OBJECTIVE:To describe the age-associated distribution of primordial follicle density (PFD) in human ovarian cortical tissue from post-pubertal individuals undergoing ovarian tissue cryopreservation, with observations concentrated in the 20-34-year range. DESIGN:Descriptive translational research study using log-transformed quantile regression to characterize conditional percentiles of PFD, with bootstrap resampling to assess uncertainty. SUBJECTS:Ovarian cortical tissue from 33 post-pubertal individuals aged 16-43 years obtained from organ donors and patients undergoing ovarian tissue cryopreservation, without prior exposure to intensive alkylating agent-based chemotherapy. EXPOSURE:Age at ovarian tissue harvesting. MAIN OUTCOME MEASURES:Age-specific distribution of PFD (follicles/mm2), modeled across the 10th, 25th, 50th, 75th, and 90th percentiles; estimates outside the 20-34-year range are exploratory owing to sparse representation. RESULTS:Primordial follicle density declined nonlinearly with age, with wide interindividual variability. Within the well-represented 20-34-year range (21 of 33 individuals), the estimated median PFD decreased from 1.18 follicles/mm2 at age 20 to 0.49 follicles/mm2 at age 34. Estimates at younger (16-19 years, n=2) and older (35-43 years, n=10) ages showed substantially wider bootstrap uncertainty and should be considered exploratory. An exploratory descriptive analysis of PFD and graft duration among eight ovarian transplant recipients was also performed. CONCLUSION:This study provides a descriptive characterization of the age-associated distribution of PFD in ovarian cortical tissue prepared under contemporary fertility-preservation conditions. These findings are concentrated in the 20-34-year range and are hypothesis-generating. Larger multicenter studies linking PFD to graft function and longevity are needed before age-specific percentiles can inform individualized ovarian tissue transplantation.
Polyendocrine metabolic ovarian syndrome (PMOS) is one of the most common endocrine conditions affecting hundreds of millions of women globally. The former name polycystic ovary syndrome (PCOS) was inaccurate, underpinning the robust nomenclature change process. This review historically traces renaming efforts up to, including and beyond the PMOS global renaming process. A systematic search of Medline and Embase screened according to PRISMA 2020 methodology, identified 30 eligible papers (1995-2026). The name PCOS was repeatedly challenged on scientific grounds, with the absence of increased ovarian cysts and neglect of the breadth of the disorder, and on systemic grounds from limited ovarian classification, research, data capture, education, provider knowledge, diagnostic delay and care dissatisfaction. Historically, isolated expert opinion predominated yet failed to gain traction. The 2026 global, patient-co-led, multistep process, involved 56 organisations and 22,000+ survey respondents and generated a mandate for change, explored risks and implementation priorities and delivered a 97% consensus on the name PMOS. Implementation and embedded evaluation spans coding and classification systems, research, education, clinical guidelines and care with early adoption and predominantly positive reception across media, social media, research and academic literature, and professional societies.
Objective To evaluate the clinical outcome potential of embryos classified by preimplantation genetic testing for aneuploidy (PGT-A) as non-mosaic whole chromosome aneuploid (WCA) or segmental aneuploid (SA) in a large multicenter consortium study. Design Multicenter retrospective cohort study. Subjects Data were obtained from eight of the 26 fertility centers participating in the International Registry of Mosaic Embryo Transfers (IRMET) network that contributed non-mosaic WCA and SA embryo transfers between 2016 and 2026. The study included 250 embryo transfers (168 WCA and 82 SA) with complete clinical outcome documentation. Transfers were performed either with knowledge of the PGT-A result at the time of transfer or as non-selective transfers performed without knowledge of the PGT-A result. Exposure Trophectoderm biopsy at blastocyst stage followed by PGT-A using whole-genome amplification (WGA) and next-generation sequencing (NGS). Main Outcome Measures Pregnancy and neonatal outcomes. Results Among 168 WCA transfers, including 111 performed without knowledge of the PGT-A result at the time of transfer, no live births occurred. Most transfers resulted in no pregnancy (78.6%), with smaller proportions showing biochemical pregnancy (8.3%), ectopic pregnancy (1.8%), early spontaneous abortion (9.5%), late spontaneous abortion (1.2%), or therapeutic termination (0.6%). In contrast, SA transfers (n = 82) resulted in a 17.1% live birth rate. Neonatal data available for 10 SA live births showed no differences in gestational age or birthweight compared with live births following euploid embryo transfer at the same centers, and prenatal or neonatal genetic testing were normal in all tested cases. Conclusions In this large multicenter dataset of non-mosaic whole chromosome and segmental aneuploid embryo transfers, embryos classified as uniformly whole chromosome aneuploid produced no live births, whereas segmental aneuploid embryos retained a modest yet clinically meaningful potential for live birth. These findings support the biological validity of PGT-A classification of whole chromosome aneuploid embryos and highlight the distinct clinical implications of whole chromosome and segmental aneuploidies.
OBJECTIVE:To investigate associations between endocrine diseases and pregnancy loss, including associations according to the number of pregnancy losses, temporal patterns, and familial clustering independent of the woman's own endocrine diagnosis. DESIGN:Nationwide population-based cohort study. SUBJECTS:366,539 women born in Denmark between 1977 and 1993 with documented pregnancies in the Danish national registers. EXPOSURE:Presence of endocrine disease diagnosed before or after pregnancy. Subgroup analyses of major endocrine diseases, including hypothyroidism, hyperthyroidism, polycystic ovary syndrome (PCOS), type 1 and 2 diabetes, and gestational diabetes. MAIN OUTCOME MEASURES:Pregnancy loss, defined as the number of pregnancy losses before 22 weeks of gestation (categorized as 0, 1, 2, or ≥3 losses) in association with endocrine disease. Multivariable multinomial logistic regression models calculated odds ratios (ORs) with 95% confidence interval adjusted for maternal age and year of pregnancy. Additional analyses examined associations according to timing of endocrine disease diagnosis relative to the first pregnancy and evaluated familial clustering. RESULTS:Endocrine disease was diagnosed in 56,618 women (15%). In analyses that did not account for temporal order, endocrine disease showed progressively stronger associations with increasing number of pregnancy losses: OR 1.15 (95% CI: 1.12-1.17) for one, OR 1.30 (95% CI: 1.24-1.37) for two, and OR 1.81 (95% CI: 1.70-1.93) for three or more (p<0.001). All major endocrine diseases were significantly associated with pregnancy loss. Women diagnosed with an endocrine disease after their first pregnancy showed a stronger association with pregnancy loss in the first pregnancy (OR 1.24 [95% CI: 1.20-1.29]) than those diagnosed before the first pregnancy (OR 1.11 [95% CI: 1.07-1.15]). Familial endocrine disease in a parent or sister was also positively associated with pregnancy loss (OR 1.07 [95% CI: 1.05-1.09] and OR 1.08 [95% CI: 1.03-1.13], respectively), independent of the woman's own endocrine diagnosis. CONCLUSION:Endocrine diseases and pregnancy loss were strongly associated regardless of temporal order, with progressively stronger associations across increasing numbers of pregnancy losses, with significant familial clustering independent of personal diagnosis, suggesting shared genetic or environmental factors. Our findings support consideration of targeted endocrine evaluation in women with pregnancy loss. Further research should determine optimal screening strategies and timing.
