Hypothalamic-pituitary-adrenal axis activity in panic disorder: Effects of alprazolam on 24 h secretion of adrenocorticotropin and cortisol

Abelson, James L.; Curtis, George C.; Cameron, Oliver G.

doi:10.1016/0022-3956(95)00035-6

Cited by 67 publications

(67 citation statements)

References 27 publications

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“…Our findings that chronic alprazolam treatment resulted in a progressive increase in predose cortisol levels contrasts with previous reports that chronic alprazolam treatment was associated with significantly lower plasma or urinary free cortisol relative to the predrug baseline (Abelson et al, 1996;Lopez et al, 1990a). The reasons for the discrepancy may be attributable to several methodological differences, such as uncontrolled dose-to-sampling intervals for cortisol determination, differences in target population, prior use of psychotropic medications, inclusion of placebo group, and pharmacokinetic factors.…”

Section: Discussioncontrasting

confidence: 99%

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Interdose Elevation in Plasma Cortisol During Chronic Treatment with Alprazolam but not Lorazepam in the Elderly

Pomara

Willoughby

Ritchie

et al. 2003

Neuropsychopharmacol

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Benzodiazepines (BZPs) have been shown to reduce hypothalamic-pituitary-adrenal (HPA) axis activity acutely in normal humans. In contrast, the effects of chronic BZP treatment on the HPA axis have not been well studied, especially in the geriatric population. This study examined the acute and chronic effects (3 weeks) of alprazolam and lorazepam on plasma cortisol in 68 subjects (60-83 years) who received 0.25 or 0.50 mg b.i.d. alprazolam, or 0.50 or 1.0 mg b.i.d. lorazepam, or placebo orally according to a randomized, doubleblind, placebo-controlled parallel design. Memory assessment and blood samples for plasma cortisol were obtained prior to the morning dose on days 0, 7, 14, and 21, and at 1, 2.5, and 5 h postdrug on days 0 and 21. Assessments of anxiety and depression were carried out at days 0, 7, 14, and 21 before drug administration. Plasma cortisol was affected compared to placebo only by the 0.5 mg alprazolam dose. During the first and the last day of treatment, there was a significant drop in cortisol at 2.5 h after alprazolam compared to placebo. The predose cortisol levels increased significantly during chronic alprazolam treatment, and correlations were found between these cortisol changes and changes in depression, anxiety, and memory scores. These findings suggest that even a short period of chronic treatment with alprazolam, but not lorazepam, may result in interdose HPA axis activation in the elderly, consistent with drug withdrawal. If confirmed, this effect may contribute to an increased risk for drug escalation and dependence during chronic alprazolam treatment.

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Section: Discussioncontrasting

confidence: 99%

“…Data on the influence of chronic BZP treatment remain sparse and the relevant studies have been limited to patients with panic disorder (Abelson et al, 1996;Fukuda et al, 1998;Lopez et al, 1990a). Interestingly, these individuals exhibit baseline hypercortisolemia (Lopez et al, 1990a), a potentially confounding effect.…”

Section: Introductionmentioning

confidence: 99%

Interdose Elevation in Plasma Cortisol During Chronic Treatment with Alprazolam but not Lorazepam in the Elderly

Pomara

Willoughby

Ritchie

et al. 2003

Neuropsychopharmacol

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“…For instance, Yehuda (2006) has reported lower cortisol levels, blunted diurnal rhythm, and increased cortisol suppression in response to dexamethasone suppression in post-traumatic stress disorder (PTSD), while others have found no differences in circadian salivary (Rasmusson et al, 2001;Altemus et al, 2003) and 24 h urinary cortisol (Baker et al, 1999;Rasmusson et al, 2001;Young and Breslau, 2004), or even higher levels of 24 h urinary (Pitman and Orr, 1990;Lemieux and Coe, 1995) and daytime salivary cortisol (Lindley et al, 2004). Similarly, some studies have characterized panic disorder by elevated cortisol concentrations at night (Abelson and Curtis, 1996) and impaired negative feedback (Erhardt et al, 2006), while others have found no differences in mean urinary cortisol levels (Uhde et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Salivary cortisol is associated with diagnosis and severity of late-life generalized anxiety disorder

