Salivary Cortisol Responses to Dexamethasone in Adolescents With Posttraumatic Stress Disorder

Lipschitz, Deborah S.; Rasmusson, Ann M.; Yehuda, Rachel; Wang, Sheila; Anyan, Walter R.; Gueoguieva, Ralitza; Grilo, Carlos M.; Fehon, Dwain C.; Southwick, Steven M.

doi:10.1097/01.chi.0000084832.67701.0d

Cited by 46 publications

(18 citation statements)

References 27 publications

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“…Further, these studies either had no control group (Goenjian et al, 1996;Kellner et al, 1997) or no healthy control group (Heim et al, 1998). Our results are in agreement with recent studies in adolescents (Lipschitz et al, 2003) and adults (Lindley et al, 2004), which also failed to find an enhanced negative feedback inhibition in PTSD in a low-dose salivary dexamethasone test. Interestingly, in our study, dexamethasone concentrations were somewhat lower in patients compared with healthy controls (Table 2).…”

Section: Posttraumatic Stress Disorder C Otte Et Alsupporting

confidence: 82%

“…In PTSD, 24-h urinary cortisol was increased (De Bellis et al, 1999;Lemieux and Coe, 1995;Maes et al, 1998;Pitman and Orr, 1990), unchanged (Baker et al, 1999;Rasmusson et al, 2001;Young and Breslau, 2004) or decreased (Thaller et al, 1999;Yehuda et al, 1995Yehuda et al, , 1990 compared to healthy controls. Also, cortisol suppression after dexamethasone was reported to be diminished (Atmaca et al, 2002;Thaller et al, 1999), unchanged (Dinan et al, 1990;Halbreich et al, 1989;Lindley et al, 2004;Lipschitz et al, 2003), or to be enhanced (Stein et al, 1997;Yehuda et al, 2002Yehuda et al, , 1993. Some of these inconsistencies might be related to differences among studies regarding the study population, age, and gender differences, use of psychotropic medication, comorbid substance abuse, and dose of dexamethasone (for reviews, see Rasmusson et al, 2003;Yehuda, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Hypothalamic–Pituitary–Adrenal Axis Activity and Sleep in Posttraumatic Stress Disorder

Otte

Lenoci

Metzler

et al. 2005

Neuropsychopharmacol

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Alterations of the hypothalamic-pituitary-adrenal (HPA) axis and sleep disturbances have been described separately in post-traumatic stress disorder (PTSD). It is not known if HPA alterations and sleep disturbances are associated in PTSD. This study examined sleep and HPA activity in 20 male medication-free subjects with PTSD and 16 matched healthy controls. Two nights of polysomnography were obtained and 24-h urinary cortisol was collected during day 2. Subjects self-administered a low-dose (0.5 mg) salivary dexamethasone test at home. Compared with controls, PTSD subjects had higher 24-h urinary mg cortisol/g creatinine (mean7SD 40717 vs 28712, p ¼ 0.03) but not significantly higher 24-h urinary cortisol (mean7SD 52715 mg/day vs 43723, p ¼ 0.19). PTSD subjects showed a trend towards less cortisol suppression after dexamethasone (73%718 vs 83%710, p ¼ 0.06). In the combined sample, delta sleep was significantly and negatively correlated with 24-h urinary cortisol (r ¼ À0.36, p ¼ 0.04), and with 24-h urinary cortisol/g creatinine on a trend level (r ¼ À0.34, p ¼ 0.06). Our results suggest that increased cortisol is negatively associated with delta sleep. This may contribute to sleep abnormalities in conditions associated with elevated cortisol, possibly including PTSD. Future studies should explore the temporal relationship between HPA activity, sleep disturbances, and psychopathology after a traumatic event.

