ABSTRACT
Ovarian hyperstimulation syndrome (OHSS) is the price patients pay for our attempt to override nature’s delicate balances that were created to assure a single oocyte ovulation. Spontaneous OHSS does occur, as we delineate later. It is, however, very rare. Indeed, natural-cycle-based assisted reproductive technologies (ART) were responsible for the birth of the first IVF baby; however, this method was abandoned because it is cumbersome and, more important, yields poor results in terms of pregnancy rate. Therefore, human menopausal gonadotropin (hMG) has been used for decades in ovulation induction cycles, particularly in the context of in vitro fer tilization (IVF). In recent years, recombinant fol licle stimulating hormone (FSH) preparations have replaced hMG in most centers. Typically, in these cycles, human chorionic gonadotropin (hCG) is used as a surrogate to luteinizing hor mone (LH) for the purpose of oocyte maturation and induction and ovulation. Given its signifi cantly longer half-life (> 24 h versus 60 min for LH1,2), hCG administration results in a pro longed luteotrophic effect, characterized by the development of multiple corpora lutea and supraphysiological levels of estradiol (E2) and prog esterone (P). This sustained luteotrophic effect
may result in the development of OHSS, still the most frequent and severe complication of ovar ian stimulation treatments as described in other chapters of this volume. Although hCG (recom binant or urinary-derived in different doses) is used routinely, other modes of ovulation trigger are also available, namely, recombinant LH, native gonadotropin-releasing hormone (GnRH) and GnRH agonists. The aim of this chapter is to explore the association between the mode of trigger and the risk of OHSS. This association culminates in an OHSS risk-free clinical proto col that is available at the end of the chapter.