Mantella

Butters

Amico

et al. 2008

Psychoneuroendocrinology

188

151

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SummaryAge-associated alterations in hypothalamic-pituitary-adrenal (HPA) axis functioning may make individuals more susceptible to HPA dysregulation in the context of mood and anxiety disorders. Little to no research has been done to examine HPA axis function in generalized anxiety disorder (GAD), particularly in late-life GAD, the most prevalent anxiety disorder in the elderly. The study sample consisted of 71 GAD subjects and 40 nonanxious comparison subjects over 60 years of age. We examined the hypotheses that elderly individuals with GAD will have elevated salivary cortisol levels compared to nonanxious subjects, and that elevated cortisol levels in GAD will be associated with measures of symptom severity. We report that late-life GAD is characterized by elevated basal salivary cortisol levels, with higher peak cortisol levels and larger areas under the curve, compared to nonanxious subjects. Additionally, severity of GAD as measured by the GAD Severity Scale and the Penn State Worry Questionnaire are positively correlated with cortisol levels. These data demonstrate HPA axis dysfunction in late-life GAD and suggest the need for additional research on the influence of aging on HPA axis function in mood and anxiety disorders.

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“…Patients with anxiety also present abnormalities in regulation of the hypothalamic-pituitary-adrenal (HPA) axis, with reports of blunted ACTH response to CRF (Curtis et al 1997;Holsboer et al 1987;Roy-Byrne et al 1986) indicative of a possible increase in negative feedback within the HPA axis in patients and abnormal circadian rhythms in cortisol secretion (Abelson and Curtis 1996). Inhalation of 35% CO 2 , a model for panic discussed above, also causes increased HPA responsivity in the form of enhanced cortisol and ACTH levels in both panic patients and control subjects (van Duinen et al 2005(van Duinen et al , 2006.…”

Section: Translational Research With Mglur Binding: Development Of a mentioning

confidence: 99%

Metabotropic glutamate receptor modulation, translational methods, and biomarkers: relationships with anxiety

Nordquist

Steckler²,

Wettstein

et al. 2008

Psychopharmacology

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Rationale The increasing awareness of the need to align clinical and preclinical research to facilitate rapid development of new drug therapies is reflected in the recent introduction of the term "translational medicine". This review examines the implications of translational medicine for psychiatric disorders, focusing on metabotropic glutamate (mGlu) receptor biology in anxiety disorders and on anxiety-related biomarkers. Objectives This review aims to (1) examine recent progress in translational medicine, emphasizing the role that translational research has played in understanding of the potential of mGlu receptor agonists and antagonists as anxiolytics, (2) identify lacunas where animal and human research have yet to be connected, and (3) suggest areas where translational research can be further developed.Results Current data show that animal and human mGlu 5 binding can be directly compared in experiments using the PET ligand 11 C-ABP688. Testing of the mGlu 2/3 receptor agonist LY354740 in the fear-potentiated startle paradigm allows direct functional comparisons between animals and humans. LY354740 has been tested in panic models, but in different models in rats and humans, hindering efforts at translation. Other potentially translatable methods, such as stress-induced hyperthermia and HPA-axis measures, either have been underexploited or are associated with technical difficulties. New techniques such as quantitative trait loci (QTL) analysis may be useful for generating novel biomarkers of anxiety. Conclusions Translational medicine approaches can be valuable to the development of anxiolytics, but the amount of cross-fertilization between clinical and pre-clinical departments will need to be expanded to realize the full potential of these approaches.

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Hypothalamic-pituitary-adrenal axis activity in panic disorder: Effects of alprazolam on 24 h secretion of adrenocorticotropin and cortisol

Cited by 67 publications

References 27 publications

Interdose Elevation in Plasma Cortisol During Chronic Treatment with Alprazolam but not Lorazepam in the Elderly

Interdose Elevation in Plasma Cortisol During Chronic Treatment with Alprazolam but not Lorazepam in the Elderly

Salivary cortisol is associated with diagnosis and severity of late-life generalized anxiety disorder

Metabotropic glutamate receptor modulation, translational methods, and biomarkers: relationships with anxiety

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