Afternoon cortisol levels before (spontaneous) and after suppression with dexamethasone or oxazepam in depressed patients

Christensen, P.; Gram, Lars F.; Kragh‐Sörensen, P.; Nielsen, Sebastian Werngreen

doi:10.1016/0165-0327(86)90001-7

Cited by 14 publications

(13 citation statements)

References 30 publications

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“…In addition, the benzodiazepine antagonist 3-carboethoxybeta-carboline (beta-CCE) raises cortisol levels in rhesus monkeys (8). Cortisol levels after benzodiazepine suppression thus might be useful in the investigation of depressed patients, and the present study was undertaken in order to confirm and extend our earlier findings (7). Cortisol levels after benzodiazepine suppression thus might be useful in the investigation of depressed patients, and the present study was undertaken in order to confirm and extend our earlier findings (7).…”

supporting

confidence: 52%

“…This suppression has been demonstrated in both healthy volunteers ( 6 ) and depressed patients (7). Earlier studies by our group have shown a relationship between high cortisol levels and the feeling of stress or distress in depressed patients (7,9). Earlier studies by our group have shown a relationship between high cortisol levels and the feeling of stress or distress in depressed patients (7,9).…”

mentioning

confidence: 64%

“…This suppression has been demonstrated in both healthy volunteers ( 6 ) and depressed patients (7). This suppression has been demonstrated in both healthy volunteers ( 6 ) and depressed patients (7).…”

mentioning

confidence: 76%

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Afternoon plasma cortisol in relation to depression A replication study

Christensen

Lolk²,

Pedersen³

et al. 1988

Acta Psychiatr Scand

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In 37 consecutive depressed inpatients afternoon plasma cortisol (1500-1520 h) was measured in 3 ways: 1) spontaneously; 2) 2 h after oral administration of 60 mg oxazepam; and 3) 16 h after oral administration of 2 mg dexamethasone. Both oxazepam and dexamethasone caused a significant suppression of cortisol secretion. Spontaneous and suppressed cortisol levels correlated significantly to stress/distress items on the Hamilton Rating Scale for Depression (sum of items 8, 9, 10 and 12), whereas no correlations to age, or type of depression were found. In an earlier similar study of 35 patients both spontaneous and suppressed cortisol levels correlated significantly with age, type and severity of depression as well as with the stress/distress items. Those patients were older, more depressed (HRSD-17) and had higher stress/distress scores compared with the present sample of 37 patients. The consistent finding of a correlation with the stress/distress items suggest that this factor is important in relation to the hypersecretion of cortisol during depression and this may explain the limited diagnostic power of spontaneous and suppressed cortisol levels.

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confidence: 52%

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confidence: 64%

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Afternoon plasma cortisol in relation to depression A replication study

Christensen

Lolk²,

Pedersen³

et al. 1988

Acta Psychiatr Scand

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“…Hence, while alprazolam failed to influence CRH-induced ACTH release from dispersed pituicytes, alprazolam significantly inhibited in vitro 5HT-induced CRH release from rat hypothalamic organ cultures at doses as low as 10~1 0 M. Moreover, alprazolam was 40 times more potent in suppressing 5HT-induced CRH secretion than diazepam. The effect of alprazolam on serotonin-induced CRH release seems mediated through interaction with the benzodiazepine component of the (19,(51)(52)(53) and depressed patients (53)(54)(55). In the rat, benzodiazepines seem to suppress plasma corticosterone levels during stress-induced hypothalamic-pituitary-adrenal axis activation (56,57), and this effect is counteracted by the imidazodiazepine Ro 15-1788 (58).…”

Section: Discussionmentioning

confidence: 98%

In Vitroandin VivoEffects of the Triazolobenzodiazepine Alprazolam on Hypothalamic Pituitary-Adrenal Function: Pharmacological and Clinical Implications*

