Abstract

BackgroundThe use of progestin (P) during ovarian stimulation is effective in blocking the luteinizing hormone (LH) surge in women with normal ovarian reserve, however, its effects have not been determined in poor responders. This study aimed to explore the follicular dynamics in P-primed minimal stimulation in poor responders.MethodsA total of 204 infertile women with diminished ovarian reserve were allocated into the medroxyprogesterone acetate (MPA) group or the natural-cycle control group in an alternating order. MPA (10 mg) was administered daily beginning from the early follicular phase and a low dose of hMG was added in the late follicular phase if the serum FSH level was lower than 8.0mIU/ml. When a dominant follicle reached maturity, triptorelin 100 μg and hCG 1000 IU were used for trigger, and oocytes were retrieved 34-36 h later.All viable embryos were cryopreserved for subsequent frozen embryo transfer. Natural cycle IVF was used as controls.ResultsCompared with the natural cycle group, the MPA group exhibited a larger pre-ovulatory follicle (18.7 ± 1.8 mm vs 17.2 ± 2.2 mm), a longer follicular phase (13.6 ± 3.6 days vs 12.3 ± 3.2 days), and higher peak oestradiol values (403.88 ± 167.16 vs 265.26 ± 122.16 pg/ml), while maintaining lower LH values (P < 0.05). The incidences of spontaneous LH surge and premature ovulation decreased significantly (1.0% vs 50%; 2% vs. 10.8%, respectively; P < 0.05). A greater number of oocytes and viable embryos were harvested from the MPA group than from the natural cycle group (P < 0.05). Moreover,the clinical pregnancy rate was slightly higher in the MPA group than in the natural cycle controls, but the difference was not significant (11.8% vs 5.9%, P > 0.05).ConclusionThis study supported the hypothesis that P-primed minimal stimulation achieved ovulation control of the dominant follicle and did not adversely affect the quality of oocytes in poor responders. Therefore, P-priming is a promising approach to overcome premature ovulation in minimal stimulation for poor responders.Trial registrationChiCTR-OCH-14004176. Registered on January 8, 2014.

Highlights

  • The use of progestin (P) during ovarian stimulation is effective in blocking the luteinizing hormone (LH) surge in women with normal ovarian reserve, its effects have not been determined in poor responders

  • Serum Follicle-stimulating hormone (FSH) values decreased slightly during the follicular phase, and LH values demonstrated a gradual increasing trend; 50% of all cases (51/102) presented a spontaneous LH surge (>20 mIU/ml), with an average LH peak value of 35.1 ± 16.0 mIU/ml, and the patients underwent oocyte retrieval after 18-30 h based on the presumed stage of ovulation.The remaining 50 cases in the natural cycle group did not exhibit spontaneous LH surges, their mean LH level on the trigger day was 9.27 ± 4.52 mIU/ ml, which was close to the onset of the LH surge

  • The implantation rate was comparable in the two groups, indicating that the administration of P did not adversely affect the embryo developmental potential in the poor responders (21.4% vs. 15.4%, P > 0.05). In this trial, we prospectively compared the follicular phase dynamics of P-primed minimal stimulation and natural cycle in vitro fertilization (IVF) in poor responders.The results indicated that ovulation of the dominant follicle in P-primed minimal stimulation was well-controlled and facilitated the IVF programme

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Summary

Introduction

The use of progestin (P) during ovarian stimulation is effective in blocking the luteinizing hormone (LH) surge in women with normal ovarian reserve, its effects have not been determined in poor responders. This study aimed to explore the follicular dynamics in P-primed minimal stimulation in poor responders. P-primed ovarian stimulation (PPOS) protocols have been confirmed to effectively block the rise of luteinizing hormone (LH) and demonstrate a comparable pregnancy outcome to that of classical protocols for infertile women with normal ovarian reserve and polycystic ovarian syndrome [1, 2, 4,5,6,7]. We explored the role of P in blocking premature ovulation in minimal stimulation for poor responders

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