Human reproduction open最新文献

{"title":"Correction to: Birth defects reporting and the use of dydrogesterone: a disproportionality analysis from the World Health Organization pharmacovigilance database (VigiBase).","authors":"","doi":"10.1093/hropen/hoaf029","DOIUrl":"https://doi.org/10.1093/hropen/hoaf029","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/hropen/hoae072.].</p>","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 2","pages":"hoaf029"},"PeriodicalIF":8.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12132097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Uterine smooth muscle tumours with uncertain malignant potential: reproductive and clinical outcomes in patients undergoing fertility-sparing management.","authors":"","doi":"10.1093/hropen/hoaf032","DOIUrl":"https://doi.org/10.1093/hropen/hoaf032","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/hropen/hoaf009.].</p>","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 2","pages":"hoaf032"},"PeriodicalIF":8.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12132096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Why does the latest pharmacovigilance data not reflect clinical experience with dydrogesterone?","authors":"Emre Pabuccu, Angela Aguilar, Roberto de Azevedo Antunes, Eran Gefen, Lee P Shulman","doi":"10.1093/hropen/hoaf030","DOIUrl":"10.1093/hropen/hoaf030","url":null,"abstract":"","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 3","pages":"hoaf030"},"PeriodicalIF":8.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply: Fetal safety of dydrogesterone: clarifying the role of pharmacovigilance.","authors":"Laurent Chouchana, Alexandra Henry, Mathilde Bourdon, Chloé Maignien, Charles Chapron, Jean-Marc Treluyer, Jean Guibourdenche, Pietro Santulli","doi":"10.1093/hropen/hoaf031","DOIUrl":"10.1093/hropen/hoaf031","url":null,"abstract":"","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 3","pages":"hoaf031"},"PeriodicalIF":8.3,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressively diminished estrogen signaling concordant with increased fibrosis in ectopic endometrium.","authors":"Jichan Nie, Yunhua Yi, Xishi Liu, Sun-Wei Guo","doi":"10.1093/hropen/hoaf028","DOIUrl":"10.1093/hropen/hoaf028","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Study question: &lt;/strong&gt;Do all ectopic endometrial lesions (endometriosis and adenomyosis) universally have activated estrogen signaling?&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary answer: &lt;/strong&gt;Estrogen signaling diminishes concordantly with increased fibrosis in ectopic endometrium, with deep endometriotic (DE) lesions exhibiting an estrogen biosynthesis capability and estrogen receptor β (ERβ) expression level comparable to that of control endometrium but having suppressed ERα.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;What is known already: &lt;/strong&gt;Endometriosis and adenomyosis are both estrogen-dependent diseases driven by estrogen-mediated lesional development, progression, and symptom manifestation. Of note, ectopic endometrium is thought to have the ability to synthesize estradiol (E&lt;sub&gt;2&lt;/sub&gt;) &lt;i&gt;in situ&lt;/i&gt; from cholesterol due to upregulation of aromatase (CYP19A1), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase type 2 (HSD3β2), and HSD17β1. In addition to increased estrogen biosynthesis, ERβ and G-protein coupled ER (GPER) are also overexpressed in ectopic endometrium. In particular, the prevailing view holds that prostaglandin E2 plays a vital role in facilitating estrogen biosynthesis and the upregulation of ERβ, positioning itself in the central nexus in a feed-forward loop linking hyperestrogenism and inflammation in all ectopic endometria.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design size duration: &lt;/strong&gt;After obtaining written informed consent, we collected lesional tissues from 19 patients with ovarian endometriosis (OE) and 20 patients each with adenomyosis (AD) and DE. As controls, normal endometrial tissue samples (CT) were procured from 20 cycling women free of endometriosis and adenomyosis, and age- and menstrual phase-matched with patients in the other groups. Additionally, primary ectopic or control endometrial stromal cells derived from eight subjects in each of the OE, AD, DE, and CT groups were cultured for experiments.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Participants/materials setting methods: &lt;/strong&gt;We performed immunohistochemistry and western blotting to assess the expression of proteins key to the estrogen biosynthesis (StAR, HSD3β2, aromatase, and HSD17β1) and estrogen receptors (ERα, ERβ, and GPER). Fibrosis was quantified via Masson trichrome staining. Real-time RT-PCR was performed to assess corresponding gene expression levels. The estrogen concentrations in cell cultures of primary stromal cells derived from different tissues were also measured by ELISA.