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Section: Posttraumatic Stress Disorder C Otte Et Alsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Hypothalamic–Pituitary–Adrenal Axis Activity and Sleep in Posttraumatic Stress Disorder

Otte

Lenoci

Metzler

et al. 2005

Neuropsychopharmacol

Self Cite

View full text Add to dashboard Cite

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“…Previous studies using the dexamethasone suppression test (DST) have shown enhanced (Stein et al, 1997) or normal (Lipschitz et al, 2003) glucocorticoid negative feedback in premenopausal women with PTSD, or have contained too few female subjects to give reliable results (Grossman et al, 2003;Rinne et al, 2002)Fespecially since menstrual phase influences DST outcome (Altemus et al, 1997) and was not controlled in any of these studies. Thus, it will be important in the future to investigate whether DHEA modulates glucocorticoid negative feedback at the level of the pituitary in premenopausal women with PTSD.…”

Section: Study Limitationsmentioning

confidence: 97%

An Increased Capacity for Adrenal DHEA Release is Associated with Decreased Avoidance and Negative Mood Symptoms in Women with PTSD

Rasmusson

Vasek

Lipschitz

et al. 2004

Neuropsychopharmacol

121

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We recently found increased adrenal cortisol responses to adrenocorticotropic hormone (ACTH)1-24 and increased pituitary ACTH and adrenal cortisol responses to corticotropin-releasing factor in premenopausal women with chronic post-traumatic stress disorder (PTSD) compared to healthy nontraumatized subjects. This pattern of hypothalamic-pituitary-adrenal axis (HPA) hyper-reactivity has been previously seen in healthy individuals treated with the antiglucocorticoid mifepristone. We therefore investigated whether endogenous plasma levels of antiglucocorticoids such as dehydroepiandrosteroine (DHEA) and progesterone were increased in premenopausal women with PTSD at baseline or in response to adrenal activation by ACTH1-24. The study revealed that DHEA responses to 250 microg ACTH1-24 were increased in 13 PTSD subjects compared to 13 healthy nontraumatized subjects, while DHEA levels were generally increased in the PTSD subjects compared to seven healthy traumatized subjects. Cortisol responses to ACTH1-24 were also higher in the women with PTSD, while progesterone levels and responses were not different among the three groups. In addition, among the PTSD subjects, the peak change in DHEA in response to ACTH1-24 was negatively correlated with the total Clinician Administered PTSD Scale score, while the peak DHEA to cortisol ratio was inversely associated with negative mood symptoms measured by the Profile of Mood States scale. This work suggests that an increased capacity for DHEA release in response to extreme adrenal activation may influence the pattern of HPA axis adaptation to extreme stress, as well as mitigate the severity of PTSD and negative mood symptoms in premenopausal women with PTSD.

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“…Similarly, some evidence suggests that adolescents who have experienced multiple or prolonged traumatic events may be more likely to present with predominately dissociative and externalizing features, including depersonalization, derealization, substance abuse, and aggressive outbursts (Goodwin, 1988;Horowitz, 1996;Terr, 1991). Recent physiological research also suggests that whereas adult trauma survivors generally demonstrate cortisol suppression, adolescents typically do not (Lipschitz et al, 2003). Whether differences in physiological experience and symptom presentation among adolescents and children reflect qualitatively distinct reactions, potentially representing separate causal pathways, or are merely developmentally influenced variations of the same underlying pathology remains unknown.…”

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confidence: 93%

The latent structure of posttraumatic stress disorder among adolescents

Broman-Fulks

Ruggiero

Green

et al. 2009

Journal of Traumatic Stress

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Debate has arisen over whether posttraumatic stress disorder (PTSD) is most accurately conceptualized as representing a discrete clinical syndrome or an extreme reaction to traumatic life events. Recent taxometric research using predominantly adult samples appears to support a dimensional model of PTSD, raising questions about the utility of current psychiatric nosology which depicts PTSD as a distinct entity. The present study sought to use taxometric procedures to examine the latent structure of posttraumatic stress reactions among a national epidemiologic sample of 2,885 adolescents. Results were consistent with previous taxometric studies in supporting a dimensional model of posttraumatic stress reactions. The implications of these findings for public policy, as well as the etiology and assessment of posttraumatic stress reactions, are discussed.

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Salivary Cortisol Responses to Dexamethasone in Adolescents With Posttraumatic Stress Disorder

Cited by 46 publications

References 27 publications

Hypothalamic–Pituitary–Adrenal Axis Activity and Sleep in Posttraumatic Stress Disorder

Hypothalamic–Pituitary–Adrenal Axis Activity and Sleep in Posttraumatic Stress Disorder

An Increased Capacity for Adrenal DHEA Release is Associated with Decreased Avoidance and Negative Mood Symptoms in Women with PTSD

The latent structure of posttraumatic stress disorder among adolescents

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