Endocrine Requirements for Oocyte Maturation Following hCG, GnRH Agonist, and Kisspeptin During IVF Treatment.

Endocrine Requirements for Oocyte Maturation Following hCG, GnRH Agonist, and Kisspeptin During IVF Treatment.
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DOI:
10.3389/fendo.2020.537205
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发表时间:
2020
影响因子:
5.2
通讯作者:
Dhillo WS
Dhillo WS
中科院分区:
医学2区
文献类型:
--
作者:
Abbara A;Hunjan T;Ho VNA;Clarke SA;Comninos AN;Izzi-Engbeaya C;Ho TM;Trew GH;Hramyka A;Kelsey T;Salim R;Humaidan P;Vuong LN;Dhillo WS

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卵母细胞成熟以获得受精能力是体外受精(IVF)治疗成功的关键。它需要通过人绒毛膜促性腺激素(hCG)或促性腺激素释放激素激动剂(GnRHa)提供的类h暴露。最近,下丘脑刺激剂kisspeptin被用于成熟卵母细胞。在此,我们研究了这些药物后的内分泌变化与卵母细胞成熟之间的关系。回顾性队列研究。从499个研究中前瞻性收集的激素数据进行了评估,这些数据是由hCG、GnRHa或kisspeptin触发的IVF周期。hCG水平(121 iU/L)在hCG后24小时达到峰值,而lh水平在GnRHa (140 iU/L)或kisspeptin (41 iU/L)后约4小时达到峰值。hcg水平与体重呈负相关,而触发前LH值与GnRHa和kisspeptin后LH升高呈正相关。hCG/LH水平增加了每次触发的成熟卵母细胞产量中位数的几率。每次触发后,黄体酮在卵母细胞成熟过程中急剧上升,并强烈预测了成熟卵母细胞的数量。黄体酮升高与hCG触发后的hCG水平呈正相关,但与所有三种触发后的LH升高呈负相关。GnRHa触发后12小时每成熟卵母细胞孕酮的升高高于hCG或kisspeptin触发后的升高。卵母细胞成熟过程中的内分泌反应因不同的触发因素而有显著差异。与直觉相反,在卵母细胞成熟过程中,黄体酮的升高与LH的升高呈负相关,即使考虑到回收的成熟卵母细胞的数量也是如此。这些数据扩大了我们对卵母细胞成熟过程中内分泌变化的理解,并为未来精确触发方案的设计提供了信息。
The maturation of oocytes to acquire competence for fertilization is critical to the success of in vitro fertilization (IVF) treatment. It requires LH-like exposure, provided by either human chorionic gonadotropin (hCG), or gonadotropin releasing hormone agonist (GnRHa). More recently, the hypothalamic stimulator, kisspeptin, was used to mature oocytes. Herein, we examine the relationship between the endocrine changes following these agents and oocyte maturation. Retrospective cohort study. Prospectively collected hormonal data from 499 research IVF cycles triggered with either hCG, GnRHa, or kisspeptin were evaluated. HCG-levels (121 iU/L) peaked at 24 h following hCG, whereas LH-levels peaked at ~4 h following GnRHa (140 iU/L), or kisspeptin (41 iU/L). HCG-levels were negatively associated with body-weight, whereas LH rises following GnRHa and kisspeptin were positively predicted by pre-trigger LH values. The odds of achieving the median mature oocyte yield for each trigger were increased by hCG/LH level. Progesterone rise during oocyte maturation occurred precipitously following each trigger and strongly predicted the number of mature oocytes retrieved. Progesterone rise was positively associated with the hCG-level following hCG trigger, but negatively with LH rise following all three triggers. The rise in progesterone per mature oocyte at 12 h was greater following GnRHa than following hCG or kisspeptin triggers. The endocrine response during oocyte maturation significantly differed by each trigger. Counter-intuitively, progesterone rise during oocyte maturation was negatively associated with LH rise, even when accounting for the number of mature oocytes retrieved. These data expand our understanding of the endocrine changes during oocyte maturation and inform the design of future precision-triggering protocols.
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