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Human Reproduction, Vol. 8, No. 12, pp. 2056-2060, 1993
© 1993 European Society of Human Reproduction and Embryology

review-article

Endocrinology: The combination of gonadotrophin-releasing hormone (GnRH) antagonist and pulsatile GnRH normalizes luteinizing hormone secretion in polycystic ovarian disease but fails to induce follicular maturation

S. Dubourdieu1, E. le Nestour2, I.M. Spitz3, B. Charbonnel and P. Bouchard2

Clinique Endocrinologique, Hôtel-Dieu, 44000 Nantes 2Service d'Endocrinologie et des Maladies de la Reproduction, Hôpital Bicêtre 94270 Le Kremlin-Bicêtre, France 3The Population Council, Center for Biomedical Research New York, NY 10021, USA

Correspondence: 1To whom correspondence should be addressed

To evaluate the role of altered luteinizing hormone (LH) release in the mechanism of polycystic ovarian disease (PCOD) anovulation, we have co-administered a gonadotrophin-releasing hormone (GnRH) antagonist and pulsatile GnRH therapy to two clomiphene citrate-resistant PCOD patients. The aim was to correct their inappropriate gonadotrophin secretion. Nal-Glu was administered s.c. every 72 h to both subjects for 3 weeks. On day 7 after commencing the study, intravenous pulsatile GnRH therapy was initiated (10 ug/ pulse) every 90 min for 15 days to both subjects. In one subject, Nal-Glu treatment was continued and the GnRH dose was increased to 20 ug/pulse for 10 additional days. Prior to Nal-Glu, mean serum LH levels were 10.4 ±1.6 and 9.3 ± 1.3 mlU/ml (mean ± SEM) and mean interpulse intervals were 67.1 and 60 min in patients 1 and 2, respectively. Mean serum FSH levels were 4.9 ± 0.4 and 4.2 ± 0.2 mIU/ml for patients 1 and 2, respectively. LH pulsatility was abolished following Nal-Glu, mean serum LH decreased to 1.1 ± 0.1 and 1.3 ± 0.5 mIU/ml and mean FSH to 1.8 ± 0.1 and

2 ± 0.1 mIU/ml in the two subjects. On the 4th day of the combined therapy, mean serum LH increased to 5.4 ± 1.3 and 3.9 ± 0.9 mIU/ml with a mean interpulse interval of 72 and 80 min, respectively. Mean FSH levels increased to 3 ± 0.1 and 2.8 ± 0.1 mIU/ml, respectively and to 5.5 ± 0.2 mIU/ml after the GnRH dose was increased in patient 2. Testosterone levels decreased but remained above the normal range following combined therapy. Levels increased to the pretreatment values after augmentation of the GnRH dose in subject 2. Oestradiol levels remained <50 pg/ml and no follicular development was observed on vaginal endosonography. Failure to obtain an ovarian response in PCOD after re-establishment of improved pituitary gonadotrophin release may reflect the presence of an inherent ovarian defect in PCOD patients.

Key words: GnRH antagonist/LH pulsatility/PCOD/pulsatile/GnRH


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K. Gordon, R. T. Scott, R. F. Williams, D. R. Danforth, H. J. J. Loozen, H. J. Kloosterboer, and G. D. Hodgen
In Vivo Effects of a Potent GnRH Antagonist ORG 30850: Physiologic Evidence That Down-Regulation of GnRH Receptors Does Not Occur
Reproductive Sciences, October 1, 1994; 1(4): 290 - 296.
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