China
Africa
Explore chapters and articles related to this topic
Principles of Pathophysiology of Infertility Assessment and Treatment*
Published in Asim Kurjak, Ultrasound and Infertility, 2020
Joseph G. Schenker, Aby Lewin, Menashe Ben-David
Until recently, women with ovarian failure suffering primary or secondary amenorrhea, hypergonadotrophism, and hypoestrinism were considered incurably sterile. Primary ovarian failure is due to gonadal dysgenesis, Turner’s syndrome, Turner-like mosaics, and in cases of mixed gonadal dysgenesis. Premature ovarian failure is a rare entity. Its incidence is 3.1% of all women. It is defined as ovarian failure characterized by secondary amenorrhea with elevated gonadotropin levels occurring prior to the age of 35 years. Premature ovarian failure may be due to premature menopause, resistant ovary syndrome, autoimmune disorders, galactosemia, ovarian destruction following surgery, radiation, and chemotherapy.
Immunopathogenesis and Therapy of Gonadal Disorders and Infertility
Published in George S. Eisenbarth, Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
Afollicular premature ovarian failure may result from a variety of causes. Infections have the most impact at periods of high follicle turnover such as at birth, puberty, and peripartum. Viral oophoritis associated with mumps is a common cause.5 Mycobacterial infections, toxins, radiation therapy, chemotherapy (e.g., cyclophosphamide), and surgery exert physical or environmental insult to the ovary.6,7 Congenital disorders may be associated with accelerated follicular atresia. Turner’s syndrome (monosomy X) is associated with a normal number of follicles at 20 weeks gestation and normal histology until the fourth intrauterine month. This is followed by accelerated follicular loss.8-11 Sex chromosome mosaicism 45, XO/46, XX improves ovarian function when compared with Turner’s syndrome, and menstruation may occur in up to 30%.12 Accelerated atresia may also occur in the presence of thymic aplasia.13 An example of this is the athymie nude mouse model. Thymic peptides may stimulate GnRH. Ataxia telangiectasia, myotonia dystrophica, and galactosemia (possible failure of germ cell migration) have all been associated with premature menopause.14 Familial afollicular premature menopause has been reported and may be X-linked dominant or possibly autosomal dominant. Autoimmune disease may also cause an afollicular (or decreased follicular number) form of premature ovarian failure.
Fertility Preservation for Cancer Patients
Published in Steven R. Bayer, Michael M. Alper, Alan S. Penzias, The Boston IVF Handbook of Infertility, 2017
Women over the age of 40 years have a 90% chance of amenorrhea subsequent to multiagent chemotherapy, whereas the potential for premature ovarian failure in younger patients varies between 20% and 90% [5]. All patients exposed to chemotherapy will have a diminished ovarian reserve and, therefore, potential infertility with a significant predisposition for developing premature ovarian failure. Chemotherapy treatments may, in fact, be the leading cause of premature ovarian senescence, since 2% of the female population between the ages of 1 and 39 will be diagnosed with cancer, and half of these patients will require treatment with chemotherapy [1].
A bibliometric analysis of primary ovarian insufficiency from 2010 to 2020
Published in Climacteric, 2022
Z.-H. Deng, H.-J. Tan, L. Wang, P.-P. Long, D. Guo, R.-P. Quan, M.-H. Zeng, H.-W. Deng, H.-M. Xiao
Primary ovarian insufficiency (POI) is defined as ovarian function recession and oligomenorrhea/amenorrhea, with gonadotropin and estrogen deficiency among women below the age of 40 years [1]. The diagnostic criteria are oligomenorrhea/amenorrhea for at least 4 months, and an elevated follicle stimulating hormone (FSH) level >25 IU/l on two occasions >4 weeks apart. Recent meta-analyses suggest that 3.7% of women are affected by POI [2,3]. The disease is heterogeneous. Potential etiologies can be divided into genetic, iatrogenic, immune and environmental causes. More than half of POI patients with unclear etiology are identified with idiopathic POI. In fact, POI is also known as premature ovarian failure. Premature ovarian failure is defined as cessation of menstruation before the expected age of menopause [4]. This age is presumed to be before 40 years old and diagnosis is confirmed by elevated serum FSH levels (>40 IU/l). The description of POI includes the entire gamut of disorders having diminished ovarian reserve – occult, subclinical and iatrogenic. Premature ovarian failure is considered the final stage of POI, but confusion still exists concerning nomenclature [4].
Targeting signaling pathways involved in primordial follicle growth or dormancy: potential application in prevention of follicular loss and infertility
Published in Expert Opinion on Biological Therapy, 2022
Sara Ali Farhat, Forouq Jabbari, Parnian Jabbari, Nima Rezaei
Despite the numerous trials conducted so far to prevent females’ premature ovarian failure and infertility, no efficient methods have been developed yet due to the challenging aspect of the complex female reproductive cycles. The limited number of ovarian follicles that might be exhausted either by environmental, genetic or iatrogenic factors requires holistic approaches to protect this reserve, especially with the expanding use of gonadotoxic agents in ovarian therapy. Hence, targeting the pathways that are involved in follicles development might be the key to controlling the exhaustion of the follicles pool by stopping the primordial follicles from transition to the other stages. This can control the main mechanism behind premature ovarian failure induced by over-recruitment of follicles. This effect was seen by the use of several elements that proved to reduce primordial to primary follicles transition through directed mechanisms targeting signaling pathways responsible for primordial follicles activation.
Young women’s opinions on the use of a blood test to predict the possibility of premature ovarian failure: a qualitative study
Published in Human Fertility, 2021
Anouk Grootenhuis, Agnes van den Hoogen, Frank Broekmans, Helen Torrance, Harmieke van Os-Medendorp, Henrietta Ockhuijsen
Every woman is born with a finite number of oocytes (around 1 million follicles/oocytes) (Gleicher, Kushnir, & Barad, 2015), and each month, the number decreases. At some point, when the number of oocytes is too low, the woman stops menstruating. A woman is considered to be menopausal when no menstrual periods have occurred for 12 consecutive months is defined as the start of the menopause (Gleicher, Weghofer, Oktay, & Barad, 2009; National Institutes of Health, 2005). Worldwide, the average age at which menopause occurs is around 51 years, with a broad range of 40–60 years (Bouma et al., 2001; Gleicher et al., 2015; Pal & Santoro, 2002; Treloar, 1981). When menstruation stops before the age of 40 years, it is called premature ovarian failure (POF). Worldwide, POF affects 1 in every 1000 women between the ages of 15 and 29, and 1 in every 100 women between the ages of 30 and 39 (Goswami & Conway, 2005; Pal & Santoro, 2002; Shuster, Rhodes, Gostout, Grossardt, & Rocca, 2010). POF can be described as a decline in both ovarian function and the ovarian response to follicle-stimulating hormone (FSH) and as a reduction of oestrogen levels (Alipour, Rasekhjahromi, Maalhagh, Sobhanian, & Hosseinpoor, 2015). Risk factors for POF include hereditary diseases, enzyme shortage (decreased oestrogen production), smoking, alcohol use and autoimmune diseases as well as damage to the ovaries as a result of chemotherapy and radiation therapy (Gleicher et al., 2015).