The Combined Dexamethasone‐Suppression/CRH‐Stimulation Test in Alcoholics During and After Acute Withdrawal

Hundt, Walter; Zimmermann, U.; Pöttig, M.; Spring, K.; Holsboer, Florian

doi:10.1111/j.1530-0277.2001.tb02268.x

Cited by 56 publications

(17 citation statements)

References 34 publications

(40 reference statements)

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“…In humans, acute exposure to alcohol profoundly activates the HPA axis, and many alcoholics develop HPA tolerance after chronic alcohol exposure [Adinoff et al, 1990;Inder et al, 1995]. In contrast, acute alcohol withdrawal transiently activates HPA axis [Hundt et al, 2001;Zimmermann et al, 2003]. Also, the noradrenergic system, the known key stress mediator that is involved in stress and anxiety responses as demonstrated before [e.g., Tunstall et al, 2017], probably interacts with AVP and CRF systems to regulate alcohol drinking and HPA activity.…”

Section: V1b Receptor and Arginine Vasopressin (Avp) Systemmentioning

confidence: 90%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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Addiction to specific drugs (such as alcohol, psychostimulants and opioids) shares some common direct or downstream effects on the brain stress-responsive systems, including arginine vasopressin and its V1b receptors, dynorphin and the kappa opioid receptors, proopiomelanocortin/β-endorphin and the mu opioid receptors, and the endocannabinoids. Further study of these systems, through laboratory-based and translational research, could lead to the discovery of novel treatment targets and the early optimization of interventions (for example, combination) for the pharmacological therapy of alcoholism.

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Section: V1b Receptor and Arginine Vasopressin (Avp) Systemmentioning

confidence: 90%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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“…There was no difference between the two groups in cortisol response to oCRF with or without alcohol administration. In alcoholic subjects, acute withdrawal (12-72 h after last alcohol use) and medium-term abstinence (13-42 days after last alcohol use) are both associated with decreased ACTH response following 100 mg hCRF (von Bardeleben et al, 1989;Hundt et al, 2001). While these findings are similar to those seen in major depression, the authors did not control for affective states.…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor Testing Reveals a Dose-Dependent Difference in Methadone Maintained Vs Control Subjects

Schluger

Bart

Green

et al. 2003

Neuropsychopharmacol

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Opiate addiction is associated with abnormal function of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis. In general, addiction and withdrawal are associated with abnormal HPA responsivity as demonstrated by baseline, dexamethasone, and metyrapone testing. Following stabilization in methadone maintenance treatment, normalization of HPA axis responsivity is observed. To further investigate HPA axis function associated with heroin addiction and its treatment, saline placebo and human corticotropin-releasing factor (hCRF) were administered intravenously in two doses, one dose lower (0.5 mg/kg) and one dose higher (2.0 mg/kg) than the dose used in standard clinical diagnostics (100 mg), to 16 normal male volunteer controls (NV) and eight male stable-dose methadone-maintained former heroin addicts without ongoing drug or alcohol abuse or dependence (MM). Plasma adrenocorticotrophic hormone (ACTH) and cortisol levels were determined at serial time points. There was no difference in hormonal measurements between the two groups following placebo. NV as well as MM displayed a dose-response effect in plasma ACTH and cortisol levels. MM displayed a significantly greater increase in plasma ACTH levels than the NV following high-dose but not low-dose hCRF (po0.05). There was no significant difference in plasma cortisol levels between the two groups following high-dose hCRF. Thus, despite earlier documented normalization of behavioral function and of several measures of neuroendocrine function during long-term methadone maintenance, some abnormalities in HPA axis responsivity that may be a consequence of heroin exposure, or that may have existed prior to the addiction, can persist during stable methadone treatment.

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“…Such chronic elevations of CRF are associated with depression, which shows significant comorbidity with alcoholism. Furthermore, during withdrawal from EtOH, the response to CRF appears to be disrupted compared with the response of normal controls (Hundt et al 2001). Recovering alcoholics show diminished sensitivity to challenge with exogenously administered CRF, demonstrating a long-lasting change in the HPA axis (von Bardeleben et al 1989;Costa et al 1996;Ehrenreich et al 1997), which is similar to the effects of chronic stress.…”

Section: Introductionmentioning

confidence: 96%

Corticotropin-releasing factor overexpression decreases ethanol drinking and increases sensitivity to the sedative effects of ethanol

et al. 2004

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The Combined Dexamethasone‐Suppression/CRH‐Stimulation Test in Alcoholics During and After Acute Withdrawal

Abstract: We conclude that the HPA system is severely disturbed during alcohol withdrawal, possibly reflecting an exaggerated release of hypothalamic corticotropin and vasopressin.

Cited by 56 publications

References 34 publications

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Corticotropin-Releasing Factor Testing Reveals a Dose-Dependent Difference in Methadone Maintained Vs Control Subjects

Corticotropin-releasing factor overexpression decreases ethanol drinking and increases sensitivity to the sedative effects of ethanol

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