Kalogeras

Calogero²,

Kuribayiashi³

et al. 1990

The Journal of Clinical Endocrinology & Metabolism

118

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We report here a study of the effects of alprazolam on in vivo pituitary-adrenal function in jacketed nonrestrained nonhuman primates and on in vitro CRH release from rat hypothalami and ACTH release from rat dispersed anterior pituicytes. We undertook this study because alprazolam is the only benzodiazepine effective in treating both major depressive and anxiety disorders, and recent data suggest that the hypercortisolism of major depression reflects hypersecretion of CRH. Moreover, the intracerebroventricular administration of CRH can reproduce many of the components of the symptom complex of major depression, including not only hypercortisolism, but also hypothalamic hypogonadism, decreased libido, anorexia, and intense anxiety. As a comparison, we also assessed the effects of diazepam on in vitro CRH release, because in contrast to alprazolam, diazepam is effective in anxiety states but not in depression. Alprazolam (0.01-0.3 mg/kg, iv) produced a dose-dependent inhibition of both plasma ACTH and cortisol secretion in non-restrained adult male rhesus monkeys. Our in vitro studies showed that alprazolam significantly inhibited serotonin (5HT)-induced CRH release in a dose-dependent fashion (10(-10)-10(-5) M). Diazepam also inhibited 5HT-induced CRH release, but was 40 times less potent than alprazolam. Alprazolam was ineffective in blocking basal or CRH-induced ACTH release from rat dispersed anterior pituicytes, suggesting that its in vivo effects are through inhibition of CRH secretion. As expected, the inactive benzodiazepine ligand Ro 15-1788 inhibited the effects of alprazolam on 5HT-induced CRH release, but this occurred only at doses below 10(-7) M. Interestingly, when incubated alone in higher doses with our rat hypothalamic organ culture, Ro 15-1788, like alprazolam, produced a dose-dependent inhibition of 5HT-induced CRH release (10(-7)-10(-5) M), suggesting an agonistic action of Ro 15-1788 at the benzodiazepine receptor at higher concentrations. We conclude that alprazolam is capable of suppressing the primate pituitary-adrenal axis, and that this suppression most likely reflects suppression of the CRH neuron rather than of the pituitary corticotroph cell. We speculate that the enhanced capacity of alprazolam to suppress the CRH neuron relative to other benzodiazepines may contribute to its unique efficacy among this class of drugs in the treatment of major depression. The capacity of Ro 15-1788 to reverse alprazolam-induced suppression of the CRH neuron indicates that the effects of alprazolam are mediated at least in part via its interaction with the benzodiazepine component of the gamma-aminobutyric acidA macromolecular complex.

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“…In preclinical studies, it has been shown that benzodiazepines attenuate stress-and drug-induced HPA-axis activation (de Souza, 1990). Moreover, both studies in healthy volunteers (Breier et al, 1992;Schuckit et al, 1992) and in patients with major depression (Christensen et al, 1986) and PD (Roy-Byrne et al, 1991) revealed that benzodiazepines reduce HPA-axis activity. A comparison of cortisol AUC before and after placebo treatment also revealed a slight but statistically significant reduction of cortisol release after the second CCK-4 challenge.…”

Section: Discussionmentioning

confidence: 99%

Effects of Alprazolam on Cholecystokinin-Tetrapeptide-Induced Panic and Hypothalamic–Pituitary–Adrenal-Axis Activity: A Placebo-Controlled Study

Zwanzger

Eser

Aicher

et al. 2002

Neuropsychopharmacol

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Cholecystokinin-tetrapeptide (CCK-4) induces panic attacks both in patients with panic disorder (PD) and healthy volunteers. It has been shown that panic elicited by CCK-4 is improved after treatment with antidepressants. Moreover, a reduction of CCK-4-induced panic has also been demonstrated after treatment with lorazepam in single subjects and after selective GABAergic treatment with vigabatrin. Although benzodiazepines are widely used as anxiolytics, no controlled study on the effects of benzodiazepines on CCK-4-induced panic symptoms is available so far. Therefore, we investigated the effects of alprazolam and placebo on CCK-4-induced panic symptoms in a double-blind, placebo-controlled study. A total of 30 healthy subjects were challenged with 50 mg CCK-4. Out of these 30 subjects, 26 showed a marked panic response to CCK-4. Subjects were rechallenged after a 7-day interval and treated with 1 mg alprazolam or placebo 1 h prior to the second CCK-4 challenge. Panic was assessed using the acute panic inventory (API) and a DSM-IV-derived panic symptom scale (PSS). Moreover, the number of reported symptoms and self-rated anxiety and arousal were recorded. We found a significant reduction of the API and PSS scores and of the number of reported symptoms compared to placebo. Moreover, compared to placebo the CCK-4-induced ACTH and cortisol release were significantly attenuated during the CCK-4 challenge after alprazolam treatment. However, also placebo treatment reduced CCK-4-induced anxiety and HPA-axis activation to a certain extent. In conclusion, our data show that alprazolam reduces CCK-4-induced panic, which supports the hypothesis of a possible interaction between the GABA and the CCK system.

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Afternoon cortisol levels before (spontaneous) and after suppression with dexamethasone or oxazepam in depressed patients

Cited by 14 publications

References 30 publications

Afternoon plasma cortisol in relation to depression A replication study

Afternoon plasma cortisol in relation to depression A replication study

In Vitroandin VivoEffects of the Triazolobenzodiazepine Alprazolam on Hypothalamic Pituitary-Adrenal Function: Pharmacological and Clinical Implications*

Effects of Alprazolam on Cholecystokinin-Tetrapeptide-Induced Panic and Hypothalamic–Pituitary–Adrenal-Axis Activity: A Placebo-Controlled Study

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