Impact of citalopram on the HPA system. A study of the combined DEX/CRH test in 30 unipolar depressed patients

Bschor, Tom; Ising, Marcus; Erbe, Sebastian; Winkelmann, Patricia; Ritter, Dirk; Uhr, Manfred; Lewitzka, Ute

doi:10.1016/j.jpsychires.2011.09.020

Cited by 41 publications

(26 citation statements)

References 50 publications

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“…Medication prior to study inclusion was very limited; in particular, selective serotonin reuptake inhibitors that indirectly regulate the HPA axis [39] were not allowed. We can effectively rule out the possibility that the different cortisol levels in psychiatric patients with or without suicidality compared to healthy controls and remitted patients were influenced by medication.…”

Section: Discussionmentioning

confidence: 99%

Impulsivity and Saliva Cortisol in Patients with Suicide Attempt and Controls

et al. 2017

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Objectives: The objective of this study was to prove concepts in the characterization of suicidal patients and the possible usefulness of those markers to potentially identify patients with a higher risk for suicidality. Methods: Patients with a recent suicide attempt were compared with patients suffering from depression, adjustment disorder, anxiety, or eating disorders without suicidality, healthy controls and remitted patients with a history of at least 1 suicide attempt (≥1 year). We analyzed impulsivity (Barratt Impulsivity Scale, BIS) and saliva cortisol concentrations. Results: Independently of suicidality and disease state patients display higher BIS scores than healthy controls. Saliva cortisol levels tend to be higher in patients in the acute disease state than in remitted patients and healthy controls. Conclusions: Saliva cortisol may be a useful marker that reveals alterations in nonsuicidal patients suffering from depression, adjustment disorder, anxiety, or eating disorders who might be at risk.

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Section: Discussionmentioning

confidence: 99%

Impulsivity and Saliva Cortisol in Patients with Suicide Attempt and Controls

et al. 2017

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“…However, other studies have failed to observe HPA axis disruption following CeA CRF-OE (Regev et al, 2011). Escitalopram has previously been shown to normalize HPA axis reactivity in depressed patients (Bschor et al, 2012; Nikisch et al, 2005b) and in animal models of stress (Uys et al, 2006). We hypothesized that CeA CRF-OE would elevate HPA axis reactivity via indirect mechanisms, which would be normalized by escitalopram administration.…”

Section: Discussionmentioning

confidence: 99%

Escitalopram alters gene expression and HPA axis reactivity in rats following chronic overexpression of corticotropin-releasing factor from the central amygdala

Flandreau

Bourke

Ressler

et al. 2013

Psychoneuroendocrinology

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Summary We have previously demonstrated that viral-mediated overexpression of corticotropin-releasing factor (CRF) within the central nucleus of the amygdala (CeA) reproduces many of the behavioral and endocrine consequences of chronic stress. The present experiment sought to determine whether administration of the selective serotonin reuptake inhibitor (SSRI) escitalopram reverses the adverse effects of CeA CRF overexpression. In a 2 × 2 design, adult male rats received bilateral infusions of a control lentivirus or a lentivirus in which a portion of the CRF promoter is used to drive increased expression of CRF peptide. Four weeks later, rats were then implanted with an Alzet minipump to deliver vehicle or 10 mg/kg/day escitalopram for a 4-week period of time. The defensive withdrawal (DW) test of anxiety and the sucrose-preference test (SPT) of anhedonia were performed both before and after pump implantation. Additional post-implant behavioral tests included the elevated plus maze (EPM) and social interaction (SI) test. Following completion of behavioral testing, the dexamethasone/CRF test was performed to assess HPA axis reactivity. Brains were collected and expression of HPA axis-relevant transcripts were measured using in situ hybridization. Amygdalar CRF overexpression increased anxiety-like behavior in the DW test at week eight, which was only partially prevented by escitalopram. In both CRF-overexpressing and control groups, escitalopram decreased hippocampal CRF expression while increasing hypothalamic and hippocampal expression of the glucocorticoid receptor (GR). These gene expression changes were associated with a significant decrease in HPA axis reactivity in rats treated with escitalopram. Interestingly, escitalopram increased the rate of weight gain only in rats overexpressing CRF. Overall these data support our hypothesis that amygdalar CRF is critical in anxiety-like behavior; because the antidepressant was unable to reverse behavioral manifestations of CeA CRF-OE. This may be a potential animal model to study treatment-resistant psychopathologies.

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“…Previous studies also reported a decreasing effect of SSRIs on HPA-axis hyperactivity (Nikisch et al, 2005;Buhl et al, 2010;Lenze et al, 2010), although contradictory findings exist (Deuschle et al, 2003;Bschor et al, 2012).…”

Section: Changes In Cortisol Parameters During Treatment and Associatmentioning

confidence: 95%

Longitudinal effects of the SSRI paroxetine on salivary cortisol in Major Depressive Disorder

Ruhé

Khoenkhoen

Ottenhof

et al. 2015

Psychoneuroendocrinology

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Hypothalamic-pituitary-adrenal (HPA)-axis dysregulation is a prominent finding in more severe Major Depressive Disorder (MDD), and is characterized by increased baseline cortisol levels at awakening (BCL), blunted cortisol awakening response (CAR) and increased area under the cortisol curve (AUC). Selective serotonin reuptake inhibitors (SSRIs) appear to normalize HPA-axis dysfunction, but this is hardly investigated longitudinally.We studied salivary BCL, CAR and AUC at awakening and 30 min thereafter. We compared measurements in initially drug-free MDD-patients with healthy controls (HCs) at study-entry. In patients, we repeated measures after 6 and 12 weeks' treatment with the SSRI paroxetine. Non-responding patients received a randomized dose-escalation after six weeks' treatment.We found no significant study-entry differences in BLC, CAR or AUC between MDD-patients (n = 70) and controls (n = 51). In MDD-patients, we found general decreases of BCL and AUC during paroxetine treatment (p ≤ 0.007), especially in late and non-responders. Importantly, while overall CAR did not change significantly over time, it robustly increased over 12 weeks especially when patients achieved remission (p ≤ 0.041). The dose-escalation intervention did not significantly influence CAR or other cortisol parameters.In conclusion, paroxetine seems to interfere with HPA-axis dysregulation, reflected in significant overall decreases in BCL and AUC during treatment. Paroxetine appears to decrease HPA-axis set-point in MDD, which might result in increased HPA-axis activity over time, which is further improved when patients achieve remission (ISRCTN register nr. ISRCTN44111488).

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Impact of citalopram on the HPA system. A study of the combined DEX/CRH test in 30 unipolar depressed patients

Cited by 41 publications

References 50 publications

Impulsivity and Saliva Cortisol in Patients with Suicide Attempt and Controls

Impulsivity and Saliva Cortisol in Patients with Suicide Attempt and Controls

Escitalopram alters gene expression and HPA axis reactivity in rats following chronic overexpression of corticotropin-releasing factor from the central amygdala

Longitudinal effects of the SSRI paroxetine on salivary cortisol in Major Depressive Disorder

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