Polycystic ovary syndrome phenotype does not have impact on oocyte morphology. - Université de Lille
Article Dans Une Revue Reprod Biol Endocrinol Année : 2022

Polycystic ovary syndrome phenotype does not have impact on oocyte morphology.

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Purpose The primary objective of the present study of women participating in an ICSI program was to determine whether the morphologic quality of oocytes was related to the polycystic ovary syndrome (PCOS) phenotype. Methods We performed a retrospective cohort study in the IVF unit at the Lille University Medical Center (Lille, France) between 2006 and 2015. Oocyte morphology (fragmented first polar body, abnormal zona pellucida, large perivitelline space, material in perivitelline space, abnormal shape of oocyte, granular cytoplasm and intracytoplasmic vacuoles) was evaluated in PCOS women and according to different subgroup (depending on the presence or absence of the cardinal features polycystic ovarian morphology (PCOM), hyperandrogenism (HA), and oligo-anovulation (OA)). Results A total of 1496 metaphase II oocytes (n = 602 for phenotype A combining PCOM + HA + OA, n = 462 oocytes for phenotype C: PCOM + HA, and n = 432 for phenotype D: PCOM + OA) were assessed. The phenotypes A, C and D did not differ significantly with regard to the proportion of normal oocytes (adjusted percentages (95%CI): 35.2% (31.5 to 39.1%), 25.8% (21.9 to 29.9%) and 34.0% (29.7 to 38.6%), respectively: adjusted p = 0.13). Likewise, there were no significant intergroup differences in oocyte morphology. The ICSI outcome was not significantly associated with the PCOS phenotype. Conclusion The present study is the first to show that the PCOS phenotype (notably the presence vs. absence of OA and/or HA) is not significantly associated with the morphological quality of oocytes.
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hal-04387940 , version 1 (11-01-2024)

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Audrey Uk, Christine Decanter, Camille Grysole, Laura Keller, Helene Behal, et al.. Polycystic ovary syndrome phenotype does not have impact on oocyte morphology.. Reprod Biol Endocrinol, 2022, Reprod Biol Endocrinol, 20, pp.7. ⟨10.1186/s12958-021-00874-2⟩. ⟨hal-04387940⟩
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