Bakgrund Polycystiskt ovarialsyndrom (PCOS) är en hormonell störning hos fertila kvinnor. Den ger symtom som oregelbunden eller utebliven menstruation, övervikt, ökad kroppsbehåring samt risk för infertilitet. Kunskapen är bristfällig både i samhället och bland vårdpersonal. Det är viktigt att öka medvetenheten om PCOS för att erbjuda en personcentrerad vård och förebygga allvarliga hälsoproblem. Syfte Syftet var att beskriva kvinnors upplevelse av att leva med polycystiskt ovarialsyndrom. Metod En litteraturöversikt utifrån tio artiklar från Pubmed samt Cinahl Complete. Alla artiklar var granskade utifrån Fribergs kvalitetgranskningsmall. Resultat Två huvudteman framkom i resultatet. Det första huvudtemat var Kvinnors erfarenheter i mötet med sjukvården och det inkluderade undertemat Bristande kunskap inom hälso- och sjukvården samt Bemötande. Hälso- och sjukvårdspersonalen hade bristande kunskap om PCOS vilket ledde till försenade diagnoser och negativt bemötande. Kvinnorna upplevde en frustration och fann stöd i form av stödgrupper och internetinformation. Det andra huvudtemat fokuserade på Kvinnlig identitet med undertemat Övervikt, Hirsutism, Infertilitet och Femininitetsnormer. Dessa teman beskrev kvinnornas erfarenheter av PCOS-symtom och deras jämförelser med andra kvinnor utifrån samhällets normer. De upplevde stigma av symtomen och den emotionella påverkan av dessa symtom ledde till en påtaglig fysisk och psykisk påfrestning på kvinnornas välbefinnande. Slutsats Kvinnor med PCOS behöver utökat stöd av vården för fysiska och psykiska symtom. Ett lidande uppstår av försenade diagnoser och bristande kunskap. / Background Polycystic Ovary Syndrome (PCOS) is a hormonal disorder in fertile women. It presents symptoms such as irregular or absent menstruation, overweight, increased body hair, and a risk of infertility. Knowledge is deficient both in society and among healthcare professionals. It is crucial to raise awareness about PCOS to provide person-centered care and prevent serious health issues. Aim The aim was to describe women's experiences of living with polycystic ovary syndrome. Method A literature review based on ten articles from PubMed and Cinahl Complete. All articles were reviewed according to Friberg's quality assessment template. Results Two main themes emerged in the results. The first main theme was Women's experiences in the encounter with healthcare, and it included the subthemes Lack of knowledge in healthcare and Interaction. Caregivers lacked knowledge about PCOS, leading to delayed diagnoses and negative treatment. Women experienced frustration and found support in the form of support groups and online information. The second main theme focused on Female identity with subthemes of Overweight, Hirsutism, Infertility, and Femininity norms. These themes described women's experiences of PCOS symptoms and their comparisons with other women based on societal norms. They faced stigma related to their symptoms and the emotional impact of these symptoms resulted in a significant physical and psychological strain on women's well-being. Conclusions Women with PCOS need expanded support from healthcare for their physical and psychological symptoms. Suffering arises from delayed diagnoses and a lack of knowledge from healthcare providers.

Between 10-15% of women suffer from polycystic ovary syndrome (PCOS), making it the most common cause of female infertility. Clinical features of PCOS include high circulating levels of ovarian androgens (T and A4), anovulation and obesity. The aetiology of this reproductive endocrinopathy is likely to be multifactorial, through the interplay of genetics, epigenetics and environmental factors. Primate research into sexual behaviour development noted that fetally androgenised monkeys developed symptoms like those of PCOS. There are now multiple animal models of PCOS using primates, sheep, rats and transgenic mice. The investigations described in this thesis use rodent models to examine the role of androgens in the pathogenesis of female infertility. An attempt to generate a granulosa cell specific androgen receptor knockout mouse model will first be described, followed by several studies into the developmental programming of female Wistar rat infertility and metabolism by steroid hormones. Initial investigations showed that testosterone proprionate (TP) administered to female rats during different windows of fetal and neonatal life alters the reproductive and metabolic axes of the adult animals. Fetal plus neonatal TP exposure led to complete ovarian dysgenesis, while postnatal exposure produced a PCOS-like phenotype. Animals which received TP postnatally were heavier and had an increased proportion of primordial follicles in their ovaries by postnatal day (pnd) 90 of life. Evaluation of this PCOS model showed that neonatally androgenised rats had ovarian follicles with larger antra and a greater ovarian stromal compartment. In addition, these animals were heavier when compared to controls. However, unlike human studies, neonatally androgenised rats showed no differences in circulating gonadotrophin or ovarian androgen levels. Nor did they show any programming effect of neonatal TP upon the theca interna by pnd 90. Further investigations to narrow the windows and dose of TP required to produce a PCOS phenotype showed that TP administered in an early window of neonatal life, between postnatal days (pnd) 1-6 not only led to anovulation, but potentially reprogrammed the hypothalamic-pituitary axis, as there was minimal gonadotrophin response to reduced ovarian negative feedback (inhibin B and estradiol) in these rats. Neonatal TP also affected the rat metabolic axis with adult animals becoming heavier after weaning without any change in food