Biomedical subjects

P Avgerinos

Publications and source records attributed to P Avgerinos.

4 recordsLinked to original sources

PubMed1988

The CRH stimulation test in bereaved subjects with and without accompanying depression.

We studied recently bereaved individuals with the corticotropin-releasing hormone (CRH) stimulation test. Subjects with a bereavement complicated by a depressive illness (n = 9) had significantly higher basal plasma cortisol levels and smaller plasma adrenocorticotropic hormone (ACTH) responses to CRH than either subjects with an uncomplicated bereavement (n = 19) or normal controls (n = 34). Subjects with depressed bereavement showed ACTH responses to CRH similar to those of depressed patients (n = 30). Bereaved subjects who had received psychotropic medications in the past (n = 13), compared with those who had not (n = 15), showed significantly smaller plasma ACTH responses to CRH. Significantly more subjects with bereavement complicated by depression, as compared to subjects whose bereavement was uncomplicated, had a past history of treatment for depression. These results suggest that predisposed individuals may respond to the stress of bereavement with a depressive illness accompanied by dysregulation of the hypothalamic-pituitary-adrenal axis.

Adjustment Disorders↗

PubMed1986

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

To further explore hypothalamic pituitary adrenal regulation in patients with affective illness, we administered 1 microgram/kg of synthetic ovine corticotropin releasing factor at 2000h to 26 drug-free patients with this disorder and to 15 healthy controls. Compared to controls, depressed patients (N = 12) showed a significant elevation in baseline cortisol and significant reductions in the net ACTH and cortisol responses to corticotropin releasing factor. These findings were normal in manic (N = 6) and improved (N = 8) subjects. An additional finding was that baseline cortisol and net ACTH and cortisol responses to CRF were negatively correlated in the entire group of patients and controls as well as in the patients alone. These data indicate that the reduced ACTH and cortisol responses to CRF in depression reflect normal functioning of the pituitary corticotroph cell (i.e., that the negative feedback effect of cortisol on ACTH secretion in depression is physiologically intact, effectively serving as a brake on the ACTH response to exogenous CRF. Thus, the hypercortisolism of depression may be due to a hypothalamic defect, possibly involving hypersecretion of endogenous CRF. This possibility may be of particular interest in light of clinical observations that depression can often be precipitated by stress and by data in experimental animals that CRF may influence several processes known to be altered in the overall symptom complex of depression.

Adrenocorticotropic Hormone↗

PubMed1985

Corticotropin releasing factor: basic studies and clinical applications.

Corticotropin releasing factor (CRF) is a newly sequenced peptide first isolated from sheep hypothalami and thought to be an important modulator of both the pituitary-adrenal axis and the sympathetic nervous system. We administered intravenous, intramuscular, and intracerebroventricular CRH to non-human primates and measured plasma ACTH, beta endorphin, cortisol, GH and PRL responses to CRF. In addition, we determined the pharmacokinetic properties of I125 in these primates. We administered CRF as an intravenous bolus or as a continuous infusion to normal volunteers and as an intravenous bolus to patients with disorders of the hypothalamic-pituitary-adrenal axis, such as Cushing's syndrome and adrenal insufficiency, and patients with endogenous depression and mild hypercortisolism, and assessed their plasma ACTH, cortisol, GH and PRL responses. In addition, we determined the pharmacokinetic properties of CRF in man by measuring CRF immunoreactivity in plasma. CRF given intravenously to primates or man is a slowly metabolized, long-acting, secretagogue of ACTH, beta-endorphin and cortisol. When given intracerebroventricularly to primates it stimulates the hypothalamic-pituitary-adrenal axis without escaping into the plasma and it is actively cleared in the CNS. It does not cross the blood brain barrier appreciably when given intravenously. CRF given to primates and men as an intravenous continuous infusion has only mild ACTH stimulating effects and this may be due to an intact cortisol negative feedback system. Finally, CRF causes characteristic plasma hormone responses in patients with Cushing's disease, adrenal insufficiency and depression.

Adrenal Insufficiency↗

PubMed1984

The corticotropin-releasing hormone stimulation test: a possible aid in the evaluation of patients with adrenal insufficiency.

Ten patients with adrenal insufficiency receiving chronic glucocorticoid therapy were studied. All had subnormal plasma cortisol responses to ovine corticotropin-releasing hormone ( CRH ) (1 microgram/kg as an iv bolus) 12-60 h after discontinuation of steroid treatment. Plasma ACTH responses to CRH fell into three different patterns. The first three patients with primary adrenal insufficiency had high basal ACTH levels and augmented ACTH responses to CRH . A fourth such patient, however, treated with pharmacologic doses of prednisone, had a low normal ACTH response. Patients with secondary adrenal insufficiency had either low basal ACTH levels and diminished responses to CRH or low basal ACTH values but prolonged and augmented plasma ACTH responses to CRH with a delayed peak. We postulate that the group of patients with the former pattern have pituitary gland destruction whereas the patients with the latter pattern have hypothalamic CRH deficiency. Thus, CRH may be useful in differentiating between hypothalamic and pituitary causes of adrenal insufficiency.

Adolescent↗