Delayed initiation of GnRH antagonist in PCOS patients undergoing IVF: a retrospective cohort study of premature ovulation and embryological outcomes


Peker N., Yücetürk A., Tığlı E., Karaosmanoğlu Ö., Elmas B., Aslan İ. Ö., ...Daha Fazla

Journal of Ovarian Research, cilt.19, sa.1, 2026 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 19 Sayı: 1
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1186/s13048-026-02161-3
  • Dergi Adı: Journal of Ovarian Research
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE, Directory of Open Access Journals, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
  • Anahtar Kelimeler: Delayed initiation, GnRH antagonist, PCOS, Premature ovulation
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Evet

Özet

Background: We aimed to evaluate whether delayed initiation of gonadotropin hormone-releasing hormone (GnRH) antagonist treatment affects premature ovulation and the number of good-quality blastocysts. We retrospectively reviewed the medical records of polycystic ovary syndrome (PCOS) patients who underwent in vitro fertilization (IVF) treatment at our clinic between 2017 and 2025. Patients were divided into two groups: Group 1: Patients in whom GnRH antagonist injections were initiated when at least three dominant follicles measured ≥17 mm. Group 2: Patients in whom GnRH antagonist was initiated upon identification of a single dominant follicle reaching ≥14 mm. The groups were compared in terms of premature ovulation, estradiol (E2) level at GnRH antagonist initiation, total number of retrieved oocytes, number and proportion of metaphase II (MII) oocytes, fertilization rate, blastocyst number and rate, and good-quality blastocyst grades. Results: A total of 89 patients were included in the study. Of these, 38 patients were assigned to Group 1 and 51 to Group 2. There were no statistically significant differences in age or body-mass index (BMI) between the groups. Serum E2 levels at GnRH antagonist initiation were significantly higher in Group 1. The “median-(Interquartile Range (IQR))” total oocyte count was 33 (27–41) in Group 1 and 30 (26–40) in Group 2. The median 2PN count was 19.5 (12.75–27) in Group 1 and 19.0 (15–22) in Group 2. There were no statistically significant differences between the groups in terms of MII oocyte or two pronuclei (2PN) count. Blastocyst outcomes were comparable between the groups; the median number of day 5–6 blastocysts was 7.0 (IQR: 5-11.5) in Group 1 and 8.0 (IQR: 5–11) in Group 2. Furthermore, the median number of Grade A blastocysts was 4.0 (IQR: 3-10) in Group 1 and 5.0 (IQR: 4-8) in Group 2, and there was no statistically significant difference between the groups regarding Grade‑A blastocyst counts. No premature ovulation occurred in either group. Conclusion: In this PCOS cohort, delayed GnRH antagonist initiation was not associated with impaired laboratory embryological outcomes or increased premature ovulation risk. Prospective randomized controlled trials are needed to confirm these preliminary findings.