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Embryos from polycystic ovary syndrome patients with hyperandrogenemia reach morula stage faster than controls

To investigate if patients with polycystic ovary syndrome (PCOS) have altered embryo morphokinetics when compared with controls. Retrospective cohort analysis. Single academic fertility clinic in a tertiary hospital setting. Age- and body mass index–matched patients who underwent in vitro fertilizat...

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Bibliographic Details
Published in:F&S Reports (Online) 2020-09, Vol.1 (2), p.125-132
Main Authors: Chappell, Neil Ryan, Barsky, Maya, Shah, Jaimin, Peavey, Mary, Yang, Liubin, Sangi-Haghpeykar, Haleh, Gibbons, William, Blesson, Chellakkan Selvanesan
Format: Article
Language:English
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Summary:To investigate if patients with polycystic ovary syndrome (PCOS) have altered embryo morphokinetics when compared with controls. Retrospective cohort analysis. Single academic fertility clinic in a tertiary hospital setting. Age- and body mass index–matched patients who underwent in vitro fertilization diagnosed with PCOS using the Rotterdam criteria. A subanalysis was performed on patients with PCOS with hyperandrogenemia. Sixty-four patients with PCOS were identified with 990 embryos that were matched with 64 control patients with 628 embryos. None. Time to blastulation. Embryos from women with PCOS displayed faster growth rate at t7, t8, and t9; all other morphokinetic points were similar. Patients with PCOS also had a higher number of oocytes retrieved. No differences were seen in the fertilization rate or blastulation rate. Patients with PCOS had a higher miscarriage rate (38.1% in PCOS vs. 18.8% in controls). Patients with hyperandrogenic PCOS showed a faster growth rate at t5, t6, t7, t8, t9, and morula. Embryos from women with PCOS grew faster until 9-cell stage and women with hyperandrogenic PCOS until morula. Patients with PCOS also showed a higher miscarriage rate. The alterations in early embryo development are consistent with altered fertility and obstetric outcomes in the population with PCOS and may be due to the hyperandrogenic microenvironment in the ovarian follicle.
ISSN:2666-3341
2666-3341
DOI:10.1016/j.xfre.2020.05.006