Dexamethasone suppression, protirelin stimulation, and insulin infusion in subtypes of recovered depressive patients

doi:10.1016/0165-1781(83)90031-8

Psychiatry Research

Volume 9, Issue 2, June 1983, Pages 99-106

https://doi.org/10.1016/0165-1781(83)90031-8 Get rights and content

Abstract

Twenty-eight patients (10 bipolar, 13 depressive spectrum disease, and 5 familial pure depressives), recovered from depression for an average of 1 year, underwent a series of basal and provocative endocrine tests. No significant differences were found among depressive subtypes in thyrotropin, cortisol, or growth hormone measurements either before or after provocative testing with the exception of growth hormone response to insulin-induced hypoglycemia. Patients with depressive spectrum disease showed a significantly different growth hormone response to insulin-induced hypoglycemia than patients with bipolar disorder, a finding which suggests differences in α-adrenergic receptor sensitivity between these groups.

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Patients with endogenous depression (major affective disorder) frequently have high cortisol levels, but the diurnal rhythm is usually maintained and they do not develop the physical signs of Cushing's syndrome. On the other hand, depression is a frequent feature of Cushing's syndrome regardless of etiology, and it is often relieved when the cortisol levels are reduced, by whatever means. The mechanisms of the hypercortisolemia and resistance to dexamethasone suppression commonly found in endogenous depression are poorly understood; contrary to expectations, ACTH levels are not clearly elevated. There is striking difference in the psychiatric features seen in endogenous hypercorticism compared to those seen after exogenous administration of glucocorticoids or ACTH. This suggests that either there are other stimulating or modifying factors besides ACTH or that the steroids stimulated by ACTH or other peptides differ from those in control subjects, i.e. there may be an alteration in the metabolism of steroids in depression. Little is known about the metabolic changes or the many steroids besides glucocorticoids produced by the hyperactive steroid-producing tissue. Preliminary studies suggest that major depression may be improved by steroid suppression. It is hypothesized that steroids themselves may be important in causing and perpetuating depression.
TSH response to TRH and family history of alcoholism
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The thyrotropin (TSH) response to intravenous thyrotropin-releasing hormone (TRH) was evaluated in 10 sons of alcoholic fathers (FHP group) and 10 matched controls (FHN group). No differences were observed between the two groups in basal TSH, peak TSH levels, on the incidence of TSH-blunting to TRH. Though there was a trend for a less intense TSH response over time after the TRH infusion, the difference between the family groups was not significant. These results are not consistent with some previous reports of an increased percentage of blunted TSH response to TRH for children of alcoholics. The clinical and research implications of these findings are discussed.
Human growth hormone releasing factor infusion effects on plasma growth hormone in affective disorder patients and normal controls
1988, Peptides
In a preliminary, prospective pilot study, five patients with major depressive disorder and eleven age and sex matched normal controls received intravenous human growth hormone releasing factor (hGRF) (1 μg/kg in 5 cc of normal saline infused over five minutes) and placebo. Thirty minutes after insertion of the catheter, blood was sampled every 15 minutes for thirty minutes prior to and for 2 hours subsequent to intravenous infusion of hGRF or placebo. hGRF but not placebo caused significant elevations of plasma growth hormone levels in all subjects. Of interest, the depressed patients had a significantly attenuated rise in plasma growth hormone concentrations when compared with the normal controls. These results must be considered preliminary awaiting replication with a larger subject population.
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The HPA axis response to insulin hypoglycemia in depression
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Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, demonstrated by failure to suppress cortisol secretion after dexamethasone, is found in approximately 50% of patients with major depression (MD). In this study, we examined the response of adrenocorticotrophic hormone (ACTH) and cortisol to insulin-induced hypoglycemia in 20 healthy controls and 18 inpatients with MD [12 dexamethasone suppressors (S) and 5 dexamethasone nonsuppressors (NS)]. After the administration of 0.15 U/kg of regular insulin, both controls and patients with MD showed an increase in plasma ACTH and cortisol levels. Controls had a significantly higher ACTH peak (p < 0.01) and ACTH increment (p < 0.01) than MD patients. There were no statistically significant differences between patients who were S and NS. Although baseline plasma cortisol levels were significantly higher in MD patients, there were no significant differences in the peak cortisol or increment in plasma cortisol after hypoglycemia between patients with MD and controls or between patients who were S and those who were NS. These findings suggest that a defect exists in the regulation of the HPA axis at the pituitary level in MD and that this defect is not necessarily reflected in the dexamethasone suppression status of the patient.

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Dexamethasone suppression, protirelin stimulation, and insulin infusion in subtypes of recovered depressive patients

Abstract

Psychoneuroendocrinology

Psychoneuroendocrinology

Psychoneuroendocrinology

Biochemical Biophysics Acta

Neuroendocrinology of depresion—A discussion

Psychopharmacology Bulletin

Hypothalamic-pituitary function in depressive illness: Insensitivity to hypoglycaemia

British Medical Journal

Neuroendodrinologische Veranderungen unter Langzeibehandlung mit Lithiumsalzen

Pharmakopsychiatrie

Diagnostic criteria for use in psychiatric research

Archives of General Psychiatry

Effects of estrogen and sex difference on secretion of human growth hormone

Journal of Clinical Endocrinology and Metabolism

A rating scale for depression

Journal of Neurology, Neurosurgery, and Psychiatry

Measurement of urinary free cortisols by competitive protein-binding radioassay in hypoadrenal states

Journal of Clinical Endocrinology and Metabolism

Effect of adrenergic receptor blockade on cortisol and GH response to insulin-induced hypoglycemia in man

International Journal of Clinical Pharmacology and Biopharmacy

Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey: II. GH and cortisol secretion

Endrocrinology

Characterization of the normal temporal pattern of plasma corticosteroid levels

Journal of Clinical Endocrinology

Differentiation of depressive subtypes by insulin insensitivity in the recovered phase

Archives of General Psychiatry