ABSTRACT
Although the first baby born after in vitro fertilization (IVF) was conceived in a non-stimulated cycle (1), it was soon accepted that the role of IVF, as an efficient therapeutic modality for subfertile couples, could only be served through multifollicular development, achieved with the use of gonadotropins (2). Gonadotropin use, however, was frequently associated with premature luteinizing hormone (LH) surge prior to oocyte retrieval, which led to cycle cancellation in approximately one out of five women (3,4). The problem of the premature LH surge was managed by the introduction of gonadotropin-releasing hormone (GnRH) agonists in ovarian stimulation (5), thanks to the pioneering work of Schally et al. in 1971 (6). Both GnRH agonists and antagonists were available in the early 1980s for suppression of endogenous LH secretion. GnRH antagonists, however, could not be used for this purpose due to the associated allergic reactions provoked by their administration (7), leaving GnRH agonists as the only available choice. Following pituitary down-regulation by GnRH agonists and avoidance of a premature LH surge, unhindered use of gonadotropins in ovarian stimulation led to the collection of more oocytes and to an increase in the number of good-quality embryos available for transfer (8). This was associated with an increase in pregnancy rates compared to cycles where no suppression of a premature LH surge was performed, as shown by one of the first meta-analyses in reproductive medicine (9).
