The Dexamethasone Suppression Test in Patients With Mood Disorders
Mental Health Clinical Research Center, University of Texas, Southwestern Medical Center at Dallas, USA. The Journal of Clinical Psychiatry
(Impact Factor: 5.5).
11/1996; 57(10):470-84. DOI: 10.4088/JCP.v57n1006
This study was undertaken to (1) determine whether the endogenous/nonendogenous mood disorder dichotomy is validated by the dexamethasone suppression test (DST); (2) determine whether other subtyping schemes (unipolar/bipolar, DSM-III melancholic/nonmelancholic, Winokur's family history subtypes) relate to the DST; (3) evaluate the relative contributions of symptom severity, weight loss, and other factors to DST status; and (4) assess the relative sensitivity of various post-dexamethasone cortisol determinations in the detection of dexamethasone nonsuppression.
487 consecutive adult inpatients (N = 131) and outpatients (N = 356) with unipolar (N = 422) or bipolar disorder (N = 65) underwent the 1.0-mg DST. Nonsuppression was defined as at least one post-dexamethasone cortisol measurement > 4.0 micrograms/dL.
Nonsuppression occurred in 27% of all patients with major depression and 43% of all bipolar depressed phase patients. For outpatients, dexamethasone nonsuppression occurred in 35.2% of subjects with endogenous (unipolar + bipolar; N = 145) and 9.0% of those with nonendogenous (unipolar only; N = 211) depressions (single 4 p.m. post-dexamethasone cortisol). For inpatients, dexamethasone nonsuppression was found in 61.5% of subjects with endogenous (N = 104) and 18.5% of those with nonendogenous (N = 27) depressions (three post-dexamethasone cortisol determinations). For the inpatient and outpatient sample together, the DST had a sensitivity of 46.2% and a specificity of 89.9% in differentiating endogenous from nonendogenous major depressive episodes. Weight loss, gender, and symptom severity added little to the endogenous/nonendogenous dichotomy. The Research Diagnostic Criteria (RDC) primary/secondary and Winokur and colleagues' family history subtypes for unipolar depression were not strongly validated by the DST. The 4 p.m. and 11 p.m. samples together detected 91.0% of those inpatients with abnormal three-sample DST results. The 8 a.m. sample alone detected 30% of those, the 4 p.m. sample alone detected 67%, and the 11 p.m. sample alone detected 62%.
The RDC endogenous/nonendogenous dichotomy was validated by the DST.
Available from: Jeff Kiesner
- "First, because PMS/PMDD demonstrates a number of similarities with major depressive disorder (MDD), and because MDD is associated with multiple indices of cortisol dysregulation, including cortisol hypersecretion (Gillespie and Nemeroff, 2005;Goodyer et al., 2001;Wong et al., 2000), non-suppression to the dexamethasone suppression test (DST;Carroll et al., 1981;Rush et al., 1996), and flattened diurnal cortisol secretion (Doane et al., 2013;Jarcho et al., 2013), researchers have also tested whether cortisol dyregulation is associated with PMS/PMDD. Specifically, because of overlapping symptoms and high comorbidity between major depression and PMS/PMDD (Endicott et al., 1981;Fava et al., 1992;Graze et al., 1990;Halbreich and Endicott, 1985;Pearlstein et al., 1990), and because some research suggests that SSRIs are effective in treating both major depression (Baker et al., 2003;Lanzenberger et al., 2012;Villafuerte et al., 2009) and PMS/PMDD (Dimmock et al., 2000), it has been hypothesized that these disorders share common neurological or neuroendocrinological substrates (Bancroft and Cook, 1995). "
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ABSTRACT: Although decades of research has examined the association between cortisol regulation and premenstrual syndrome/premenstrual dysphoric disorder (PMS/PMDD), no review exists to provide a general set of conclusions from the extant research. In the present review we summarize and interpret research that has tested for associations between PMS/PMDD and cortisol levels and reactivity (n = 38 original research articles). Three types of studies are examined: correlational studies, environmental-challenge studies, and pharmacological-challenge studies.
Available from: Theodore Beauchaine
- "Even though the DST is a more efficient biomarker of depression than either basal cortisol or CRH infusion, a medium effect size does not confer adequate sensitivity or specificity to render the test useful for diagnostic purposes (Casat and Powell 1988; Arana et al. 1985), especially if one assumes that all depressions are etiologically homogenous. However, depression is not a homogeneous construct, and the DST is much more effective in identifying those who suffer from melancholic depression (Arana et al. 1985; Rush et al. 1996), and those with high-risk glucocorticoid receptor polymorphisms (Ruiz et al. 2001). Such findings suggest that HPA axis dysfunction may be associated more specifically with endogenous forms of depression, which portend greater risk of eventual suicide than other forms of depression, especially among women (e.g., Thompson 2012). "
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ABSTRACT: Although the dexamethasone suppression test (DST) has limited use as a marker of depression given inadequate sensitivity and specificity, it marks prospective risk for suicide among adults. However, few studies have examined associations between the DST, suicidal ideation, and self-inflicted injury (SII) among adolescents, even though SII is the single best predictor of eventual suicide. We evaluated the DST as a correlate of suicidal ideation and retrospective reports of self-inflicted injury (SII) among adolescent girls, ages 13-17, with histories of depression (n=28) or depression/self-harm (n=29). Lower post-DST cortisol was associated with suicidal ideation and SII, over-and-above parent-reports and combined parent-/self-reports of internalizing and externalizing behavior. These findings are consistent with recent acquired capacity models of stress-related psychopathology in which hypothalamic-pituitary adrenal (HPA) axis function is altered through epigenetic/allostatic mechanisms among vulnerable individuals who incur adversity early in life.
Available from: Christiaan Vinkers
- "Our findings should be interpreted in light of the existing data on HPA-axis activity in bipolar disorder. Several studies in which the HPA-axis was pharmacologically challenged showed that there is a reduced negative feedback in bipolar disorder patients, associated with hypercortisolism (Watson et al., 2004; Rush et al., 1996; Rybakowski and Twardowska, 1999; Schmider et al., 1995). This disrupted feedback has further been related to decreased glucocorticoid receptor (GR) sensitivity in bi polar disorder (for review see (Spijker et al., 2011)). "
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ABSTRACT: There is ample evidence that the acute stress response is altered in schizophrenia and bipolar disorder. However, it is not clear whether such changes are related to the illness, a genetic vulnerability, or is the result of medication that is used in the majority of these patients. Therefore, we investigated determinants of the acute endocrine and autonomic stress response in healthy controls (n=48), euthymic BD1 patients (n=49) and unaffected siblings of BD1 patients (n=27). All participants completed a validated psychosocial stress task, the Trier Social Stress Test for Groups (TSST-G). Saliva levels of alpha-amylase and cortisol were measured before, during, and after exposure to stress. Compared to controls, we found a significantly blunted cortisol stress response in BD1 patients. Conversely, BD1 patients displayed exaggerated alpha-amylase levels in response to stress. Antipsychotic use was a significant contributing factor to the blunted cortisol stress response in BD1 patients. Unaffected BD1 siblings displayed similar stress-induced cortisol and alpha-amylase levels as controls, suggesting that familial risk for BD1 did not have a large effect on the functionality of the stress system. In conclusion, this study shows that euthymic BD1 patients have a substantially blunted endocrine stress response but an exaggerated autonomic stress response and that the endocrine stress response differences can be largely contributed to antipsychotic use rather than constitute a specific BD1 phenotype or vulnerability.
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