Abstract

BackgroundPrevious studies have investigated the effects of anti-Müllerian hormone (AMH) and AMH type II receptor (AMHR2) polymorphisms on ovarian stimulation outcomes, but the results were inconsistent.MethodsWe searched PubMed, Web of Science, Embase, and Cochrane Central Register of Controlled Trials databases for the literature used in this meta-analysis. The meta-analysis was performed with a random effects model with RevMan 5.3.5. Results were expressed as the relative risk (RR) for discrete data and the mean difference (MD) for continuous outcomes with a 95% confidence interval (CI).ResultsSeven studies with 2078 participants were included. More metaphase II (MII) oocytes were retrieved in the T allele carrier of AMH (rs10407022) in the dominant model (MD: 1.20, 95% CI: 0.76 to 1.65, I2 = 0%, P < 0.00001), homozygote model (MD: 1.68, 95% CI: 0.35 to 3.01, I2 = 70%, P = 0.01) and heterogeneity model (MD: 1.20, 95% CI: 0.74 to 1.66, I2 = 0%, P < 0.00001). Oocytes retrieved from the Asian region in the TT carrier were significantly lesser than those in the GG/GT carrier in AMH (rs10407022) (MD: -1.41, 95% CI: − 1.75 to − 1.07, I2 = 0%). Differences in the stimulation duration, gonadotropin (Gn) dosage, and pregnancy rate were insignificant.ConclusionsOur analysis indicated that the polymorphisms of AMH/AMHR2 could influence the ovarian stimulation outcomes. Prospective studies with a larger sample size and more rigorous design are needed in the future to further confirm these findings.

Highlights

  • The anti-Müllerian hormone (AMH), known as Müllerian-inhibiting substance, belongs to the transforming growth factor-beta (TGF-β) superfamily of growth and differentiation factors [1]

  • Eligibility criteria The criteria of the inclusion of studies were as follows: (1) participants underwent in vitro fertilization (IVF)/ intracytoplasmic sperm injection (ICSI); (2) single nucleotide polymorphisms (SNPs) of AMH and AMHR2 were detected in some or all of the participants; (3) controlled ovarian stimulation (COS) outcomes based on the gene polymorphisms were available

  • Six studies [15,16,17,18,19, 21] including 1907 participants reported the number of retrieved oocytes regarding the distribution of AMHR2 genotypes

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Summary

Introduction

The anti-Müllerian hormone (AMH), known as Müllerian-inhibiting substance, belongs to the transforming growth factor-beta (TGF-β) superfamily of growth and differentiation factors [1]. AMH is synthesized by granulosa cells of preantral and small antral follicles [2], and its level strongly correlates with the size of primordial follicle pool and the number of antral follicles [3], which has made AMH an ideal marker of the ovarian reserve [4]. Through modulating the threshold of follicle-Stimulating Hormone (FSH) sensitivity, AMH could inhibit FSH-induced antral follicle growth and limit the transition of follicles from the primordial to primary stage [5, 6]. AMH exerts its specific biological function mainly through the AMH type II receptor (AMHR2), which is expressed on granulosa and theca cells [7]. Previous studies have investigated the effects of anti-Müllerian hormone (AMH) and AMH type II receptor (AMHR2) polymorphisms on ovarian stimulation outcomes, but the results were inconsistent

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