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Service d'Endocrinologie et Uniuersité Paris-Sud, Hopital de Bicêtr 94270 Le Kremlin-Bicêtre
Département de Biochimie, Faculté de Médecine Pitié-Salpètriere, National Institute of Child Health and Human Development 75013 Paris
Groupe de Recherches sur la Biochimie Endocrinienne et la Reproduction, (INSERM U 135) Faculté de Médecine de Bicêtre, Université Paris-Sud 94270 le Kremlin-Bicêtre, France
Service d'Endocrinologie et Uniuersité Paris-Sud, Hopital de Bicêtr 94270 Le Kremlin-Bicetre
Address requests for reprints to: Dr. G. Schaison, Service d''Endo crinologie, Hopital de Bicetre, 94270 Le Kremlin-Bicetre, France.
Hyperprolactinemia in men is frequently associated with hypogonadism. Normalization of serum PRL levels s i generally associated with an increase in serum testosterone (T) to normal. To determine the mechanism of the inhibitory effect of hyperprolactinemia on the hypothalamic-pituitary-gonadal axis, we studied the effect of intermittent pulsatile GnRH administration on LH pulsatility and T levels in four men with prolactinomas. All patients had high PRL values (100–3000 ng/ ml), low LH (mean ± SEM, 2.2 ± 0.1 mlU/ml), and low T values (2.3 ± 0.3 ng/ml), with no other apparent abnormality of pituitary function. GnRH was administered iv using a pump delivering a bolus dose of 10 fig every 90 min for 12 days. No LH pulses were detected before treatment. Pulsatile GnRH administration resulted in a significant increase in basal LH levels (6.7 ± 0.6 mlU/ml; P < 0.001) and restored LH pulsatility. In addition, T levels increased significantly to normal values in all patients (7.8 ± 0.4 ng/ml; P < 0.001) and were normal or supranormal as long as the pump was in use, although PRL levels remained elevated. These data, therefore, suggest that hyperprolactinemia produces hypogonadism primarily by interfering with pulsatile GnRH release.
* Presented in part at the Seventh International Congress of Endo-crinology, Quebec, Canada, 1984.
Received June 20, 1984.
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