Racial and ethnic disparities in assisted reproductive technology: a systematic review.

There is emergent scientific literature examining the disparities in reproductive care of women in the United States. Reproduction is a basic human right and there are unique challenges that racial and ethnic minorities face in accessing fertility care and assisted reproductive technology. The identification of these disparities can aid in identifying areas for interventions to improve and resolve, the inequities that exist in providing care for minority populations. A literature search was performed using PubMed to identify articles with data specific to racial and ethnic differences in study populations as it related to infertility, access to care, and treatment outcomes. The following review and collection of articles provide a comprehensive overview of the disparities that exist, the factors that contribute to these disparities, and recommendations for how providers and health care systems may begin to resolve the gaps in equitable care.

Use of gonadotropin-releasing hormone (GnRH) agonist trigger in fertility preservation for patients with inherited genetic disorders.

In patients with varying hematologic disorders (thalassemia, sickle cell anemia, aplastic anemia, etc.), inherited bone marrow failure syndromes, and immune deficiencies due to a single gene disorder, the advent of stem cell transplantation (SCT) as a treatment option has allowed for significant disease improvement, and possibly cure. This specific treatment option often requires exposure to chemotherapeutic agents and sometimes whole body radiation; therefore, primary ovarian insufficiency is often sequelae of the therapy. The optimization of fertility preservation protocols within this patient population is of extreme importance. This review aims to detail the use of GnRH agonist use within this patient population, within the context of fertility preservation cycles.

Fetal programming of polycystic ovary syndrome: Effects of androgen exposure on prenatal ovarian development.

Polycystic ovary syndrome (PCOS) is a common form of anovulatory infertility with a strong hereditary component but no candidate genes have been found. The inheritance pattern may be due to in utero androgen programming on gene expression and mitochondria. Mitochondria are maternally inherited and alterations to mitochondria after fetal androgen exposure may explain one of the mechanisms of fetal programming in PCOS. Our aim was to investigate the role of excessive prenatal androgens in ovarian development by identifying how hyperandrogenemia affects gene expression and mitochondria in neonatal ovary. Pregnant dams were injected with dihydrotestosterone on days 16-18 of pregnancy. Day 0 ovaries were collected for gene expression and mitochondrial studies. RNAseq showed differential gene expressions which were related to mitochondrial dysfunction, fetal gonadal development, oocyte maturation, metabolism, angiogenesis, and PCOS. Top 20 up and downregulated genes were validated with qPCR and Western Blot. Transcriptional pathways involved in folliculogenesis and genes involved in ovarian and mitochondrial function were dysregulated. Further, DHT exposure altered mitochondrial ultrastructure and function by increasing mitochondrial oxygen consumption and decreasing mitochondrial efficiency with increased proton leak within the first day of life. Our data indicates that one path that leads to PCOS begins at birth and is programmed in utero by androgens.