Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism

F. Cordido
R. Peino
T. Martínez-Ramonde
52

Abstract

Endogenous Cushing's syndrome, obesity and chronic glucocorticod treatment are characterized by blunted GH secretion. The administration of GHRH is capable of stimulating a small but significant PRL increase in normal subjects. The current study was designed to determine plasma PRL levels in response to GHRH, studied in three different situations characterized by a blunted GH secretion. Obese patients (n = 6) with a weight over 30% of ideal body weight, patients with active Cushing's syndrome, and normal volunteers treated with dexamethasone 22 mg per os over two days before the pituitary challenge were studied. As a control group 18 normal subjects of similar age and sex were studied. GH and PRL was determined at intervals after GHRH (1 microgram/kg). GHRH-induced GH secretion was markedly reduced in patients with obesity, patients with endogenous Cushing's syndrome and volunteers treated with dexamethasone. In contrast, GHRH-induced PRL secretion was not affected in these three clinical situations. In summary, in three situations characterized for an impairment of the somatotroph cell, due to a primary intrinsic defect or to a functional hypothalamic alteration, there is a persistent GHRH-induced PRL secretion, suggesting that prolactin could be released by mammosomatotrophs that function normally in spite of hyposomatotropism.

Keywords:
Gonadotropin-Releasing Hormone, Adult, Anterior/drug effects/physiopathology, Chemical, Cushing Syndrome/physiopathology, Dexamethasone/pharmacology, Female, Growth Hormone/metabolism, Humans, Hydrocortisone/blood/metabolism, Hypothalamo-Hypophyseal System/physiopathology, Male, Middle Aged, Obesity/physiopathology, Pituitary Gland, Prolactin/metabolism, Secretory Rate/drug effects, Stimulation, Prolactin, GHRH, Hyposomatotropism, Obesity, Hypercortisolism

Authors

F. Cordido
R. Peino
T. Martínez-Ramonde


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