The relationship of premature progesterone rise with serum estradiol levels and number of follicles in GnRH antagonist/recombinant FSH-stimulated cycles.

نویسندگان

  • D Kyrou
  • M Al-Azemi
  • E G Papanikolaou
  • P Donoso
  • K Tziomalos
  • P Devroey
  • H M Fatemi
چکیده

OBJECTIVE(S) To investigate the relationship between premature progesterone (P) rise and serum estradiol (E(2)) levels and the number of follicles in GnRH antagonist/rec-FSH stimulated cycles. STUDY DESIGN Two hundred and seven patients treated by IVF/ICSI at the Centre for Reproductive Medicine of the Dutch-Speaking Brussels Free University were included in this observational study. They received 200 IU/day rec-FSH from day 2 of the cycle and daily GnRH antagonist starting on day 6 of stimulation. The criteria for hCG administration included the presence of ≥3 follicles of ≥17 mm diameter. Serum P, E(2) and LH were determined on the day of hCG administration. The outcome measure was to identify a threshold of E(2) and number of follicles on the day of hCG administration which would define a progesterone rise on the day of hCG administration (cut-off value of 1.5 ng/ml). RESULT(S) Patients with a P >1.5 ng/ml had significantly higher concentrations of E(2) and increased number of follicles on the day of hCG administration compared to those with P ≤1.5 ng/ml. However, patients with a P >1.5 ng/ml the day of hCG showed lower pregnancy rates than those with P <1.5 ng/ml (17.8 vs. 32.7%, respectively; p<0.05). A ROC curve was employed in order to estimate a cut-off for E(2) on day of hCG >1790.5 pg/ml and more than 9.5 follicles of ≥11 mm in diameter for progesterone rise over 1.5 ng/ml. CONCLUSION(S) A significant impact is shown on progesterone rise by E(2) and number of follicles on the day of hCG administration in GnRH antagonist/rec-FSH-stimulated cycles. With this knowledge, an upcoming progesterone rise during follicular phase can be anticipated and prevented.

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عنوان ژورنال:
  • European journal of obstetrics, gynecology, and reproductive biology

دوره 162 2  شماره 

صفحات  -

تاریخ انتشار 2012