Pituitary-adrenal responses to standard and low-dose dexamethasone suppression tests in adult survivors of child abuse (original) (raw)
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Journal of Psychiatric Research, 2008
Reports about alterations of hypothalamic-pituitary-adrenocortical (HPA) function in patients with chronic posttraumatic stress disorder (PTSD) are inconsistent and controversial. More refined laboratory tests and subgrouping of PTSD patients might help to decrease variance of findings. 14 subjects with chronic PTSD and 14 healthy controls were examined between 13:00 and 17:00 using a modified combined dexamethasone/CRH test (0.5 mg dexamethasone at 23:00, 100 microg CRH at 15:00). Plasma adenocorticotropic hormone (ACTH), cortisol and blood pressure were measured every 15 min from 14:45 until 17:00. No significant differences between patients and controls were found in the analyses of ACTH and cortisol levels, but a significantly elevated systolic and diastolic blood pressure in PTSD. Severity of depressive symptoms had no influence. However, explorative analyses showed that patients with a history of childhood traumatization had significantly higher post-dexamethasone-ACTH levels and a significantly lower diastolic blood pressure in comparison to patients without early trauma. In this first pilot study in a typical clinical sample of patients with chronic PTSD we found effects of severe adverse events in childhood on HPA axis regulation. Maybe, childhood traumatization could influence HPA axis findings in PTSD. Further research is needed, especially dose-response studies with different doses of dexamethasone in dexamethasone/CRH tests in PTSD.
American Journal of Psychiatry, 2001
Objective: Early adverse life events may predispose individuals to the development of mood and anxiety disorders in adulthood, perhaps by inducing persistent changes in corticotropin-releasing factor (CRF) neuronal systems. The present study sought to evaluate pituitary-adrenal responses to standard hypothalamic-pituitary-adrenal axis challenge tests in adult female survivors of childhood abuse with and without major depressive disorder.
Psychoneuroendocrinology, 2003
Preclinical studies show that animals with a history of chronic stress exposure have increased hypothalamic-pituitary-adrenal (HPA) axis reactivity following reexposure to stress. Patients with posttraumatic stress disorder (PTSD) have been found to have normal or decreased function of the HPA axis, however no studies have looked at the HPA response to stress in PTSD. The purpose of this study was to assess cortisol responsivity to a stressful cognitive challenge in patients with PTSD related to childhood abuse. Salivary cortisol levels, as well as heart rate and blood pressure, were measured before and after a stressful cognitive challenge in * Corresponding author. Present address: patients with abuse-related PTSD (N = 23) and healthy comparison subjects (N = 18). PTSD patients had 61% higher group mean cortisol levels in the time period leading up to the cognitive challenge, and 46% higher cortisol levels during the time period of the cognitive challenge, compared to controls. Both PTSD patients and controls had a similar 66-68% increase in cortisol levels from their own baseline with the cognitive challenge. Following the cognitive challenge, cortisol levels fell in both groups and were similar in PTSD and control groups. PTSD patients appeared to have an increased cortisol response in anticipation of a cognitive challenge relative to controls. Although cortisol has been found to be low at baseline, there does not appear to be an impairment in cortisol response to stressors in PTSD. Published by Elsevier Science Ltd.
Implications of Hypothalamic-Pituitary-Adrenal Axis Functioning in Posttraumatic Stress Disorder
Journal of the American Psychiatric Nurses Association, 2011
BACkgrounD: Cortisol secretions serve as the barometer of the hypothalamic-pituitary-adrenal (HPA) axis, which regulates and controls responses to stress. Studies of cortisol secretions in patients with posttraumatic stress disorder (PTSD) reveal inconsistent results. PurPoSe: Current research on HPA axis functioning in PTSD is examined to elucidate the neuroendocrine contributions in the disorder, identify current treatment's impact on the HPA axis, and consider implications for nursing care and areas for future research. FInDIngS: There is evidence for HPA dysregulation in PTSD, which contributes to widespread impairment in functions such as memory and stress reactivity and to physical morbidity via processes such as allostatic load. There is limited, but building, evidence that dehydroepiandrosterone (DHEA), which is released simultaneously with cortisol, may provide anti-glucocorticoid and neuroprotective effects. ConCluSIon: Current treatments such as selective serotonin reuptake inhibitors and psychotherapy may have a beneficial impact on the HPA axis in PTSD populations. Somatic approaches to treating PTSD have not yet been studied in relation to their impact on HPA axis parameters in PTSD patients. Treatment studies of DHEA or glucocorticoids have not yet used HPA axis endpoints. PTSD treatment studies that include measures of HPA axis target mechanisms and consider HPA axis regulation as an additional treatment outcome are warranted.