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main results and the role of chance: &lt;/strong&gt;Among all ectopic endometrial tissue samples, the extent of lesional fibrosis was the highest in the DE lesions, followed by the AD and then the OE lesions. The protein and gene expression levels of StAR, HSD3β2, aromatase, and HSD17β1, the four proteins critically involved in estrogen biosynthesis, were significantly higher than in the CT group in OE and AD lesions, but were lowest in DE lesions, which were comparable to that of c","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 3","pages":"hoaf028"},"PeriodicalIF":8.3,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12165729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144303844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia exposure impairs male fertility via inhibiting Septin2-mediated spermatogonial proliferation.","authors":"Zhibin Li, Shuying Li, Yufeng Xiao, Junfeng Guo, Jianchun Zhou, Yang Chen, Juan Yang, Chunli Gong, Bing He, Yuyun Wu, Nannan Gao, Huan Yang, Limin Gao, Hua Hu, Yunfang Zhang, Shiming Yang","doi":"10.1093/hropen/hoaf027","DOIUrl":"10.1093/hropen/hoaf027","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Study question: &lt;/strong&gt;What are the molecular mechanisms underlying hypoxia-induced male reproductive impairment?&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary answer: &lt;/strong&gt;Hypoxia compromises Septin2 (&lt;i&gt;Sept2&lt;/i&gt;) transcription in spermatogonia, which impedes spermatogonial proliferation through protein phosphatase 2A (PP2A)-dependent AKT dephosphorylation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;What is known already: &lt;/strong&gt;Hypoxia is associated with impaired spermatogenesis and poor sperm parameters in men. Spermatogonia proliferation, a crucial early step in spermatogenesis, is essential for maintaining the spermatogenic cell population and ensuring sperm quality. However, the connection between hypoxia and spermatogonial proliferation remains poorly understood, and treatment options for hypoxia-related reproductive disorders are limited.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design size duration: &lt;/strong&gt;A cross-sectional study analyzed semen samples from 24 high-altitude (HA) residents, 6 pathological hypoxia (PH) patients, and 19 healthy controls to evaluate hypoxia-associated sperm parameter alterations. Complementary animal studies employing a hypobaric chamber-induced hypoxic mouse model (n = 5) confirmed reproductive impairments through assessment of birth rates, sperm quality, and testicular histopathology. Transcriptomic profiling of hypoxic versus normoxic mouse testes (n = 3/group) identified spermatogonial proliferation defects as a predominant pathological feature and pinpointed &lt;i&gt;Sept2&lt;/i&gt; as a candidate mediator. Subsequent mechanistic investigations employed &lt;i&gt;in vitro&lt;/i&gt; hypoxic culture of spermatogonial cell lines under hypoxic conditions coupled with pharmacological modulation of PP2A activity in mice (n = 3-5 per intervention group) to delineate the underlying molecular pathways.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Participants/materials setting methods: &lt;/strong&gt;Semen parameters were evaluated using computer-assisted sperm analysis (CASA; for sperm concentration, count, and motility), morphological staining (Pap staining for sperm deformity), and eosin-nigrosin staining (for sperm viability). In the hypoxic mouse model, fertility outcomes were assessed through fertility assessment (mating experiments), sperm parameters (CASA), testicular histology (H&E staining), and spermatogonia proliferation (immunohistochemistry and qPCR). In hypoxic spermatogonial cell models, cell proliferation was detected using CCK-8, EdU incorporation, flow cytometry, and western blotting. &lt;i&gt;Sept2&lt;/i&gt; manipulation (knockdown/overexpression), followed by mechanistic analyses (dual-luciferase reporter assay, DNA pulldown/mass spectrometry, TMT-based quantitative proteomics, co-immunoprecipitation, etc.), was performed to investigate the mechanism underlying hypoxia-regulated spermatogonia proliferation. The SEPT2 inhibitor forchlorfenuron (FCF), the PP2A agonists celastrol, erlotinib, and FTY720, as well as PP2A inhibitor okadaic acid (OA) were used to investigate the role of the SEPT2-PP2A-AKT axis in male fer","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 3","pages":"hoaf027"},"PeriodicalIF":8.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12145212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of pubertal induction with combined gonadotropin therapy on testes development and spermatogenesis in males with gonadotropin deficiency: a cohort study.","authors":"Sebastian Castro, Kyla Ng Yin, Francesco d'Aniello, Emma C Alexander, Emily Connolly, Claire Hughes, Lee Martin, Rathi Prasad, Helen L Storr, Ruben H Willemsen, Leo Dunkel, Gary Butler, Sasha R Howard","doi":"10.1093/hropen/hoaf026","DOIUrl":"10.1093/hropen/hoaf026","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Study question: &lt;/strong&gt;Are recombinant FSH (rFSH) and hCG effective therapies for promoting testicular growth and spermatogenesis in male adolescents and young adults with gonadotropin deficiency?