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Submitted on June 30, 2004
Accepted on November 24, 2004
Department of Endocrinology, CHU Cochin & Institut Cochin, INSERM U567, CNRS UMR8104, IFR 116, Université Paris V-René Descartes (J.B., L.G., X.B.), 75014 Paris, France, European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U413, UA CNRS, University of Rouen (V.C., E.L., C.D., J.M.K., H.V., H.L.), 76821 Mont-Saint-Aignan, France, and Department of Endocrinology, CHR of Orléans (G.B., P.E.), 45067 Orléans, France
* To whom correspondence should be addressed. E-mail: herve.lefebvre{at}chu-rouen.fr.
In ACTH-independent macronodular adrenal hyperplasia (AIMAH) causing Cushing's syndrome, cortisol production can be controlled by illegitimate membrane receptors. The aim of the present study was to evaluate in vivo and in vitro the sensitivity of AIMAH to various regulatory factors to detect the expression of illegitimate receptors by the tissues. Four consecutive patients with AIMAH and hypercortisolism (H1-H4) underwent preoperatively a series of pharmacological and/or physiological tests. After adrenalectomy, in vitro studies were conducted to investigate the cortisol responses of cultured cells, derived from hyperplastic tissues, to various membrane receptor ligands. The adrenal tissues of the two patients (H2 and H4) who responded in vivo to food intake were stimulated in vitro by gastric inhibitory polypeptide (GIP). GnRH and hCG but not FSH stimulated cortisol secretion in patients H2 and H4. In these two cases, hCG but not GnRH stimulated cortisol production from cultured adrenocortical cells. Cisapride induced a significant increase in cortisol levels in patient H1. In addition, serotonin (5-HT) was more efficient to stimulate cortisol production in H1 cells than in normal adrenocortical cells. Upright stimulation test provoked an increase in cortisol levels in patients H1, H2 and H3. H1 and H2 cells were more sensitive to the stimulatory action of angiotensin II than normal cells. Similarly, arginine vasopressin (AVP) more efficiently activated steroidogenesis in H1 cells than in normal cells. In H1 tissue, immunohistochemical studies revealed the presence of 5-HT- and AVP-like immunoreactivities within clusters of steroidogenic cells, suggesting that these two factors acted through an autocrine/paracrine mechanism to stimulate cortisol secretion. The present study provides the first demonstration of primary adrenal Cushing's syndrome dependent from both gonadotropin and GIP. Our data also show an hyperresponsiveness of hyperplastic adrenal tissues to 5-HT, Ang II and AVP. Finally, they reveal for the first time the presence of paracrine regulatory signals in adrenal hyperplasia tissues.
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