Pretreatment DST and Hypothalamic-Pituitary-Adrenocortical Function in Depressed Patients and Comparison Groups

Stokes, Peter E.

doi:10.1001/archpsyc.1984.01790140047006

Cited by 361 publications

(82 citation statements)

References 36 publications

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“…These data add to studies showing blunted adrenocorticotropic hormone (ACTH) response to intravenous CRH in depressed patients, which was interpreted to reflect increased hypothalamic CRH secretion stimulating pituitary corticotrophs (Holsboer et al, 1984;Gold et al, 1986). In addition, there appears to be an altered feedback regulation of the HPA-axis via the glucocorticoid receptors in these patients, which is reflected by a basal hypercortisolemia (Halbreich et al, 1985) and cortisol escape from dexamethasone suppression (Stokes et al, 1984) as well as an increased ACTH and cortisol release in the combined dexamethasone-suppression/CRH-stimulation test (Dex-CRH test) (Heuser et al, 1994b;von Bardeleben and Holsboer, 1991;Modell et al, 1997). So far, the Dex-CRH test appears to be the most sensitive tool to detect depression-related changes in the HPA-axis (Heuser et al, 1994b).…”

Section: Introductionsupporting

confidence: 51%

Pharmacological and Nonpharmacological Factors Influencing Hypothalamic–Pituitary–Adrenocortical Axis Reactivity in Acutely Depressed Psychiatric In-patients, Measured by the Dex-CRH Test

Künzel

Binder

Nickel

et al. 2003

Neuropsychopharmacol

135

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The most consistent biological findings in patients with depression are abnormalities in the hypothalamic-pituitary-adrenal (HPA)-axis, which can be measured using the combined dexamethasone-suppression/CRH-stimulation (Dex-CRH) test. The reactivity of the HPAaxis in this test, however, ranges over several orders of magnitude in depressed patients with comparable severity of symptoms. In this present study, we investigate which factors influence the magnitude of the response in the Dex-CRH test in 235 acutely depressed inpatients. We first examined the effects of common confounders shown to influence the HPA-axis, such as caffeine and nicotine consumption, acute stressors during the test, weight, gender, and age. Of all these variables, only female sex and nicotine consumption were positively correlated with the cortisol or ACTH response, respectively. As for the effects of psychopharmacological treatment, only the intake of carbamazepine and the fact of having relapsed under an established pharmacotherapy significantly increased the response in the Dex-CRH test, whereas the presence or absence of antidepressant treatment, the type of antidepressant treatment, or the number of ineffective antidepressant treatment trials during the index episode up to admission did not have any effect. We also found a positive correlation of the number of previous episodes, the overall HAM-D score and the severity of somatic/vegetative symptoms with the results in the Dex-CRH test. These results underline that in depressed patients this test is not majorly influenced by disease-unrelated factors. In addition, current antidepressant treatment does not appear to affect test outcome in the absence of clinical response. The influence of the number of previous episodes and relapse under pharmacotherapy suggests that HPA-axis reactivity may be altered by repetitive states of hypercortisolemia or continuous antidepressant treatment. Finally, more severe vegetative symptoms are associated with an enhanced HPA-axis activity.

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Section: Introductionsupporting

confidence: 51%

Pharmacological and Nonpharmacological Factors Influencing Hypothalamic–Pituitary–Adrenocortical Axis Reactivity in Acutely Depressed Psychiatric In-patients, Measured by the Dex-CRH Test

Künzel

Binder

Nickel

et al. 2003

Neuropsychopharmacol

135

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“…The NIMH study (Stokes et al, 1984) on drug-free patients reported mean pre-dexamethasone UFC levels of 148 @tmg/24hours in unipolar depressed patients, a result very similar to our own. Moreover, the post-dexamethasone UFC results in the two studies were remarkably similar with the NIMH study reporting levels of 59 @tgms per 24 hours, (and 65 @tgmper 24 hours in patients with unipolar depression), as compared to 65.4 @tgm per 24 hours in our study of mainly unipolar depressed patients (Calloway et al, 1984).…”

supporting

confidence: 88%

“…It has been established that RIA gives comparable results to competitive protein binding (Wilens et al, 1983) and RIA is now the most widely used method for assaying cortisols in DST studies of depressed patients (e.g., Stokes et al, 1984).…”

mentioning

confidence: 99%

Depression and Urinary Free Cortisol

Calloway

Dolan

1986

Br J Psychiatry

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after their partners' death (Bornstein & Clayton, 1972) probably are common, though are mostly so mild as not to require the attention of psychiatrists. My own study suggests that age-correspondence precipitated reactions are rare. When they do occur it is important that they be recognised as such, since they can sometimes present as florid psychotic states (Hilgard & Newman, 1959). I would be interested to know if any readers have experience of one.

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“…The HPA axis is the interaction between the hypothalamus, pituitary gland, and the adrenal cortex, and is a major part of the neuroendocrine system that controls reactions to stress [16]. The clinical manifestation of its dysfunction in depression includes basal hypercortisolemia [17], elevated cortisol secretion in the dexamethasone suppression test [18], and increased cortisol release in the combined dexamethasone suppression-corticotropine releasing hormone stimulation test [19,20]. The first line of treatment for depression is the use of antidepressants [21].…”

Section: Introductionmentioning

confidence: 99%

Aerobic Exercise Does Not Predict Brain Derived Neurotrophic Factor And Cortisol Alterations in Depressed Patients

Lamego¹,

Moura²,

Paes³

et al. 2015

CNSNDDT

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The pathophysiology of depression is related to neurobiological changes that occur in the monoamine system, hypothalamic-pituitary-adrenal axis, neurogenesis system and the neuroimmune system. In recent years, there has been a growing interest in the research of the effects of exercise on brain function, with a special focus on its effects on brainderived neurotrophic factor (BDNF), cortisol and other biomarkers. Thus, the aim of this study is to present a review investigating the acute and chronic effects of aerobic exercise on BDNF and cortisol levels in individuals with depression. It was not possible to establish an interaction between aerobic exercise and concentration of BDNF and cortisol, which may actually be the result of the divergence of methods, such as type of exercises, duration of the sessions, and prescribed intensity and frequency of sessions.

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Pretreatment DST and Hypothalamic-Pituitary-Adrenocortical Function in Depressed Patients and Comparison Groups

Cited by 361 publications

References 36 publications

Pharmacological and Nonpharmacological Factors Influencing Hypothalamic–Pituitary–Adrenocortical Axis Reactivity in Acutely Depressed Psychiatric In-patients, Measured by the Dex-CRH Test

Pharmacological and Nonpharmacological Factors Influencing Hypothalamic–Pituitary–Adrenocortical Axis Reactivity in Acutely Depressed Psychiatric In-patients, Measured by the Dex-CRH Test

Depression and Urinary Free Cortisol

Aerobic Exercise Does Not Predict Brain Derived Neurotrophic Factor And Cortisol Alterations in Depressed Patients

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