&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary answer: &lt;/strong&gt;Combined gonadotropin therapy is effective in inducing puberty and promoting spermatogenesis in male adolescents and young adults with gonadotropin deficiency and has the potential to improve adult outcomes relating to both fertility and quality of life.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;What is known already: &lt;/strong&gt;Deficiency of pituitary gonadotropins (LH and FSH) due to hypogonadotropic hypogonadism (HH) can result in poor testicular development, low testicular volumes, micropenis and cryptorchidism. Inadequate hormonal replacement can lead to long-term issues, including subfertility or infertility, and reduced quality of life. Exogenous testosterone for pubertal induction can elevate serum testosterone concentrations and induce virilization, but it does not promote testicular development nor induce spermatogenesis. Fertility and testes growth remain primary concerns for patients seeking treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design size duration: &lt;/strong&gt;We conducted a retrospective observational review of male adolescents and young adults with gonadotropin deficiency and seeking puberty replacement therapy at two large tertiary centre hospitals in London, UK, from 2010 to 2024.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Participants/materials setting methods: &lt;/strong&gt;A total of 35 males, with diagnosis of congenital hypogonadotropic hypogonadism (CHH: n = 23; further subdivided into those with partial [pHH: n = 8] and those with complete gonadotropin deficiency [cHH: n = 15]), acquired HH (AHH: n = 4) or Kallmann syndrome (KS: n = 8), received combined gonadotropin therapy. We assessed testicular growth and semen quality post-treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main results and the role of chance: &lt;/strong&gt;The majority of patients were referred for pubertal delay, alone or in combination with cryptorchidism, micropenis or microorchidism. Out of 35 patients, 22 (63%) had previously received testosterone, and the median age at gonadotropin treatment initiation was 15.8 years (range: 11.8-22.7). Semen analysis was obtained in 18 out of 19 patients who had received gonadotropin therapy for a median treatment duration of 21.1 months (range: 4.5-66.9) for rFSH and 19.5 months (range: 8.3-61.1) for hCG. The median sperm count on semen analysis was 8.9 × 10&lt;sup&gt;6&lt;/sup&gt;/ml (range: 0.0-54.9). Significant increases were noted in testicular volume (median change after therapy: 10.5 ml [95% CI 9.5-13.6], &lt;i&gt;P&lt;/i&gt; &lt; 0.0001), testosterone (median increase: 25.7 nmol/l [95% CI 19.8-31.5], &lt;i&gt;P&lt;/i&gt; &lt; 0.0001) and inhibin B levels (67.7 pg/ml [95% CI 18.4-86.7], &lt;i&gt;P&lt;/i&gt; = 0.0008).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Limitations reasons for caution: &lt;/strong&gt;The relatively low representation of patients with acquired HH in our study emphasizes the need to extrapolate the findings with caution in thi","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 2","pages":"hoaf026"},"PeriodicalIF":8.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12132099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Automatic identification of human spermatozoa with zona pellucida-binding capability using deep learning.","authors":"Erica T Y Leung, Xianghan Mei, Brayden K M Lee, Kevin K W Lam, Cheuk-Lun Lee, Raymond H W Li, Ernest H Y Ng, William S B Yeung, Lequan Yu, Philip C N Chiu","doi":"10.1093/hropen/hoaf024","DOIUrl":"10.1093/hropen/hoaf024","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Study question: &lt;/strong&gt;Can a deep-learning algorithm, independent of World Health Organization (WHO) sperm morphology grading, be used to identify human spermatozoa with zona pellucida (ZP)-binding capability in assisted reproductive technology (ART)?&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary answer: &lt;/strong&gt;A novel deep-learning model, irrespective of the conventional semen analysis, was established to identify human spermatozoa capable of binding to ZP for predicting their fertilization potential.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;What is known already: &lt;/strong&gt;Sperm morphology evaluation is crucial in semen analysis to investigate male infertility and to determine the appropriate insemination methods in ART. The current manual assessment, which relies on microscopically examining individual spermatozoa based on WHO criteria, has shown limited predictive power for fertilization outcomes due to its highly subjective, labour-intensive nature, and high inter-/intra-assay variations. Deep learning is a rapidly evolving method for automated image analysis. Recent studies have explored its potential for automating sperm morphology analysis. However, algorithms trained on manually annotated datasets using existing WHO criteria have had little success in predicting ART outcomes. To date, no study has established an independent set of morphology evaluation standards based on sperm fertilizing ability for clinical prediction.