In the present study, it was observed that the longer duration of GnRH-ant use did not have a detrimental effect on oocyte quality, fertilization rate, implantation rate or pregnancy rate. It is still controversial whether pregnancy rate is lower with GnRH-ant protocols compared to the well established GnRH-agonist regimens
9. Gonadotrophin releasing hormone and its receptors were found in extrapituitary tissues such as ovary, myometrium, endometrium, mammary gland, placenta, and embryo
10. Thus, the extrapituitary actions of GnRH-ant were thought to affect ovarian stimulation outcomes and could be one of the causes of lower pregnancy rates
6. It is still unclear whether lower pregnancy rates are the result of detrimental effects of GnRH-ant on oocyte quality, embryo development, or endometrial maturation. Kinay et al
11, reported no relation between endometrial thickness and pregnancy rates in GnRH-ant cycles. In our study there was no difference between groups for endometrial thickness on the day of hCG administration and implantation rate.
The quality of oocytes12-15 and embryos16 are among the most significant factors determining the success of an IVF treatment. Increased cytoplasmic abnormalities in the retrieved oocytes, lower rate of zygotes showing normal pronuclear morphology and, higher rate of embryos on day 2 with an increased number of blastomeres were reported in GnRH-ant cycles17. In our study we did not observe any relation between antagonist duration and oocyte and embryo quality. Blastocyst development did not show significant difference according to antagonist duration, but in group2 blastocyst transfer percentage was higher than group 1 and 3. This difference could not be attributed to only antagonist duration, because embryo development is a multifactorial process.
GnRH-ant did not show any difference in terms of follicular growth, the maturity of the oocytes, embryo quality, implantation, clinical pregnancy, ongoing pregnancy and miscarriage rates when compared to GnRH agonists18. Ovarian stimulation response of GnRH-ant cycles were not inferior to agonist cycles, thus the reduced embryo implantation and pregnancy rates could be the result of possible deteriorating effects on the endometrium19. The endometrial thickness on the day of hCG administration < 9.8 mm in GnRH-ant cycles was reported to be inversely related to the early pregnancy loss20. In our study we did not observe any detrimental effect of antagonist duration on endometrial thickness. Early pregnancy loss was reported to be significantly higher after day 3 single embryo transfer than after day 5 single blastocyst transfer in GnRH-ant stimulated IVF cycles and this result might be explained with asynchronization between endometrium and cleavage-stage embryos21. In our study we also observed increased abortion rate for day 3 embryo transfer (29%) compared to day 5 embryo transfer (23%). It was also reported that the achievement of ongoing pregnancy in frozen embryo transfer cycles was not affected from the duration of GnRH-ant administration in the fresh cycle22.
The hyper-responder patient’s duration of stimulation was longer than of normo- and hypo-responders. This duration was correlated with antagonist administration. It could not be thought that longer antagonist administration improved the ovarian response. Higher estradiol levels and more retrieved oocytes were the result of ovarian reserve. In this study, we used two different kind of gonadotrophins and GnRH antagonists. This difference may have influence on our results. We demonstrated that longer GnRH-ant use was associated with higher estradiol levels, increased numbers of total and mature oocytes retrieved, but had no effect on fertilization rate, implantation rate or pregnancy results. In conclusion we thought that longer GnRH-ant use did not have a detrimental effect on IVF outcome.