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Management of the poor responder remains one of the greatest challenges of controlled ovarian hyperstimulation (COH) in preparation for the assisted reproductive technologies. This chapter reviews a variety of approaches which have been employed in this poorly defined patient group. The profound suppression of gonadotropins induced by traditional long luteal gonadotropin-releasing hormone agonist (GnRHa) protocols may be particularly devastating for poor responders. Decreasing the GnRHa dose during the luteal phase prior to COH would theoretically decrease the extent of endogenous gonadotropin suppression while preventing premature ovulation. The administration of estradiol in the luteal phase may induce follicle-stimulating hormone (FSH) receptor formation in more resistant follicles and result in a more coordinated gonadotropin response. The ability to enhance endogenous follicular phase gonadotropin release by the administration of either clomiphene citrate or an aromatase inhibitor would represent an attractive adjunct to GnRHant protocols in poor-responder patients.
This chapter discusses the process of in vitro maturation (IVM) of human oocytes. Oocyte maturation in vitro is profoundly affected by culture conditions. Different media have been used for in vitro oocyte maturation. The presence of estradiol in the culture medium of immature oocytes has no effect on the progression of meiosis, but improves fertilization and cleavage rates. Oocyte retrieval in IVM cycles is also largely performed in the follicular phase in routine practice. Immature human oocytes can be recovered from the ovaries during both the follicular and luteal phase. Polycystic ovary syndrome (PCOS) patients having the highest risk of ovarian hyperstimulation syndrome (OHSS), and the best chance for pregnancy due to a higher antral follicle count (AFC) have been the most appropriate candidates for routine IVM treatment. Luteal support is started on the day that maturation is achieved and intracytoplasmic sperm injection (ICSI) is performed.
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