Blunted cortisol response to a psychosocial stressor in schizophrenia

Jansen, Lucres M. C.; Wied, Christine C. Gispen‐de; Gademan, P. J.; Jonge, Rogier C. J. de; Linden, J.A. van der; Kahn, René S.

doi:10.1016/s0920-9964(98)00066-8

Cited by 126 publications

(72 citation statements)

References 27 publications

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“…Elevated levels of cortisol in SCH found in the present study are in agreement with some previous studies (Newcomer et al, 1991;Tandon et al, 1991;Lammers et al, 1995;Meltzer et al, 2001), but not with others (Jansen et al, 1998;Kaneda et al, 2002). Our finding of positive correlation between cortisol and negative symptoms is consistent with some previous studies (Newcomer et al, 1991;Tandon et al, 1991;Shirayama et al, 2002).…”

Section: Discussionsupporting

confidence: 92%

“…Nonsuppression, due to the lack of glucocorticoid secretion feedback mechanisms, occurs frequently in SCH, with percentages varying between 11 and 55% (Sharma et al, 1988;Yeragani, 1990;Coryell and Tsuang, 1992). Moreover, several studies showed that basal cortisol levels are significantly higher in schizophrenic (SCH) patients compared to normal controls (Walker and Diforio, 1997;Lammers et al, 1995), although these findings have not been consistent between studies (Jansen et al, 1998;Kaneda et al, 2002). Studies also suggest a relationship between HPA activity and symptomatology in SCH.…”

Section: Introductionmentioning

confidence: 99%

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Cortisol and Cytokines in Chronic and Treatment-Resistant Patients with Schizophrenia: Association with Psychopathology and Response to Antipsychotics

Zhang

Zhou

Cao

et al. 2005

Neuropsychopharmacol

178

110

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The bilateral communication between the immune and neuroendocrine systems plays an essential role in modulating the adequate response of the hypothalamic-pituitary-adrenal (HPA) axis to the stimulatory influence of cytokines and stress-related mediators. Growing evidence suggests that neuro-immune-endocrine crosstalk may be impaired in schizophrenia. We determined the relationship between cortisol, cytokines interleukin-2 (IL-2) and interleukin-6 (IL-6), and symptoms in schizophrenia during treatment with typical and atypical antipsychotic drugs. Subjects included 30 healthy controls (HC) and 78 schizophrenic (SCH) in-patients. SCH were randomly assigned to 12-week treatment with 6 mg/day of risperidone or 20 mg/day of haloperidol using a double-blind design. Clinical efficacy was determined using the Positive and Negative Syndrome Scale (PANSS). Serum cortisol and IL-2 levels were assayed by radioimmunometric assay, and serum IL-6 levels by quantitative enzyme-linked immunosorbent assay. Following a 2-week washout period, serum levels of cortisol, IL-2, and IL-6 were increased in patients with schizophrenia compared to HC. Elevations in cortisol were associated with increase in both IL-2 and IL-6 in SCH. Moreover, elevations in cortisol were associated with negative symptoms and IL-2 with positive symptoms. In all, 12 weeks of risperidone treatment significantly decreased elevated cortisol and improved negative symptoms, but produced similar effects on IL-2 and IL-6 as well as on positive symptoms compared to haloperidol. The improvement of negative symptoms was related to the change in cortisol. Our results suggest that the imbalance in the HPA axis and cytokine system in patients with SCH is implicated in clinical symptoms, and is improved with atypical antipsychotic treatment.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Cortisol and Cytokines in Chronic and Treatment-Resistant Patients with Schizophrenia: Association with Psychopathology and Response to Antipsychotics

Zhang

Zhou

Cao

et al. 2005

Neuropsychopharmacol

178

110

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“…Stress axis dysfunction may occur in schizophrenia as is indicated by the high levels of corticotropin-releasing hormone within the cerebrospinal fluid, failure to suppress plasma levels of cortisol in response to dexamethasone and overactivity of the pituitary-adrenal as demonstrated by high levels of resting cortisol and corticotropin (ACTH). Schizophrenia is associated with a reduced capacity to excrete water, high rates of polydipsia and hyponatremia, and a greater release of arginine vasopressin [10] . Yet, in a previous study researchers have found that patients with schizophrenia had higher plasma levels of ACTH and cortisol from 13.00 to 14.00 h, a time frame which strongly correlates with a 24-hour period supporting the contention that there is basal overactivity of the pituitary-adrenal in this disorder [10] .…”

Section: Discussionmentioning

confidence: 99%

Increased Levels of Nitric Oxide, Cortisol and Adrenomedullin in Patients with Chronic Schizophrenia

