Abnormal acth and cortisol responses to ovine corticotropin releasing factor in patients with primary affective disorder

Gold, Philip W.; Calabkese, Joseph R.; Kling, Mitchel A.; Avgerinos, Peter C.; Khan, Ijaz Ahmad; Gallucci, William T.; Tomai, Thomas P.; Chrousos, George P.

doi:10.1016/0278-5846(86)90044-8

Cited by 41 publications

(20 citation statements)

References 26 publications

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“…GH in response to CRF has been also reported in acromegalics (Pieters et al, 1984a) and in patients with primary affective disorders (Gold et al, 1983). The frequency of a paradoxical increase in GH in response to CRF in this study was comparable to that in acromegalic reported previously (Pieters et al, 1984a), but much lower than that caused by TRH (Faglia et al, 1973a).…”

Section: Discussionsupporting

confidence: 73%

Comparative in vivo and in vitro Studies on Abnormal GH Secretion in Patients with Acromegaly.

et al. 1989

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Section: Discussionsupporting

confidence: 73%

Comparative in vivo and in vitro Studies on Abnormal GH Secretion in Patients with Acromegaly.

et al. 1989

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“…Because the overall pool of CSF CRH and plasma ACTH levels are glucocorticoid suppressible, 75 we previously suggested that quantitatively 'normal' CSF CRH and plasma ACTH levels in the face of hypercortisolism are, nevertheless, inappropriate for the patients' degree of hypercortisolism. 76 Our reasoning was as follows: we compared levels of CSF CRH in patients with depression associated with Cushing's disease (a pituitary disorder), who had matching degrees of hypercortisolism. We found extremely low levels of CSF CRH in our patients with Cushing's disease, whose CNS was normal but in whom very high levels of pituitary driven cortisol bombarded the hypothalamic CRH system, profoundly suppressing it.…”

Section: Role Of the Stress System In The Pathophysiology Of Melanchomentioning

confidence: 99%

“…Therefore, detecting a centrally mediated decrement in HPA axis function patients with atyical depression was initially difficult until we developed an endocrine paradigm for the differential diagnosis between adrenal, pituitary, and hypothalamic CRH-mediated hypoactivity of the HPA axis. 76,147 Prior efforts to document a centrally-mediated hypoactivity of the HPA axis were complicated by the facts that the HPA axis could be normally quiescent for many hours per day, and that low level pulses occurring many times a day were missing in sampling studies.…”

Section: Atypical Depressionmentioning

confidence: 99%

Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE states

2002

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Stress precipitates depression and alters its natural history. Major depression and the stress response share similar phenomena, mediators and circuitries. Thus, many of the features of major depression potentially reflect dysregulations of the stress response. The stress response itself consists of alterations in levels of anxiety, a loss of cognitive and affective flexibility, activation of the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, and inhibition of vegetative processes that are likely to impede survival during a life-threatening situation (eg sleep, sexual activity, and endocrine programs for growth and reproduction). Because depression is a heterogeneous illness, we studied two diagnostic subtypes, melancholic and atypical depression. In melancholia, the stress response seems hyperactive, and patients are anxious, dread the future, lose responsiveness to the environment, have insomnia, lose their appetite, and a diurnal variation with depression at its worst in the morning. They also have an activated CRH system and may have diminished activities of the growth hormone and reproductive axes. Patients with atypical depression present with a syndrome that seems the antithesis of melancholia. They are lethargic, fatigued, hyperphagic, hypersomnic, reactive to the environment, and show diurnal variation of depression that is at its best in the morning. In contrast to melancholia, we have advanced several lines of evidence of a down-regulated hypothalamic-pituitary adrenal axis and CRH deficiency in atypical depression, and our data show us that these are of central origin. Given the diversity of effects exerted by CRH and cortisol, the differences in melancholic and atypical depression suggest that studies of depression should examine each subtype separately. In the present paper, we shall first review the mediators and circuitries of the stress system to lay the groundwork for placing in context physiologic and structural alterations in depression that may occur as part of stress system dysfunction. Molecular Psychiatry (2002) 7, 254-275. DOI: 10.1038/sj/mp/4001032 Keywords: atypical depression; corticotropin releasing hormone (CRH); melancholic depression; norepinephrine (NE); stress Stress precipitates major depression and influences its incidence, severity and course. 1,2 The stress response and major depression share many features because of similar brain circuitries and mediators (reviewed in 3-5 ). Each is associated with a diminution of cognitive and affective flexibility, alterations in arousal, and perturbations in neuroendocrine and autonomic function (reviewed in 5 ). Because major depression is a heterogeneous disorder, we focus here on two subtypes, melancholic and atypical depression. Our data and those of others indicate that the principal arousal producing mediators of the stress response, such as the corticotropin releasing hormone (CRH) system, are hyperactive in melancholic depression. 6 Not surprisingly, melan- cholia is associated with anxiety, dread of the ...

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“…It has been shown that GH levels are not influenced by the administrations of CRH to normal subjects, whether ovine CRH (Grossman et al, 1982;Orth et al, 1983;Hermus et al, 1984) or human CRH (Schurmeyer et al, 1984). However, paradoxical GH responses to oCRH have been reported in patients with primary affective disorders (Gold et al, 1983), and these responses were observed to be abolished by alpha-adrenergic blockade in subhuman primates in the same study. We recently demonstrated that metoclopramide acts additively with hCRH to stimulate ACTH secretion in normal men through a dopamine antagonist-mediated mechanism and that a normal cortisol response to metoclopramide-CRH was absent in acromegalic patients (Nishida et al, 1987).…”

mentioning

confidence: 51%

Provocation of a Paradoxical Growth Hormone Response to Corticotropin-Releasing Hormone by Pretreatment with Metoclopramide in Patients with Acromegaly and Normal Subjects.

Nishida¹,

Matsuki²,

Adachi³

et al. 1988

Endocrinol Japon

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Two of 7 patients with acromegaly and one of 7 normal subjects exhibited a paradoxical rise in growth hormone (GH) to human corticotropin-releasing hormone (CRH) when pretreated with metoclopramide, although CRH alone did not induce an increase in GH. In one of these two patients with acromegaly, the GH increase to metoclopramide alone also reached the criteria of a paradoxical response.These two acromegalic patients showed a GH increase to metoclopramide pretreatment before and up to two months after surgery. In another acromegalic patient, whose GH level remained high 5 months after surgery, metoclopramide induced an increase in GH level, while in a patient who had an above-normal GH level 18 months after surgery, the resumption of physiological GH secretion after surgery was evidenced by a postoperative absence of a GH response to metoclopramide.It is suggested from these results that the GH response to metoclopramide and the metoclopramideprovoked GH response to CRH in patients with acromegaly result from the secretion of GH from nonadenomatous cells of the pituitary.

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Abnormal acth and cortisol responses to ovine corticotropin releasing factor in patients with primary affective disorder

Cited by 41 publications

References 26 publications

Comparative in vivo and in vitro Studies on Abnormal GH Secretion in Patients with Acromegaly.

Comparative in vivo and in vitro Studies on Abnormal GH Secretion in Patients with Acromegaly.

Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE states

Provocation of a Paradoxical Growth Hormone Response to Corticotropin-Releasing Hormone by Pretreatment with Metoclopramide in Patients with Acromegaly and Normal Subjects.

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