2010Gynecologic and Obstetric InvestigationRequires access

Failure to Improve Ovarian Response by Combined Gonadotropin-Releasing Hormone Agonist and Gonadotropin Therapy

David Bider, Ehud Kokia, Shlomo Lipitz, Joseph Blankstein, Shlomo Mashiach, David M. Serr, Zion Ben‐Rafael

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Abstract

Nineteen women were treated with the gonadotropin-releasing hormone (GnRH) agonist buserelin in order to suppress the pituitary prior to gonadotropin treatment. Eight women were oligomenorrheic, 6 had polycystic ovarian disease (PCOD) and 5 women had normal cycles. Buserelin was administered for 3 weeks before ovarian stimulation, and the pituitary down-regulation was proven by provocative tests. Ovarian stimulation was then achieved by human menopausal gonadotropin (hMG) 2 ampules a day. Several abnormal responses to the combined buserelin/hMG treatment were noted in some patients. This included a sudden decrease in E2 level without LH surge (2 patients), induced follicular growth with buserelin instead of ovarian suppression (2 patients) and ovarian hyperstimulation syndrome in 3 patients with PCOD. From this we conclude that although pituitary suppression can easily be achieved by GnRH analog administration, this does not ensure the prevention of unwanted responses. It is possible that the common denominator for these abnormal responses is that they are ovarian in origin, hence they occur in spite of pituitary down-regulation. Close monitoring of the suppression and stimulation stages will detect most cases of such failures. Furthermore it is possible that not all patients are suitable for the combined treatment of gonadotropin and GnRH agonist.

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What this paper is about

Nineteen women were treated with the gonadotropin-releasing hormone (GnRH) agonist buserelin in order to suppress the pituitary prior to gonadotropin treatment. Eight women were oligomenorrheic, 6 had polycystic ovarian disease (PCOD) and 5 women had normal cycles. Buserelin was administered for 3 weeks before ovarian stimulation, and the pituitary down-regulation was proven by provocative tests. Ovarian stimulation was then achieved by human menopausal gonadotropin (hMG) 2 ampules a day. Several abnormal responses to the combined buserelin/hMG treatment were noted in some patients. This included a sudden decrease in E2 level without LH surge (2 patients), induced follicular growth with buserelin instead of ovarian suppression (2 patients) and ovarian hyperstimulation syndrome in 3 patients with PCOD. From this we conclude that although pituitary suppression can easily be achieved by GnRH analog administration, this does not ensure the prevention of unwanted responses. It is possible that the common denominator for these abnormal responses is that they are ovarian in origin, hence they occur in spite of pituitary down-regulation. Close monitoring of the suppression and stimulation stages will detect most cases of such failures. Furthermore it is possible that not all patients are suitable for the combined treatment of gonadotropin and GnRH agonist.

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Available abstract

Nineteen women were treated with the gonadotropin-releasing hormone (GnRH) agonist buserelin in order to suppress the pituitary prior to gonadotropin treatment. Eight women were oligomenorrheic, 6 had polycystic ovarian disease (PCOD) and 5 women had normal cycles. Buserelin was administered for 3 weeks before ovarian stimulation, and the pituitary down-regulation was proven by provocative tests. Ovarian stimulation was then achieved by human menopausal gonadotropin (hMG) 2 ampules a day. Several abnormal responses to the combined buserelin/hMG treatment were noted in some patients. This included a sudden decrease in E2 level without LH surge (2 patients), induced follicular growth with buserelin instead of ovarian suppression (2 patients) and ovarian hyperstimulation syndrome in 3 patients with PCOD. From this we conclude that although pituitary suppression can easily be achieved by GnRH analog administration, this does not ensure the prevention of unwanted responses. It is possible that the common denominator for these abnormal responses is that they are ovarian in origin, hence they occur in spite of pituitary down-regulation. Close monitoring of the suppression and stimulation stages will detect most cases of such failures. Furthermore it is possible that not all patients are suitable for the combined treatment of gonadotropin and GnRH agonist.

Key concepts: Buserelin, Polycystic ovarian disease, Gonadotropin, Internal medicine, Gonadotropin-releasing hormone agonist, Ovarian hyperstimulation syndrome, Endocrinology, Medicine

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Failure to Improve Ovarian Response by Combined Gonadotropin-Releasing Hormone Agonist and Gonadotropin Therapy — Research Paper | ScholarLens