Exp Clin Endocrinol Diabetes 1995; 103(3): 184-190
DOI: 10.1055/s-0029-1211348
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Changes in anterior pituitary response in patients with idiopathic hypothalamic hypogonadism caused by pulsatile GnRH therapy and testosterone replacement*

J. Schopohl, J. Mojto, M. Losa, G. Mehltretter, O. A. Müller, K. v. Werder
  • Medizinische Klinik, Klinikum Innenstadt, Ludwig Maximilian Universität München, München, Germany
* Presented in part at the 33th Meeting of the German Endocrine Society, Karlsruhe, Germany, February 22 to 25, 1989 and at the 9th International Congress of Endocrinology, Nizza, France, August 30 to September 5, 1992.
Further Information

Publication History

Publication Date:
15 July 2009 (online)

Summary

Objective. This study evaluated in male patients with idiopathic hypothalamic hypogonadism the effect of pulsatile GnRH therapy or testosterone replacement on the response of all anterior pituitary hormones to adequate dynamic stimuli.

Patients and design. In nine patients with idiopathic hypothalamic hypogonadism — mean age 21 ± 1 (mean ± SE) — a combined pituitary stimulation (CPS) with 200 µg TRH, 100 µg GnRH, 100 µg CRH and 100 µg GRH and an insulin tolerance-test (ITT) with 0.1 U insulin/kg body weight were performed. Both tests were repeated during pulsatile GnRH therapy and thereafter on testosterone replacement.

Measurements. Hormone levels were measured by immunometric assays. For statistical analysis the area under the curve (AUC) was used as a measure for hormone response.

Results. Testosterone levels did not differ significantly during GnRH therapy (16.6 ± 2.1 nmol/L) and testosterone replacement (18.5 ± 1.7 nmol/L). No significant differences were observed before and during the two treatment modalities for TSH and ACTH. PRL increase was significantly higher during GnRH therapy (AUC: 7358 ± 8940) compared to the rise before treatment (AUC: 36161 ± 5853; p < 0.01) and on testosterone replacement (AUC: 49995 ± 6158; p <0.01). The GH responsible to CPS and ITT was higher under testosterone replacement (AUC: 1826 ± 353 and 1423 ± 125) compared with the pretreatment situation (AUC: 727 ± 115; p < 0.05 and 541 ± 110; p < 0.01) and also more pronounced; than under GnRH therapy (AUC: 1148 ± 180 and 798 ± 129; p < 0.05). FSH and LH after CPS rose significantly more during GnRH therapy (AUC: 864 ± and 2215 ± 219) than before (AUC: 418 ± 61 and 1424 ± 277; p < 0.01) and on testosterone treatment (342 ± 83 and 1153 ± 323; p < 0.05).

Conclusion. These results show that GnRH exerts and stimulatory effect on PRL secretion and may modulate! GH secretion independently from sex steroids.

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