4.8%，P=0.002）和基底CD40L（31% 对 22%，P=0.025）高于对照组。此外，可溶性CD40配体（52.7 对 44.4ng/ml，P=0.023）和β-TG在抑郁症患者中也是显著不同的（206.9 对 182.8ng/ml，P=0.001）。但研究结果表明，研究组之间的基底CD41（97% 对 96.3%，P=0.57）、CD42b（96.7% 对 94.7%，P=0.28）、结缔组织生长因子（89.61 对 81.75 IU /ml，P=0.10）和血小板聚集结果没有显著差异。

与抑郁症相关的拓展阅读：

• Eur J Prev Cardiol：生活方式干预延缓抑郁症状进展
• Am J Psychiatry：老年抑郁症转归的调节因素
• 生活方式干预延缓抑郁症状进展
• EPA 2013：正念治疗可减少TBI的抑郁症状
• Clin J Pain：以疼痛患者的精神挫败感为治疗标靶可预防抑郁症 更多信息请点击：有关抑郁症更多资讯

Newly diagnosed depression is associated with increased beta-thromboglobulin levels and increased expression of platelet activation markers and platelet derived CD40-CD40L.
BACKGROUND
Inflammation plays a key role in atherosclerotic disease. Up until now only limited evidence exists on the mechanism of cardiovascular complications in patients with depression. In addition depression was also linked to an increase in cardiovascular mortality. The present study was designed to evaluate the extent of platelet activation and platelet-derived markers of atherosclerotic disease in patients with newly diagnosed depression.
METHODS
This study used whole blood aggregometry, flow cytometry and ELISA to investigate platelet CD62P (P-selectin) expression and atherosclerotic markers (CD40, CD40L) as well as serum platelet factor 4 (PF-4) and beta-thromboglobulin (β-TG) levels in 46 participants. Patients with newly diagnosed, but not yet medically treated depression (n = 21) were compared to healthy control patients.
RESULTS
The platelet activation marker CD62P was significantly higher in patients with depression (2.62% depression versus 1.27% controls; p = 0.006). Further we found basal CD40 (6.7% vs. 4.8%; p = 0.002) and basal CD40L (31.0% vs. 22.0%; p = 0.025) to be elevated in patients with depression as compared to control persons. In addition sCD40L (52.7 vs. 44.4 ng/ml; p = 0.023) and β-TG differed significantly in depressed patients (206.9 vs. 182.8 ng/ml; p = 0.001). However, basal CD41 (97.0% vs. 96.3%; p = 0.57), CD42b (96.7% vs. 94.7%; p = 0.28) and PF-4 (89.61 vs. 81.75 IU/ml; p = 0.10) and the aggregometry results did not differ significantly between the study groups.
CONCLUSIONS
Our findings with elevated CD40 and CD40L as well as CD62P and β-TG in newly diagnosed patients emphasize that depression is linked to a prothrombotic and proinflammatory state and this possibly contributes to accelerated atherosclerosis.