Background: Premature ovarian failure (POF) is a disorder of multi causal etiology. Autoimmunity has been proposed as a mechanism for some cases of ovarian follicle dysfunction which is evident in POF. The aim of this study was to identify the level of auto-antibodies in POF and FAMILIAL POF patients.Materials and Methods: In this study, auto-antibodies including anti-ovarian antibody (AOA), anti thyroid peroxidase (TPO) and anti thyroglobulin (TG) antibodies were assessed in the sera of 43 cases with spontaneous POF including 12 cases affected by FAMILIAL POF. The control samples were obtained from sera of 39 women with normal ovulatory or post menopause women.Results: AOA were detected in 46.5% of the POF group, 41.7% of the FAMILIAL POF group and 41% of the control group without significant statistical difference between the three groups. Thyroid peroxidase (TPO) antibody was found in 32.6% of the POF group, 41.6% of the FAMILIAL POF group and 10.3% of the control group. Anti TPO was detected significantly high in both POF and FAMILIAL POF groups (p<0.02 and p<0.01, respectively). Thyroglobulin (TG) antibody was found in 48.8% of the POF group, 75% of the FAMILIAL POF group and 23.1% of the control group with meaningful difference (p<0.02 and p<0.001, respectively). TG antibody was significantly higher in FAMILIAL POF group in comparison to POF group (p<0.03).Conclusion: Although measurement of AOA is not a reliable method for diagnosis of auto-immune POF, but existence of anti thyroid antibodies in FAMILIAL POF (mainly anti TG) can potentially represent an autoimmune mechanism. It is possible to propose a genetic component for developing autoimmune POF supported by presence of anti thyroid antibodies in FAMILIAL POF.

Premature ovarian failure (POF) is a heterogeneous disorder, defined as menopause under age 40 years. The prevalence is 1%; POF before age 30 years is much less common. Chromosomal causes have long been recognized - visible deletions of the X chromosome, 45, X/46, XX mosaicism, and autosomal rearrangements (balanced translocations). Toxins or iatrogenic causes (e.g., chemotherapeutic agents) are occasionally implicated; autoimmune causes exist. However, lack of explanations for most cases has led to the deduction that single gene mutations (autosomal or X-linked) must be responsible for most cases of POF. With molecular technology it is now possible to determine if a single cell is perturbed in POF. Many attractive candidate genes exist, usually based on animal models (mice).The most common single gene responsible for POF if perturbed is FMR1 (fragile X), CGG expansion explaining perhaps 5% of sporadic cases. A predictable set of genes whose perturbations cause POF are those encoding gonadotropins (FISH, LH) or their receptors (FSHR, LHR). Mutations in these gonadotropin-related genes are known but rare except for FSHR mutations in Finland. Other genes expressed during oogenesis have been interrogated by ourselves, including DNA binding proteins and transcription factors (NOBOX and LHX8), RNA binding proteins (NANOS, TGFb family members such as GDF9), and G protein receptors (GPR3). Additional genes expressed in oocytes (AT2, KIT, NOGGIN, MIS, MISR, BAX, RFPL4), are attractive candidates. To date causative mutations have still been identified in only a few genes (NOBOX, GDF9, LDX8, BMP 15) each explaining perhaps 1-2% of POF cases. However, population-specific studies are still limited, and a single mutation may prove important in certain populations like FSHR in Finland. Genome wide association studies (GWAS) are in progress and exome-sequencing planned.Clinical significance will arise from identifying POF genes. 1) Better prognosis and ovarian preservation can be offered for younger for younger family members having the same mutation; 2) Therapeutic replacement products can be envisioned to militate against ovarian failure.

Introduction: Premature ovarian failure (POF) occurs in women younger than 40 with 1-5 % prevalence. POF is a pathological condition and has negative effect on the health of affected women and leads to infertility. The main etiology of this disease is unknown but in many studies, immunological disturbances especially against thyroid glands have been introduced as possible causes. However, it hasn’t been proven by other studies. The aim of this study is the evaluation of several immunological tests in the POF women in comparison with normal ovulatory women.Materials and Methods: This prospective clinical case-control trial was done in Avicenna Infertility Clinic on 30 nonsmoking women with spontaneous POF at least for 1 year who didn’t have any previous history of bilateral oophorectomy, chemotherapy and radiotherapy with the serum FSH 3rd level more than 30U/L (case group) and compared with 30 nonsmoking normal ovulatory women (<40 years.old) who were under infertility workup for male factor with serum FSH level lower than 8 U/L (control group). The below stated tests were done in each group: ANA, dsDNA, RF, anti thymoglobulin Ab, anti TPO (anti microsomal Ab) and hormonal tests including: FSH-LH-TSH.Results: In control group, there were 4 cases of thyroid disease vs. 0 in case group (P=0.02). The mean average of ANA, dsDNA, RF, anti thyroglobulin Ab, anti TPO (anti microsomal Ab) and TSH didn’t have any significant differences between two groups.Conclusion: Based on our study, we couldn’t find any disturbances either in immunological tests or in thyroid function of POF women as compared with normal ovulatory women.

Premature ovarian failure (POF), is a condition characterized by the early decline of ovulation function. POF is a complex disorder that can be caused by various factors, and the idiopathic form represents a significant proportion of POF patients. Hormone replacement therapy (HRT) is currently considered the first-line treatment for POF. This review aims to provide a comprehensive overview of recent advancements in platelet-rich plasma (PRP), in vitro activation (IVA), stem cell therapy, exosome therapy, microRNAs, and mitochondrial targeting therapies as a promising cell-free therapeutic approach in reproductive medicine. PLT-Exos, a new generation of cells, has been used to treat POF for more than a decade and has been shown to attenuate oocyte morphology and promote the differentiation of theca cells through the upregulation of PI3K/Akt and Bcl2, as well as the downregulation of the Smad and Bax signaling pathways. This review summarizes the current state of the art in the field of PLT-Exos and discusses the advantages and limitations of their potential clinical applications.