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design size duration: &lt;/strong&gt;Spare semen samples were collected from men undergoing premarital check-ups at a family planning clinic. Immature oocytes at germinal vesicle/metaphase I stage, or mature metaphase II oocytes were donated from women attending the infertility clinic for assisted reproduction treatments. Acrosome-intact, ZP-bound spermatozoa were collected by our previously modified spermatozoa-ZP coincubation assay. ZP-unbound spermatozoa were collected from normozoospermic samples with defective ZP-binding ability, as evidenced by complete fertilization failure following conventional &lt;i&gt;in vitro&lt;/i&gt; fertilization (IVF) and the absence of ZP-bound spermatozoa on the inseminated oocytes. A total of 1083 Diff-Quik stained images of ZP-bound and unbound spermatozoa were collected to create a training database, with an additional 220 images serving as an independent test set. Clinical data were obtained from 117 men undergoing IVF due to male factor or unexplained infertility to validate the model's ability to generalize to new data. These participants were categorized into three groups based on their fertilization rates following IVF: low (0-40%), intermediate (41-70%), and high (71-100%).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Participants/materials setting methods: &lt;/strong&gt;A pre-trained VGG13 model was fine-tuned using our database to classify individual spermatozoa as either ZP-bound or unbound based on their automatically extracted morphological features. Confusion matrix was used to assess the model's classification performance, expressed in term","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 3","pages":"hoaf024"},"PeriodicalIF":8.3,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12145210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Controlled ovarian stimulation for oocyte preservation in childhood cancer survivors who have undergone chemotherapy.","authors":"Moran Shapira, Dror Meirow, Dani Raved, Leyla Levy, Noah Gruber, Dalit Modan-Moses, Raoul Orvieto, Myriam Safrai","doi":"10.1093/hropen/hoaf023","DOIUrl":"10.1093/hropen/hoaf023","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Study question: &lt;/strong&gt;What are the outcomes of controlled ovarian stimulation (COS) in childhood cancer survivors (CCS) undergoing fertility preservation (FP) after cancer treatment?&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary answer: &lt;/strong&gt;CCS who have undergone chemotherapy often show poor outcomes with COS and may need multiple cycles to achieve an adequate number of oocytes for future pregnancy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;What is known already: &lt;/strong&gt;Up to 65% of CCS experience infertility from gonadotoxic treatments. Although it is ideal to consider FP at diagnosis, age and oncological factors often limit this option. After recovery, pubescent survivors, especially those who could not preserve fertility earlier, may be offered oocyte cryopreservation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design size duration: &lt;/strong&gt;A retrospective study including 20 CCS who underwent COS for oocyte storage between 2015 and 2022.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Participants/materials setting methods: &lt;/strong&gt;This study involved young CCS who had been previously treated with chemotherapy and were evaluated at an FP center in a tertiary medical center. CCS were encouraged to pursue endocrine surveillance after recovering from cancer and were offered oocyte storage in case diminished ovarian reserve was evident, as dictated by elevated basal FSH (&gt;10 IU/l), decreased anti-Müllerian hormone (AMH; &lt;25th percentile for age), or low antral follicle count (&lt;7).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main results and the role of chance: &lt;/strong&gt;Mean age at cancer diagnosis was 13.24 ± 5.6 years. Seventeen patients (85%) had been treated with alkylating agents, with five receiving cumulative doses greater than 4000 mg/m&lt;sup&gt;2&lt;/sup&gt;. At the time of FP, a median of 4.25 years after cancer diagnosis, the mean age of patients was 20.6 ± 3.56 years. Mean Day 3 FSH levels were 9.26 ± 3.4 IU/l, and 12 patients had AMH levels below 1 ng/ml. The first stimulation cycle lasted 9.4 ± 2.1 days, with a mean gonadotropin dose of 3246 ± 1057 IU and a median peak estradiol (E2) level of 3733 pmol/ml (IQR 1424-6796). The median number of oocytes retrieved in the first stimulation cycle was 5.5, with a median of four mature oocytes. By the end of the FP process, which involved 1-7 cycles per patient, the median number of oocytes stored was 13.5 (IQR 3.5-18.5). Twelve patients managed to store more than 10 oocytes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Limitations reasons for caution: &lt;/strong&gt;The study is exploratory in its nature, limited by its small sample size and its retrospective design.