24-Hour Monitoring of Cortisol and Corticotropin Secretion in Psychotic and Nonpsychotic Major Depression

Posener, Joel A.; DeBattista, Charles; Williams, Gordon H.; Kraemer, Helena C.; Kalehzan, B. Michelle; Schatzberg, Alan F.

doi:10.1001/archpsyc.57.8.755

Cited by 189 publications

(100 citation statements)

References 31 publications

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“…A series of studies have observed an increased HPA-axis activity in psychotic patients. A consistent finding in these studies is the fact that psychotic depressed patients are significantly more often nonsuppressors in the DST and a more recent paper described an increased 24 h ACTH secretion in psychotic depressed vs nonpsychotic depressed patients and healthy controls (Nelson and Davis, 1997;Posener et al, 2000). In accordance with these findings, we found a trend for higher CORT 1500 values in psychotic patients.…”

Section: Factors Influencing the Dex-crh Testsupporting

confidence: 91%

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: Factors Influencing the Dex-crh Testsupporting

confidence: 91%

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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“…Interestingly, increased concentrations of DHEA sulfate have recently been shown to predict also nonresponse to electroconvulsive therapy (Maayan et al, 2000), which is in line with our results. Our observation that baseline cortisol levels did not differ between responders and nonresponders to PSD may be due to the fact that single-point measurements of basal cortisol secretion are often insufficient and intensive monitoring of HPA axis hormones over time is needed to detect elevated cortisol levels in depression (Posener et al, 2000). Since DHEA is a steroid with antiglucocorticoid properties (Kalimi et al, 1994), an enhanced cortisol/DHEA ratio has recently been suggested to be a more precise method to assess the 'functional' hypercortisolemia in depression (Young et al, 2002).…”

Section: Discussionmentioning

confidence: 89%

Influence of Sleep Deprivation on Neuroactive Steroids in Major Depression

Schüle

Michele

Baghai

et al. 2002

Neuropsychopharmacol

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There is evidence from preclinical and clinical studies that concentrations of neuroactive steroids are altered in depression and normalize after antidepressant pharmacotherapy. However, no data are available concerning the impact of sleep deprivation on the concentrations of neuroactive steroids. A total of 29 drug-free patients (12 men, 17 women) suffering from major depression according to DSM-IV criteria were treated with partial sleep deprivation (PSD). Response to PSD was defined as a reduction of at least 30% according to the six-item version of the Hamilton depression scale (6-HAMD). Plasma samples were taken the day before and after PSD (days 0 and 1) and after one night of recovery sleep (day 2) at 8:00 am. The samples were quantified for neuroactive steroids by means of a highly sensitive and specific combined gas chromatography/mass spectrometry analysis. There was no influence of PSD on the concentrations of neuroactive steroids either in PSD responders (n ¼ 20) or in nonresponders (n ¼ 9). However, nonresponders showed significantly higher concentrations of 3a,5a-tetrahydroprogesterone (3a,5a-THP), 3a,5b-tetrahydroprogesterone (3a,5b-THP), and dehydroepiandrosterone (DHEA) before or after PSD compared to responders. In contrast to antidepressant drugs, which correct the dysequilibrium of neuroactive steroids in major depression within several weeks, PSD does not affect the concentrations of neuroactive steroids either in responders or in nonresponders.

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“…Depressed patients with (11 subjects) and without (17 subjects) psychosis were included. All depressed subjects were required to have a minimum score of 21 on the HDRS and a minimum score of 7 on the Thase Core Endogenomorphic Scale (Thase et al 1983) modified for the 21-item HDRS (Posener et al 2000). These latter two criteria were designed to ensure inclusion of participants with similar minimum levels of severity of endogenous-type symptoms.…”

Section: Subjectsmentioning

confidence: 99%

Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus

Greicius

Flores

Menon

et al. 2007

Biological Psychiatry

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2,038

120

1,486

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Background: Positron emission tomography (PET) studies of major depression have revealed resting-state abnormalities in the prefrontal and cingulate cortices. Recently, fMRI has been adapted to examine connectivity within a specific resting-state neural network-the default-mode network -that includes the medial prefrontal and anterior cingulate cortices. The goal of this study was to examine resting-state, default-mode network functional connectivity in subjects with major depression and in healthy comparison subjects.

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24-Hour Monitoring of Cortisol and Corticotropin Secretion in Psychotic and Nonpsychotic Major Depression

Abstract: In the population studied, PMD and NPMD patients have distinct profiles of HPA axis dysregulation.

Cited by 189 publications

References 31 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

Influence of Sleep Deprivation on Neuroactive Steroids in Major Depression

Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus

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