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Cortisol response to acute trauma and risk of posttraumatic stress disorder.

机译:皮质醇对急性创伤的反应和创伤后应激障碍的风险。

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摘要

This study sought to characterize the variability of the acute cortisol response following trauma and its relationship to posttraumatic stress disorder (PTSD). Forty eight participants were recruited within 24h of a traumatic accident requiring hospital admission. A saliva sample was collected at 08.00 h and 16.00 h 2 days, 1 month and 6 months after hospital admission, together with 24-h urine collection. Participants completed a dexamethasone suppression test (0.5mg DEX at 21.00 h) at each follow up, together with self-report questionnaires. The Clinician Administered PTSD Scale (CAPS) was administered at 1 and 6 months to identify PTSD. Prevalence of PTSD was 27% at 1 month and 21% at 6 months. PTSD symptoms at 6 months were negatively correlated with salivary cortisol at 08.00 h on day 2 (r=-0.36, p=0.04), but positively correlated with 16.00 h cortisols (r=0.41, p=0.03). A lower rise in cortisol at 08.00 h on day 2 was associated with an increase in risk of PTSD at both 1 month (OR=1.411 (1.017, 1.957)) and 6 months (OR=1.411 (1.066, 1.866)). At 1 month, 70% of participants with PTSD suppressed cortisol to more than 90% of pre-dex levels compared with 25% without PTSD (chi(2)=6.77, p=0.034). Urinary cortisol excretion was not different between groups at any time point. The findings support a hypothesis that sensitization of the HPA axis and enhanced suppression of cortisol following the dexamethasone suppression test are established early in the disease process.
机译:这项研究试图表征创伤后急性皮质醇反应的变异性及其与创伤后应激障碍(PTSD)的关系。在需要住院的外伤事故发生24小时内招募了48名参与者。入院后2天,1个月和6个月的08.00 h和16.00 h收集唾液样本,并收集24 h尿液。参加者在每次随访中均完成了地塞米松抑制试验(0.5mg DEX,21.00 h),并完成了自我报告调查表。在第1和6个月时进行临床医生管理的PTSD量表(CAPS),以鉴定PTSD。 PTSD的患病率在1个月时为27%,在6个月时为21%。在第2天的08.00 h时,PTSD症状在6个月时与唾液皮质醇呈负相关(r = -0.36,p = 0.04),而与16.00 h皮质醇呈正相关(r = 0.41,p = 0.03)。第2天08.00 h皮质醇的升高与1个月(OR = 1.411(1.017,1.957))和6个月(OR = 1.411(1.066,1.866))的PTSD风险增加相关。在1个月时,有PTSD的参与者中70%抑制了皮质醇至90%以上,而没有PTSD的参与者中抑制了25%(chi(2)= 6.77,p = 0.034)。两组之间的尿皮质醇排泄在任何时间都没有差异。这些发现支持一个假说,即在疾病过程的早期就建立了地塞米松抑制试验后,对HPA轴的敏感性和对皮质醇的增强抑制作用。

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