CRF serum levels differentiate PTSD from healthy controls and TBI in military veterans.
CRF serum levels differentiate PTSD from healthy controls and TBI in military veterans.
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DOI：
10.1176/appi.prcp.20210017
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发表时间：
2021
影响因子：
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通讯作者：
Fossati S
中科院分区：
文献类型：
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作者：
Ramos-Cejudo J;Genfi A;Abu-Amara D;Debure L;Qian M;Laska E;Siegel C;Milton N;Newman J;Blessing E;Li M;Etkin A;Marmar CR;Fossati S
创伤后应激障碍(PTSD)是一种严重的、经常使人虚弱的精神疾病，可发生在经历过创伤应激源的人身上，如战争、暴力、性侵犯和其他危及生命的事件。退伍军人创伤后应激障碍和创伤性脑损伤(TBI)的治疗面临着诊断复杂性的挑战，部分原因是PTSD和创伤性脑损伤的症状重叠，以及主观自我报告评估可能受到患者分享其创伤经历和由此产生的症状的意愿的影响。促肾上腺皮质激素释放因子(CRF)是应激和焦虑状态下下丘脑-垂体-肾上腺(HPA)轴反应的主要介质之一。我们用酶免疫分析法(EIA)分析了230名受试者的血清CRF水平，其中包括健康对照组()、创伤后应激障碍(PTSD)患者(53例)、创伤后应激障碍患者(70例)和创伤后应激障碍患者(43例)。创伤后应激障碍组和创伤后应激障碍+颅脑损伤组的CRF水平均显著低于健康对照组(创伤后应激障碍与对照组：P=0.0014，创伤后应激障碍+脑外伤组与对照组：P=0.0011)和慢性脑创伤组(创伤后应激障碍与脑外伤组：P=0.0001，创伤后应激障碍+脑外伤组与脑外伤组：P>0.0001)，提示一种独立于脑外伤并与CRF减少相关的创伤后应激障碍相关机制。在整个研究组中，CRF水平与临床用药PTSD量表(CAPS-5)上的PTSD严重程度呈负相关。HPA轴的过度激活在急性应激中被经典地识别出来。然而，公认的慢性应激对HPA轴的反馈抑制增强支持了我们的发现，即PTSD患者的CRF较低。本研究提示创伤后应激障碍患者血清CRF水平降低值得进一步研究。未来的验证研究将确定CRF是否是创伤后应激障碍和/或区分创伤后应激障碍和慢性脑损伤症状的可能血液生物标志物。HPA轴在急性应激条件下被激活，但在慢性应激条件下，如创伤后应激障碍，可能普遍存在增强的反馈抑制。我们观察到患有创伤后应激障碍和创伤后应激障碍+颅脑损伤的退伍军人血清CRF水平降低，但不是仅在患有慢性颅脑损伤的退伍军人中。血清CRF的降低可能预示着PTSD特有的中枢神经系统机制，应进一步评估其作为一种可能的外周生物标志物。
Posttraumatic stress disorder (PTSD) is a serious and frequently debilitating psychiatric condition that can occur in people who have experienced traumatic stressors, such as war, violence, sexual assault and other life‐threatening events. Treatment of PTSD and traumatic brain injury (TBI) in veterans is challenged by diagnostic complexity, partially due to PTSD and TBI symptoms overlap and to the fact that subjective self‐report assessments may be influenced by a patient's willingness to share their traumatic experiences and resulting symptoms. Corticotropin‐releasing factor (CRF) is one of the main mediators of hypothalamic pituitary adrenal (HPA)‐axis responses in stress and anxiety. We analyzed serum CRF levels in 230 participants including heathy controls (64), and individuals with PTSD (53), TBI (70) or PTSD + TBI (43) by enzyme immunoassay (EIA). Significantly lower CRF levels were found in both the PTSD and PTSD + TBI groups compared to healthy control (PTSD vs. Controls: P = 0.0014, PTSD + TBI vs. Controls: P = 0.0011) and chronic TBI participants (PTSD vs. TBI: P < 0.0001, PTSD + TBI vs. TBI: P < 0.0001), suggesting a PTSD‐related mechanism independent from TBI and associated with CRF reduction. CRF levels negatively correlated with PTSD severity on the Clinically Administered PTSD Scale (CAPS‐5) scale in the whole study group. Hyperactivation of the HPA axis has been classically identified in acute stress. However, the recognized enhanced feedback inhibition of the HPA axis in chronic stress supports our findings of lower CRF in PTSD patients. This study suggests that reduced serum CRF in PTSD should be further investigated. Future validation studies will establish if CRF is a possible blood biomarker for PTSD and/or for differentiating PTSD and chronic TBI symptomatology. The HPA axis is activated under acute stress conditions, but an enhanced feedback inhibition may be prevalent in chronic stress conditions such as PTSD. We observed a reduction in serum CRF levels in veterans with PTSD and PTSD + TBI, but not in veterans with chronic TBI alone. A serum CRF reduction may be indicative of CNS mechanisms specific to PTSD and should be further evaluated as a possible peripheral biomarker.