ABSTRACT
OBJECTIVES: The undeniable asset of the antagonist protocols in in vitro fertilization is the decrease of the risks of ovarian hyperstimulation syndrome, by the use of a release by GnRH agonist. Nevertheless, questioning persist concerning the rates of clinical pregnancies, the oocyte quantity and the empty follicle syndrome. We thus studied these parameters in our center. METHODS: A retrospective study was realized from January 1st, 2013 till July 31st, 2015. The main objective was the evaluation of the rate of clinical pregnancies in antagonist protocol. A first group of 775 cycles have benefited from a release of the ovulation by HCG, while a second group of 204 cycles, by GnRH agonist. The secondary objectives were the oocyte quantity, the rate of ovarian hyperstimulation syndrome, and the rate of empty follicle syndrome. RESULTS: No statistically significant difference was found between both groups concerning the rates of clinical pregnancies, oocytes quantity, and the rate of empty follicle syndrome, whatever is the type of used release, in fresh embryo transfer. A syndrome of premature ovarian hyperstimulation syndrome was found at 7.9 % of the patients in the group 2 versus 2.3 % in the group 1, with a statistically significant difference (P<0.05). At these patients, a strategy of frozen embryo transfer ("freeze all") was proposed. The accumulated rates by pregnancy in both groups were not statistically different. CONCLUSION: The release by GnRH agonist does not show inferiority in terms of clinical pregnancy, in comparison to HCG.
Subject(s)
Fertilization in Vitro/methods , Gonadotropin-Releasing Hormone/agonists , Adult , Chorionic Gonadotropin/administration & dosage , Embryo Transfer , Female , Humans , Oocytes , Ovarian Hyperstimulation Syndrome/epidemiology , Ovarian Hyperstimulation Syndrome/prevention & control , Ovulation Induction/methods , Pregnancy , Pregnancy Rate , Retrospective StudiesABSTRACT
Chromosomal abnormalities are common in patients with oligozoospermia or azoospermia. We report the case of a 32-year patient, with male phenotype, and without hormonal or morphological abnormalities, with a severely reduced spermatogenesis. It was revealed a 45,X/46,XY gonadal dysgenesis. We have reviewed the various problems inherent in the discovery of this rare gonadal dysgenesis, including genetic, cancer and fertility risks.