intake. Animals developed mesenteric and retroperitoneal obesity along with insulin resistance (IR). Increased hepatic glucocorticoid turnover and altered adipokine expression were also noted in neonatally androgenised females, possibly contributing to the pathogenesis of obesity. No effect of TP dose upon the severity of infertility or metabolic abnormalities in adult animals was observed. To delineate which features of the rat PCOS model resulted from androgenic, estrogenic or corticosteroid action, a final study used administration of different steroids during the early window of postnatal life: TP, estradiol valerate (EV), dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA) and dexamethasone (DEX). The anovulatory PCO-like phenotype observed with TP was also seen in animals which received EV, but not those which received DHT, DHEA or DEX. TP and EV treatment also resulted in a reduction of ovarian follicle numbers and activated follicle proportions, with an increase in primordial follicle proportions. Although glucose tolerant, animals treated with TP and EV were highly IR. Unlike dexamethasone, DHT and DHEA also produced IR in adult animals, to a lesser extent than TP and EV. Taken collectively, the results described in this thesis demonstrate that the PCOS-like phenotype observed in the neonatally androgenised female rat is likely to be due to the estrogenic actions of testosterone, potentially through as yet unknown epigenetic mechanisms. The programming of the metabolic components described may additionally be due to the actions of androgens. Furthermore, these studies demonstrate a novel estrogenic effect of neonatal steroids upon primordial follicle populations and show that the neonatally androgenised rat may be a rational PCOS model in a poly-ovulatory species.

Polycystic ovary syndrome (PCOS) is a common reproductive, endocrine and metabolic disorder present in women of reproductive age. Despite the widespread prevalence and heritability of PCOS, the heterogeneous and polygenic traits have made the successful identification of candidate genes difficult. Animal models have been developed on the premise that early exposure to sex steroids can programme epigenetic changes that predispose the fetus to the adult features of PCOS. Past research has modelled ovarian dysfunction, endocrine abnormalities and metabolic perturbances in rodent, non-human primate and sheep PCOS models, through the enhanced neonatal or prenatal exposure to the male sex hormone, testosterone. The modelling of PCOS in a large domestic species such as the sheep is advantageous due to similar biological reproductive function as the human. In this regard the sheep has been extensively used to model PCOS by the treatment of pregnant ewes from early to midgestation with androgens such as testosterone propionate (TP). These experiments have demonstrated the fetal programming effects of androgens on offspring that go on to develop PCOS-like characteristics in adulthood. One of the caveats of assessing steroid effects in this way is the effect of the placenta in mediating the transfer of these hormones. TP is an aromatisable androgen and thus some of its effects in the fetus may be attributable to placental by-products such as estrogens. This thesis describes the development and assessment of a novel model of prenatal androgenisation. Two models were compared: the indirect maternal exposure to TP (the current model) and the direct fetal injection of TP. In directly treating the fetus this allowed control over the dose of TP administered and avoidance of secondary effects that androgens may exert in the mother that could be transferred to the fetus. For the maternal model, pregnant Scottish Greyface ewes were administered TP twice weekly from day (d)62-102 of a 147 day gestation. For the fetal model, fetuses were injected twice while the ewe was anaesthetised with graded doses of TP during the same period of treatment as the maternal model. The effects of prenatal androgenisation were assessed in the female fetus shortly after treatment and also in young adult sheep. Fetal ovarian and adrenal steroidogenic gene expression was monitored and found to be altered in response to elevated levels of sex steroids. At d90 the morphology of the developing ovary was not changed by prenatal androgens. In the adult a detailed ovarian and endocrine assessment was undertaken, by examination of ovarian morphology, hormone levels, ovulatory cycles, hypothalamic pituitary ovarian function and follicle steroidogenesis, during the first breeding season. In addition, the metabolic effects of prenatal androgens were monitored by measuring body fat, insulin and glucose homeostasis and liver function. Neither maternal nor fetal prenatal androgenisation during mid-gestation resulted in a perturbed hormonal milieu or polycystic ovaries in young adults. These treatments did however programme a clear ovarian phenotype demonstrated by the increased capacity of follicles to secrete androgens, independently of an abnormal endocrine environment and disordered folliculogenesis. Furthermore, animals that were exposed maternally to TP developed fatty liver and had increased insulin secretion in response to glucose load. A major outcome of this study was the finding that the fetally injected control animals were phenotypically different than the maternal control animals. In fact, some of the reproductive and metabolic features of maternal TP exposure were found in the fetal control group. This unexpected finding has raised the possibility that it is the fetal exposure to stress, that is secondary to elevated maternal androgens, rather than androgens per se that is responsible for at least some of the multitude of anomalies encountered in PCOS.

