Rauch Sheila A M, King Anthony P, Liberzon Israel, Sripada Rebecca K
Emory University School of Medicine, 12 Executive Park Dr, Ste 300, Atlanta, GA 30329.
Emory University School of Medicine, Atlanta, Georgia, USA.
J Clin Psychiatry. 2017 May;78(5):599-603. doi: 10.4088/JCP.15m10596.
Convergent evidence suggests that the hypothalamic-pituitary-adrenal (HPA) axis is disrupted in posttraumatic stress disorder (PTSD) and that HPA axis normalization may be associated with symptom improvement. Thus, the current study was designed to test the association between HPA axis reactivity and treatment response in psychotherapy for PTSD.
Thirty returning veterans with DSM-IV-TR PTSD were randomly assigned to receive 10 sessions of prolonged exposure therapy or present-centered therapy as part of a previously published randomized clinical trial (2008-2010). Treatment groups were collapsed for the current analyses. Salivary cortisol was collected 3 times during 3 therapy sessions. Cortisol reactivity was calculated by area under the curve with respect to ground. Hierarchical linear modeling was used to measure longitudinal change in salivary cortisol nested within patients and to test the effects of treatment responder status at both levels.
Session number was significant in the final model, indicating linear increases in cortisol output across sessions (β = 1.06, P = .02). In addition, responder status significantly predicted slope of cortisol reactivity across sessions (β = 1.35, P = .04). Compared to high responders, low responders exhibited a 1.35 (μg/dL) mean increase in cortisol reactivity between sessions. Responder status accounted for 6% of the previously unexplained variance in cortisol reactivity.
As compared to high treatment responders, low treatment responders showed greater increases in salivary cortisol output over the course of treatment. These results indicate that increases in HPA axis reactivity over the course of psychotherapy may be associated with worse treatment response. Future work is needed to investigate how modulation of HPA axis reactivity may be targeted in order to optimize PTSD treatment outcomes.
ClinicalTrials.gov identifier: NCT00475241.
越来越多的证据表明，创伤后应激障碍（PTSD）患者的下丘脑 - 垂体 - 肾上腺（HPA）轴功能紊乱，而HPA轴功能恢复正常可能与症状改善相关。因此，本研究旨在测试PTSD心理治疗中HPA轴反应性与治疗反应之间的关联。
30名符合DSM-IV-TR创伤后应激障碍诊断标准的退伍军人被随机分配接受10次延长暴露疗法或当前关注疗法，这是一项先前发表的随机临床试验（2008 - 2010年）的一部分。为了当前分析，将治疗组合并。在3次治疗过程中，分3次采集唾液皮质醇。皮质醇反应性通过相对于基线的曲线下面积计算。采用分层线性模型测量患者内唾液皮质醇的纵向变化，并在两个层面上测试治疗反应者状态的影响。
疗程数在最终模型中具有显著意义，表明各疗程皮质醇分泌呈线性增加（β = 1.06，P = 0.02）。此外，反应者状态显著预测了各疗程皮质醇反应性的斜率（β = 1.35，P = 0.04）。与高反应者相比，低反应者在各疗程间皮质醇反应性平均增加1.35（μg/dL）。反应者状态占皮质醇反应性先前未解释变异的6%。
与高治疗反应者相比，低治疗反应者在治疗过程中唾液皮质醇分泌增加更多。这些结果表明，心理治疗过程中HPA轴反应性增加可能与较差的治疗反应相关。未来需要开展研究，以探讨如何针对HPA轴反应性进行调节，从而优化PTSD治疗效果。
ClinicalTrials.gov标识符：NCT00475241
