Robicsek Odile, Makhoul Badira, Klein Ehud, Brenner Benjamin, Sarig Galit
Department of Psychiatry, Rambam Health Care Campus affiliated to Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Isr Med Assoc J. 2011 Sep;13(9):548-52.
Whereas procoagulation abnormalities in acute stress are well established, little is known about the mechanism of hypercoagulation in chronic stress, such as post-traumatic stress disorder (PTSD). This is crucial, given the fact that chronic coagulation disturbances have been associated with increased morbidity and premature mortality due to thromboembolism and cardiovascular disorders, complications recently described in PTSD patients.
To explore the mechanisms of hypercoagulation in chronic PTSD.
Thirty patients diagnosed with chronic PTSD were enrolled and compared with a control group matched for age, gender and ethnicity. Hypercoagulation state was evaluated by levels of fibrinogen, D-dimer, prothrombin fragment F 1+2, von Willebrand factor (vWF) antigen, factor VIII activity, activated protein C resistance, ProC Global assay, and tissue factor antigen. Psychiatric evaluation was performed using the Mini-International Neuropsychiatric Interview and Clinician Administered PTSD Scale (CAPS).
vWF antigen levels were significantly higher in patients with chronic PTSD compared with the controls (121.3 +/- 42 vs. 99.7 +/- 23, respectively, P = 0.034). Higher levels of vWF antigen and factor VIII activity were found in patients with severe chronic PTSD (CAPS > 80), compared to controls and patients with chronic PTSD and less severe symptoms (CAPS < or = 80). However, no differences were observed in any other studied coagulation parameters between patients and controls.
Increased levels of vWF antigen and factor VIII activity were documented in severe chronic PTSD. These findings suggest that the higher risk of arterial and venous thromboembolic events in PTSD patients could be related to endothelial damage or endothelial activation.
急性应激时的促凝血异常已得到充分证实，但对于慢性应激（如创伤后应激障碍，PTSD）中的高凝机制却知之甚少。鉴于慢性凝血紊乱与血栓栓塞和心血管疾病导致的发病率增加及过早死亡相关，而这些并发症最近在PTSD患者中已有描述，这一点至关重要。
探讨慢性PTSD中高凝的机制。
招募30例被诊断为慢性PTSD的患者，并与年龄、性别和种族匹配的对照组进行比较。通过纤维蛋白原、D - 二聚体、凝血酶原片段F1 + 2、血管性血友病因子（vWF）抗原、凝血因子VIII活性、活化蛋白C抵抗、ProC全球检测法和组织因子抗原水平评估高凝状态。使用迷你国际神经精神访谈和临床医生管理的PTSD量表（CAPS）进行精神评估。
慢性PTSD患者的vWF抗原水平显著高于对照组（分别为121.3±42和99.7±23，P = 0.034）。与对照组以及慢性PTSD且症状较轻（CAPS≤80）的患者相比，重度慢性PTSD（CAPS>80）患者的vWF抗原和凝血因子VIII活性水平更高。然而，患者与对照组之间在任何其他研究的凝血参数上均未观察到差异。
重度慢性PTSD患者中记录到vWF抗原和凝血因子VIII活性水平升高。这些发现表明，PTSD患者发生动脉和静脉血栓栓塞事件的较高风险可能与内皮损伤或内皮激活有关。
