ECE2011 Poster Presentations Neuroendocrinology (36 abstracts)
Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia, Belgrade, Serbia.
Introduction: Posttraumatic stress disorder (PTSD) is anxious disorder that occurs following exposure to trauma. In the last two decades, numerous studies showed that dysregulation of hipothalamopituitaryadrenal axis (HPAA) is a core feature of the PTSD. Still, results are heterogeneous and often conflicted with one another. Therefore, we conducted strictly controlled study in order to characterize relationship between ACTH and cortisol secretion in patients with chronic war-related PTSD.
Methods: We examined HPAA basal function (ACTH and cortisol concentrations measured hourly from 2200 h to 0900 h) and sensitivity (overnight low-dose (0.5 mg) dexamethason suppression test-DST0.5 mg) in men with chronic war-related PTSD (group PTSD, N=59) in comparison to healthy non-traumatized men (group Healthy, N=53). Participants with depressive disorder and other major psychiatric and somatic comorbidities were excluded from the study. There were no group differences in age (PTSP: 44.1 (9.3) years, Healthy: 42.2 (9.7) years; P=0.28) and body mass index (PTSP: 26.9 (3.6) kg/m2; Healthy: 27.0 (3.6) kg/m2, P=0.92).
Results: During the time period from 2200 h to 0900 h, PTSD had lower ACTH (P=0.043) and the same cortisol concentration (P=0.37) which resulted in lower ACTH/cortisol ratio (P=0.029) in comparison to Healthy group. There were no group differences either in ACTH secretion amplitude (P=0.63) or in cortisol secretion amplitude (P=0.24). In comparison to Healthy, PTSD showed enhanced cortisol suppression during DST0.5 mg (P=0.030).
Conclusion: Results of our study implicate that patients with chronic war-related PTSD without somatic comorbidities and depression, in comparison to healthy non-traumatized subjects of the same gender, age and body mass index, have concomitantly enhanced HPA axis sensitivity to cortisol at the level of anterior pituitary and enhanced adrenal reactivity to ACTH. It is yet to be determined which of these disturbances is primary and which is compensatory.