GnRH Peptides and Corpus Luteum Regulation

Abstract

Agonist analogues of the hypothalamic decapeptide, gonadotrophin-releasing hormone (GnRH) have superior potency, resistance to degradation and longer duration of gonadotrophin release that GnRH. Repeated or continuous administration of agonist analogues to women induces a short period of gonadotropin release, followed by down-regulation of pituitary GnRH-receptors, an ensuing decrease in gonadotropin levels, and diminished secretion of ovarian steroids. A state of reversible hypogonadotrophic hypogonadism can be induced, with plasma oestrogen reduced to castrate levels (‘medical gonadectomy’). GnRH agonist have had a profound impact on the treatment of a number of malignant and nonmalignant gynecological diseases which are oestrogen-dependent (Vickery and Nestor, 1987; McLachan et al., 1986). Recendy, GnRH agonists have been used increasingly in the induction of ovarian hyperstimulation in women undergoing in vitro fertilization and embryo transfer. The reversible hypogonadotrophic state induced by these analogues is followed by better follicular recruitment by exogenous gonadotropins and suppression of premature luteinizing hormone (LH) surges which cause inappropriate early luteinization (Fleming and Coutts, 1986; Porter et al., 1984), a common cause of cancellation of the procedure (Kerin et al., 1984) and poor outcome of IVF (Bryski et al., 1988; Macnamee et al., 1988). GnRH agonist treatment allows the programming of oocyte recoveries (Zom et al., 1987), and has been of particular benefit for women with polycystic ovarian disease (Filicori et al., 1988) and certain groups who respond poorly to other treatment regimens( Belaisch-Allart et al., 1989; Crosignani et al., 1988,1989).