PERSISTENT GHRH-INDUCED PRL SECRETION IN CUSHINGS-SYNDROME, OBESITY AND EXOGENOUS HYPERCORTISOLISM

Endogenous Cushing's syndrome, obesity and chronic glucocorticod treat ment 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 P RL levels in response to GHRH, studied in three different situations c haracterized by a blunted GH secretion. Obese patients (n = 6) with a weight over 30% of ideal body weight, patients with active Cushing's s yndrome, and normal volunteers treated with dexamethasone 22 mg per os over two days before the pituitary challenge were studied. As a contr ol group 18 normal subjects of similar age and sex were studied. GH an d PRL was determined at intervals after GHRH (1 mu g/kg). GHRH-induced GH secretion was markedly reduced in patients with obesity, patients with endogenous Cushing's syndrome and volunteers treated with dexamet hasone. In contrast, GHRH-induced PRL secretion was not affected in th ese three clinical situations. In summary, in three situations charact erized for an impairment of the somatotroph cell, due to a primary int rinsic defect or to a functional hypothalamic alteration, there is a p ersistent GHRH-induced PRL secretion, suggesting that prolactin could be released by mammosomatotrophs that function normally in spite of hy posomatotropism.