GnRH agonist for triggering final oocyte maturation in the GnRH antagonist ovarian hyperstimulation protocol: a systematic review and meta-analysis

Abstract Study question Does the use of double dose of GnRH antagonists during COH in women with risk of premature LH surge alter luteinization after final oocyte maturation induction? Summary answer The use of double dose of GnRH antagonist in women with risk of premature luteinizing hormone surge dosent affect luteinization after final oocyte maturation induction. What is known already GnRH antagonists are used to prevent a premature LH surge during controlled ovarian hyperstimulation. The antagonists directly inhibit gonadotrophin release within several hours through competitive binding to pituitary GnRH receptors, producing a rapid suppression of LH and FSH, with no initial flare effect. In women with diminished ovarian reserve (DOR) it is not uncommon that premature luteinization cannot be completely prevented using a daily dose GnRH antagonist. To date, no study has evaluated the effects of using a daily double dose of GnRH antagonists to prevent a premature LH surge and its effect on luteinization after final oocyte maturation induction. Study design, size, duration This monocentric retrospective analysis evaluated the effect on luteinization after final oocyte maturation induction in twenty women during COH who received a daily double dose of GnRH antagonists (Cetrotide 0.25 mg/mL, Merck) from January 2020 to December 2020. Participants/materials, setting, methods Women with severe DOR and history of premature luteinization during COH received a double dose of GnRH antagonist when the leading follicle reached 12–14 mm (am and pm). When two follicles reached ≥18 mm in diameter, final oocyte maturation was induced with dual trigger using Leuprolide acetate and hCG. Progesterone, estradiol, bHCG, and LH levels were measured the day after final oocyte maturation induction to assure adequate luteinization. Main results and the role of chance In total twenty women were included in the analysis. Mean age 36.8± 4.2, AMH 0.65± 0.32 ng/ml, baseline antral follicle count 4± 2.3, serum hormone levels the day of ovulation induction trigger: progesterone 0.89± 0.34 ng/ml, LH 1.6± 2.1 ng/ml, estradiol 1235 ± 1420 pg/ml. Post-surge serum hormone levels average reached adequate levels: estradiol 1645 ± 1116 pg/ml, progesterone 20.4 ±2.2 ng/ml, LH 62.66± 10.5 IU/ml and, bHCG 247±115 IU/ml. A total of 76 oocytes were retrieved (3.8± 0.8 oocytes per patient), 63.1% (48/76) MII, 22% (17/76) MI, 14% (11/76) GV. Limitations, reasons for caution The retrospective nature of the study, small sample size, and potential variability in the study center’s laboratory protocol(s) compared to other reproductive treatment centers may limit the external validity of our findings. Wider implications of the findings: The daily use of double dose of GnRH antagonists during COH offers the possibility of preventing a premature LH surge in women with DOR with high risk of early ovulation, without compromising luteinization after final oocyte maturation induction. Trial registration number NA

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Prevention of Ovarian Hyperstimulation Syndrome (OHSS) With the Use of Gonadotropin Releasing Hormone (GnRH) Agonist to Trigger Final Oocyte Maturation After Cotreatment With GnRH Antagonist in Patients With Polycystic Ovarian Syndrome (PCOS) or Previous High Response Undergoing IVF Treatment—A Prospective Randomized Clinical Trial

Fertility and Sterility ◽

10.1016/j.fertnstert.2005.07.232 ◽

2005 ◽

Vol 84 ◽

pp. S96 ◽

Cited By ~ 3

Author(s):

L. Engmann ◽

A. Diluigi ◽

D. Schmidt ◽

J. Nulsen ◽

D. Maier ◽

...

Keyword(s):

Clinical Trial ◽

Gnrh Agonist ◽

Ovarian Hyperstimulation Syndrome ◽

Polycystic Ovarian Syndrome ◽

Gnrh Antagonist ◽

Gonadotropin Releasing Hormone ◽

Ovarian Hyperstimulation ◽

Prospective Randomized Clinical Trial ◽

Final Oocyte Maturation ◽

Ovarian Syndrome

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Switching from a GnRH agonist to a GnRH antagonist in prostate cancer patients: A systematic review and meta-analysis

Canadian Urological Association Journal ◽

10.5489/cuaj.5996 ◽

2019 ◽

Vol 14 (2) ◽

Cited By ~ 1

Author(s):

Kaleem S. Atchia ◽

Christopher J.D. Wallis ◽

Neil Fleshner ◽

Paul Toren

Keyword(s):

Prostate Cancer ◽

Systematic Review ◽

Gnrh Agonist ◽

Gnrh Antagonist ◽

Meta Analysis ◽

Specific Antigen ◽

Patient Characteristics ◽

Agonist Therapy ◽

Clinical Responses ◽

Key Terms

Introduction: We sought to address whether there are clinical responses when patients who are failing gonadotropin-releasing hormone (GnRH) agonist therapy are switched to degarelix. Androgen-deprivation therapy remains the backbone of treatment for disseminated prostate cancer and may be achieved with orchiectomy, GnRH agonists, or degarelix, a GnRH antagonist. Methods: To perform a systematic review and meta-analysis, a search of the BIOSIS Previews, Embase, International Pharmaceutical Abstracts, MEDLINE, and Google Scholar databases was performed using key terms. Quantitative meta-analysis was performed to provide a pooled estimate of prostate-specific antigen (PSA) response at three months. Results: Thirteen studies were identified, eight of which were included in the qualitative and quantitative analyses. Patient characteristics were broadly similar between the studies. Out of 155 patients across all included studies, 20 had stable PSA after the switch (12.9%), 14 had between 10‒30% decrease in PSA (9.0%), three had between 30‒50% decrease (1.9%), and 13 had more than 50% decrease (8.4%). Random effects meta-analysis of these data demonstrated a pooled response rate of 27.75 (95% confidence interval 18.9‒36.5%; I2=7.9%). Changes in testosterone levels following the switch could not be quantitatively assessed due to lack of sufficient data. Conclusions: Our results suggest that a switch to GnRH antagonist following progression on a GnRH agonist may result in a stable or decreased PSA at three months in about 30% of patients. This information should be considered among the potential options to discuss with patients with a rising PSA on GnRH agonist therapy.

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