Gynäkologie und Geburtshilfe
Offener Zugang
ISSN: 2161-0932
ISSN: 2161-0932
Mark S. Denker MD, Kari Caswell, MA
The incidence of poor response to ovarian hyperstimulation during in vitro fertilization has been shown to vary from 9% to 30 [1]As patients become older and environmental factors have an adverse effect on egg quality, a larger and larger number of patients have diminished ovarian reserve and poor response to gonadotropins. [2] These adverse effects are seen more and more frequently in our clinic. Various factors including exposure to environmental toxins, [3] aging, endometriosis, hormones, antibiotics, previous ovarian surgery, and pesticides in the food and water supply, cause premature depletion of ovarian reserve and are associated with poor ovarian reserve. Poor response to ovulation stimulation results and high cancellation rates of up to 70% and extremely low pregnancy rates of 3% to 14%. [2] [4] Various strategies for poor responders including microdose flare protocols, estrogen priming protocols, and agonist/antagonist conversion protocols as well as augmentation with various adjuncts including human growth hormone, have been tried with varying degrees of success. [5, 4] [6] However, the lack of uniform consensus on which protocol is best is a testament to the lack of stellar performance of any one of these protocols in this particular patient population. [7] The etiology of poor response to gonadotropins is partly unknown and may result from a shortened follicular phase as well as decreased sensitivity to gonadotropins. It is known that patients with decreased ovarian reserve are more susceptible to the suppressive effects of oral contraceptive pills and gonadotropin releasing hormone agonists. [8] Although these drugs are commonly used to suppress ovarian function, these drugs can adversely affect ovarian responsiveness. [8] Moreover, patients with diminished ovarian reserve appear especially susceptible to the suppressive effects of pituitary desensitizers leading to low oocyte yield and low response. It has been shown that estradiol pretreatment prior to GnRH antagonist stimulation has a beneficial effect on oocyte yield. [9] Estradiol exerts a negative feedback on the reproductive axis, which inhibits GnRH secretion and suppression of GnRH responsiveness. Previous studies have shown that utilizing the natural negative feedback of the hypothalamic pituitary ovarian axis induced by estradiol pretreatment can prevent premature increase in FSH levels as well as improve follicular synchronization and result in better coordination of the developing follicles and improved oocyte maturity. [10]