OVARIAN ESTRADIOL PRODUCTION IN-VIVO - INHIBITORY EFFECT OF LEUPROLIDE ACETATE

Citation
A. Kowalik et al., OVARIAN ESTRADIOL PRODUCTION IN-VIVO - INHIBITORY EFFECT OF LEUPROLIDE ACETATE, Journal of reproductive medicine, 43(5), 1998, pp. 413-417
Citations number
20
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
00247758
Volume
43
Issue
5
Year of publication
1998
Pages
413 - 417
Database
ISI
SICI code
0024-7758(1998)43:5<413:OEPI-I>2.0.ZU;2-7
Abstract
OBJECTIVE: To determine the impact of reducing the dose of gonadotropi n-releasing hormone agonist (GnRH-a) for controlled ovarian stimulatio n in in vitro fertilization (IVF) on subsequent response to stimulatio n and cycle outcome. STUDY DESIGN: An IVF database was searched to ide ntify patients who underwent at least two cycles of ovarian stimulatio n at a university-based medical center, and a retrospective chart revi ew was performed. Fifty-one patients whose IVF stimulation protocols d uring the two cycles were identical except for the leuprolide dosage u tilized for luteal pituitary suppression were included in the study. T wo leuprolide dosages were utilized for suppression: a low dose, 0.5 m g daily, and a high nose, 2 mg daily. The leuprolide dose was uniforml y halved upon initiation of gonadotropin stimulation; the gonadotropin dose and preparation were identical in the two protocols. Day 3 folli cle-stimulating hormone levels, duration of stimulation, amount of gon adotropins required, midcycle and peak estradiol levels, oocyte yield and implantation rates were compared. RESULTS: Lowering the dose of Gn RH-a while maintaining the same stimulation protocol resulted in a fas ter estradiol rise and higher mean peak estradiol level. The higher es tradiol levels were obtained with a lower total gonadotropin nose. The oocyte yield was not affected by the stimulation protocol utilized. C ONCLUSION: Lowering the dosage of leuprolide allows higher estradiol l evels in those patients. This suggests an inhibitory in vivo effect of leuprolide acetate on ovarian steroidogenesis.