Can polymorphisms of AMH/AMHR2 affect ovarian stimulation outcomes? A systematic review and meta-analysis
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RESEARCH
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Can polymorphisms of AMH/AMHR2 affect ovarian stimulation outcomes? A systematic review and meta-analysis Di Chen1†, Xiangyu Zhu1† and Jielei Wu2*
Abstract Background: 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. Methods: We 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). Results: Seven 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. Conclusions: Our 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. Keywords: AMH, AMHR2, Meta-analysis, Polymorphism, SNP
Introduction The anti-Müllerian hormone (AMH), also 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]. * Correspondence: [email protected] † Di Chen and Xiangyu Zhu contributed equally to this work. 2 Center for Reproductive medicine, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, China Full list of author information is available at the end of the article
AMH plays a key role in the regulation of primordial follicle recruitment and cyclic selection. 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]. Considering the potential role of AMH in affecting ovarian response to stimulation, it has
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