Journal of the American Psychiatric Nurses Association, 2017
Studies of the relationship between cortisol and posttraumatic stress disorder (PTSD) have had inconsistent results. Gender, trauma type, and age at trauma exposure may explain the inconsistencies. The objective of the review was to examine cortisol levels in relation to PTSD in women with a history of child maltreatment trauma. A review of literature found 13 articles eligible for inclusion. Despite limiting focus to the relatively homogeneous population, the patterns of associations between PTSD and cortisol levels were still inconsistent. The reasons for the inconsistencies likely include highly varied methods across studies, small convenience samples, and unmeasured neuroendocrine hormones that may be stronger predictors of PTSD. The review does not point to a clear bio-behavioral target for psychiatric nursing intervention. It is important to continue to address the developmental and clinical stress response aspects of child maltreatment trauma-related PTSD without assuming tha...
Biological Psychiatry, 2001
Background: Decreased basal cortisol levels have been reported in individuals with posttraumatic stress disorder (PTSD). There is evidence for enhanced negative feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis in PTSD, which could account for this, but other possible mechanisms have not been ruled out. We examined the HPA axis employing a metyrapone-cortisol infusion protocol designed to study negative feedback sensitivity. Methods: Vietnam combat trauma-exposed subjects met DSM-IV criteria for PTSD. Exclusion criteria included substance abuse and most medications. Endogenous feedback inhibition was removed by blocking cortisol synthesis with oral metyrapone and reintroduced by intravenous infusion of cortisol. In a placebo condition, subjects received oral placebo and normal saline infusion. Serial blood samples drawn over 4 hours were assayed for adrenocorticotrophic hormone (ACTH), cortisol, and 11deoxycortisol. Selected samples were assayed for cortisol binding globulin (CBG) and dehydroepiandrosterone (DHEA). Results: Basal plasma cortisol was significantly decreased in PTSD subjects (n ϭ 13) compared with control subjects (n ϭ 16). No significant difference in the ACTH response to cortisol infusion following metyrapone was observed; however 11-deoxycortisol was significantly decreased in PTSD subjects. In addition, CBG was significantly increased in PTSD subjects, and DHEA was significantly decreased in both PTSD and combat-exposed control subjects. Conclusions: These observations suggest decreased adrenocortical responsiveness may be an additional or alternative mechanism accounting for low cortisol in PTSD.
Sensitization of the Hypothalamic-Pituitary-Adrenal Axis in Posttraumatic Stress Disorder
Annals of the New York Academy of Sciences, 1997
Posttraumatic stress disorder (PTSD) is a psychiatric condition that can occur in individuals who have experienced traumatic events. The symptoms of PTSD were initially conceptualized as reflecting a natural process of adaptation to extraordinarily adverse life event~.l-~ However, in recent years prevalence studies have clarified that PTSD only occurs in a percentage of those exposed to trauma."' Furthermore, among trauma survivors who develop this disorder, a substantial proportion appear to show full remission of their symptoms over time.6 This observation demonstrates that chronic PTSD represents a specific type of adaptation to trauma, which may not necessarily reflect typical or even normative stress responsiveness.1°
Psychoneuroendocrinology, 1989
We studied the hypothalamo-pituitary-adrenal (HPA) system in Vietnam veterans with posttraumatic stress disorder (PTSD) who also met Research Diagnostic Criteria for endogenous depression (MDD-ED). Over half also abused alcohol, and many complained of pain-confounding factors usually associated with increased HPA activity. Nonetheless, not even one patient had elevated basal plasma cortisol concentrations or an abnormal dexamethasone suppression test (DST); the subjects' post-dexamethasone cortisol values and plasma cortisol per ng plasma dexamethasone were in the lownormal range. These results highlight the biological heterogeneity of endogenous depression and its possible influence by past psychological trauma, and they raise questions about the use of current typological criteria for research purposes.
Open Access Macedonian Journal of Medical Sciences, 2014
Aim: To further examine the neurobiological mechanisms and their outcomes responsible for the PTSD sequelae induced by laboratory animal model and to explore the effects of chronic psychosocial paradigm. We tested the hypothesis that our animal model of PTSD would display abnormalities in glucocorticoid levels that are manifest in people with PTSD and that psychosocially stressed rats exhibit a significantly greater suppression of corticosterone levels than control rats following the administration of dexamethasone.Methods: Animals were divided into two groups. The experimental group was scheduled to exposure to two types of stressors: double exposure to acute immobilization stress, and combined predator-threat stress and daily social stress. There was also administration of dexamethasone in combination with stress exposure.Results: There was a statistical difference between masses of thymus in the stress group and stress group with dexamethasone appliance (p=0.024). We found statis...