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Wider implications of the findings: &lt;/strong&gt;Oocyte storage is feasible yet limited in young CCS. Despite their young age at the time of FP, CCS who have undergone chemotherapy often show poor outcomes with COS. Ongoing reproductive monitoring after recovery is crucial to identify those who would benefit from FP following cancer treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study funding/competing interests: &lt;/strong&gt;The Fertility Preservation Unit funds (Sheba Medical Center) were used to suppor","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 2","pages":"hoaf023"},"PeriodicalIF":8.3,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12122208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144200992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perinatal risks associated with infertility and medically assisted reproduction: a population-based cohort study.","authors":"Stephanie K Y Choi, Wentao Li, Christos Venetis, William Ledger, Kei Lui, Katie Harris, Robert J Norman, Louisa R Jorm, Georgina M Chambers","doi":"10.1093/hropen/hoaf020","DOIUrl":"10.1093/hropen/hoaf020","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Study question: &lt;/strong&gt;Are the risks of adverse perinatal outcomes in singletons born from medically assisted reproduction (MAR) mainly associated with underlying parental infertility, or are they primarily linked to the MAR treatments?&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary answer: &lt;/strong&gt;While MAR-conceived singletons have increased risks of preterm birth, admission to neonatal intensive care unit (NICU), and hospital admission in early life, these risks are mainly associated with the underlying parental infertility that led to the use of MAR technologies.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;What is known already: &lt;/strong&gt;Children born from MAR are at increased risk for some adverse perinatal and infant outcomes. However, to what extent this risk is associated with infertility or MAR treatment remains unclear. This knowledge gap arises from the challenge in disentangling the effects of infertility and MAR treatment, given that parental infertility necessitates the use of MAR treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study design size duration: &lt;/strong&gt;This is a statewide longitudinally data-linked population-based cohort study conducted in New South Wales, Australia, involving all singleton infants born (liveborn or stillborn) between 2009 and 2017.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Participants/materials setting methods: &lt;/strong&gt;We applied two comparisons to isolate the associations of infertility from its treatment: (i) MAR infants versus naturally conceived infants from fertile parents (NC-fertile), and (ii) MAR infants versus naturally conceived infants from parents who had a history of infertility (NC-infertile). The study cohort consisted of 824 639 singleton infants, of whom 27 796 (3.4%) were conceived through ART and 13 574 (1.6%) through ovulation induction/intrauterine insemination (OI/IUI), while 783 269 (95.0%) of the infants were naturally conceived (747 018 NC-fertile controls and 36 251 NC-infertile controls). We used the inverse probability of treatment weighting method to make MAR infants comparable with each of the two NC control groups. We then calculated the adjusted risk differences (aRDs) in these propensity score-weighted cohorts. In the subgroup analyses of different forms of ART treatment (ICSI vs IVF and fresh vs frozen embryo transfer), we reweighted the study cohort and compared these subgroups with the two NC control groups separately.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main results and the role of chance: &lt;/strong&gt;Singletons conceived through ART had a higher risk for preterm birth (aRD 25.7 per 1000 infants, 95% CI 21.3-30.0), admission to NICU (aRD 8.4 per 1000 infants, 95% CI 1.2-15.6), and hospital admission within 2 years of life (aRD 24.6 per 1000 infants, 95% CI 17.2-32.0) compared to NC-fertile controls. These risks were notably reduced when compared to NC-infertile controls (aRD 9.5 per 1000 infants, 95% CI 4.8-14.2 for preterm birth; -0.7 per 1000 infants, 95% CI -8.0 to 6.6 for NICU admission; and 10.6 per 1000 infants, 95% CI 2.5-18.7 for hospital admission within 2 years of life","PeriodicalId":73264,"journal":{"name":"Human reproduction open","volume":"2025 2","pages":"hoaf020"},"PeriodicalIF":8.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144200993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}