Yılmaz¹,

Herken

Çiçek³

et al. 2007

Med Princ Pract

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Objective: To investigate the levels of serum cortisol, dehydroepiandrosterone sulfate (DHEA-S), nitric oxide (NO) and adrenomedullin (AM) in schizophrenic patients. Subjects and Methods: Sixty-six male patients with chronic schizophrenia and 28 normal male subjects participated in this study. The duration of disease was 145 ± 120 (mean ± SD) months. Serum levels of cortisol and DHEA-S were measured by electrochemiluminescence; plasma nitrite levels as an index of NO were measured with the Griess reaction, while plasma AM concentration was measured by using high-performance liquid chromatography. Results: Patients (12.48 ± 3.2 µg/dl), as compared to controls (10.31 ± 3.1 µg/dl), had higher levels of baseline cortisol (p < 0.05). DHEA-S levels were lower in patients though this did not reach statistical significance (302 ± 156 µg/dl compared to control, 322 ± 96 µg/dl, p > 0.05). The mean levels of plasma AM and NO in the schizophrenic group (44.33 ± 5.07 pmol/l and 36.27 ± 17.6 µmol/l) were significantly higher than the levels in the control group (14.56 ± 4.03 pmol/l and 32.54 ± 7.14 µmol/l; p < 0.001, p < 0.03, respectively). There was a positive association between duration of disease and cortisol/DHEA-S ratio and cortisol level. Conclusion: The data show that schizophrenia is associated with abnormal levels of cortisol, DHEA-S, NO and AM.

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“…Changes in hypothalamic-pituitaryadrenal (HPA) axis and arginine vasopressin (AVP: antidiuretic hormone) activity, stress sensitive markers of hippocampal function (Herman et al, 2002(Herman et al, , 2005Nettles et al, 2000;Onaka and Yagi, 1998), however, generally are normal or even blunted in schizophrenia (Albus et al, 1982;Breier et al, 1988;Gispen-de Wied, 2000;Jansen et al, 1998Jansen et al, , 2000Kudoh et al, 1999;Marcelis et al, 2004). Previous reports of enhanced activity may instead be attributable to responses to specific stressors, systemic effects of the stimulus, severity, or lability of psychiatric symptoms, or to acute hospital admission, per se (Herman et al, 2005;Walder et al, 2000;Walsh et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine Responses to a Cold Pressor Stimulus in Polydipsic Hyponatremic and in Matched Schizophrenic Patients

Goldman

Gnerlich

Hussain

2006

Neuropsychopharmacol

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Schizophrenia, many believe, reflects an enhanced vulnerability to psychological stress. Controlled exposure to stressors, however, has produced inconclusive results, particularly with regards to neurohormones. Some of the variability may be attributable to the nature and psychological significance of the stimulus and failure to control physiologic confounds. In addition, it is possible that the heterogeneity of schizophrenia is an important factor. In a carefully designed study and in a controlled setting, we measured the neuroendocrine response of eight polydipsic hyponatremic (PHS), seven polydipsic normonatremic (PNS), and nine nonpolydipsic normonatremic (NNS) (ie normal water balance) schizophrenic in-patients as well as 12 healthy controls (HC) to two different stressors: one of which appears to influence neuroendocrine secretion through its psychological (cold pressor) and the other (upright posture) through its systemic actions. Subjects in the three psychiatric groups were stabilized and acclimated to the research setting, and all received saline to normalize plasma osmolality. Following the cold pressor, plasma adrenocorticotropin and cortisol levels showed a more prolonged rise in PHS patients relative to PNS patients. NNS patients, in contrast, exhibited blunted responses relative to both of the polydipsic groups and the HC. Peak vasopressin responses were also greater in PHS and blunted in NNS patients. Responses to the postural stimulus were similar across patient groups. These findings provide a mechanism for life threatening water intoxication in schizophrenia; help to reconcile conflicting findings of stress responsiveness in schizophrenia; and potentially identify a discrete patient subset with enhanced vulnerability to psychological stress.

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Blunted cortisol response to a psychosocial stressor in schizophrenia

Cited by 126 publications

References 27 publications

Cortisol and Cytokines in Chronic and Treatment-Resistant Patients with Schizophrenia: Association with Psychopathology and Response to Antipsychotics

Cortisol and Cytokines in Chronic and Treatment-Resistant Patients with Schizophrenia: Association with Psychopathology and Response to Antipsychotics

Increased Levels of Nitric Oxide, Cortisol and Adrenomedullin in Patients with Chronic Schizophrenia

Neuroendocrine Responses to a Cold Pressor Stimulus in Polydipsic Hyponatremic and in Matched Schizophrenic Patients

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