Reproductive Medicine and Biology (Jan 2022)

Clinical efficacy of dual trigger with human chorionic gonadotropin and a gonadotropin‐releasing hormone agonist for women undergoing fertility preservation

  • Yeon Hee Hong,
  • Seul Ki Kim,
  • Jung Ryeol Lee,
  • Byung Chul Jee,
  • Chang Suk Suh

DOI
https://doi.org/10.1002/rmb2.12440
Journal volume & issue
Vol. 21, no. 1
pp. n/a – n/a

Abstract

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Abstract Purpose To determine the optimal maturation method to increase the yield of mature oocytes, especially for cancer patients with fewer chances of fertility preservation (FP) before gonadotoxic therapy. Methods A total of 373 cycles in 293 patients undergoing controlled ovarian stimulation (COS) for FP using a gonadotropin‐releasing hormone (GnRH) antagonist protocol were enrolled. The control group (n = 225) received 250 µg of recombinant human chorionic gonadotropin (rhCG) while the study group (n = 148) received 250 µg of rhCG and 0.2 mg of triptorelin for triggering. Subgroup analyses were performed for stimulation cycles with diminished ovarian reserve (DOR; anti‐Müllerian hormone (AMH) levels <1.1 ng/ml, n = 86), with endometrioma (n = 104), or with breast cancer and endometrial cancer using 5 mg of letrozole during the COS cycles (n = 84). Results There was no significant difference in the baseline characteristics or the number of total and mature oocytes between the two groups. Subgroup analyses for women with endometrioma or DOR showed similar results. However, the dual trigger group had a significantly higher number of mature oocytes than the rhCG trigger group in breast and endometrial cancer patients using letrozole during the COS cycles (6.9 ± 6.0 vs. 4.6 ± 3.6, p = 0.034). The maturation rate was higher in the dual trigger group, although the difference was not statistically significant (59.3 ± 26.7 vs. 50.0 ± 28.0, p = 0.124). Conclusions Dual triggering can be an efficient maturation method to maximize the yield of mature oocytes in breast or endometrial cancer patients using letrozole‐combined GnRH antagonist protocol for FP.

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