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  • Title: Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism.
    Author: Cordido F, Peino R, Martínez-Ramonde T.
    Journal: Rev Esp Fisiol; 1994 Sep; 50(3):139-43. PubMed ID: 7886270.
    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.
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