Thesis (DMed (Obstetrics and Gynaecology))--Stellenbosch University, 2008. / Chapter 1 presents a literature study on the diagnostic debate of PCOS. The literature study includes a discussion of the recent Rotterdam consensus statement regarding the diagnosis of PCOS. This is followed by a discussion on the essential work-up of the patient presenting with PCOS. Finally, chapter 1 presents a discussion on the complexity of the different variations in women presenting with PCOS. Chapter 2 is a literature review on ovulation induction methods in patients who present with PCOS. This literature study puts special emphasis on the different available methods used for ovulation induction in women with PCOS and the profounding effect weight loss will have in managing these patients. This chapter also addresses the use of newer agents, like aromatase inhibitors (Letrozole), and the current role of each of these agents in ovulation induction protocols. Chapter 3 is a literature overview on the effect of Metformin in Clomiphene-resistant PCOS women. The inclusion criteria of this review was all prospective randomized trials where Metformin was added for ovulation in the Clomiphene-resistant PCOS patient. The data is presented as a metaanalysis. Chapter 4 is a prospective randomise control trial to evaluate the benefit of metformin if added to Clomiphene in a primary ovulation induction protocol in comparison to Clomiphene alone. This chapter also evaluates all factors influencing ovulation outcome. Finally in the discussion section all the recent studies published addressing this topic were reviewed. Chapter 5 is a literature review to evaluate the classification systems for semen parameters and the in vivo fertility potential. This data is also used to establish fertility/subfertility thresholds for semen parameters. This chapter also presents the results of a prospective and retrospective study of the semen analysis of the partners of women with PCOS. We believe that this population presents the best reference group to study the semen profile of the general male population. Chapter 6 is a summary of the results of these studies and serves as an evidence based approach for ovulation induction in women with PCOS.

Polycystic ovary syndrome is a complex, heterogeneous disease that affects 5-10% of reproductive-aged women. It is characterized by clinical or biochemical hyperandrogenism, oligo-anovulation, and polycystic ovary morphology. Instigating endocrine findings include aberrantly rapid gonadotropin-releasing hormone pulsatile secretion, elevated luteinizing hormone, sub-optimal levels of follicle-stimulating hormone, and hyperandrogenism. Metabolic symptoms are also present including hyperinsulinemia, insulin resistance, and dyslipidemia. These endocrine and metabolic findings are also accompanied by ovarian dysfunction and improper folliculogenesis. Because aberrant functioning of the hypothalamic-pituitary-gonadal axis is central to the pathophysiology of polycystic ovary syndrome, it is beneficial to examine it for abnormalities. Polycystic ovary syndrome has been shown to have both genetic and environmental components. Its strong genetic component has been demonstrated in twin studies, family association studies, candidate gene studies, and genome-wide association studies. Previous genome-wide association studies have found many candidate genes including those for DENND1A (differentially expressed in normal and neoplastic cells domain containing 1A), THADA (thyroid adenoma-associated protein), FSHR (follicle-stimulating hormone receptor), and LHR (luteinizing hormone receptor). This, together with the central endocrine abnormalities, prompted this review on polymorphisms of receptors of the hypothalamic-pituitary-gonadal axis, including those for gonadotropin-releasing hormone, luteinzing hormone, follicle-stimulating hormone, estrogen, and progesterone, as well as anti-müllerian hormone. Studies on single-nucleotide polymorphisms of these receptors were found on PubMed, Web of Science, and Google Scholar and subsequently analyzed. Many different single-nucleotide polymorphisms were studied, but only a handful of them have been subjected to repeated studies. Only rs2293275 of the luteinizing hormone receptor and rs2349415 of the follicle-stimulating hormone receptor, both at 2p16.3, were found to have a possible role in the etiology of polycystic ovary syndrome, but all eight were found to have a possible phenotypic role: rs13405728, rs2293275, and rs4539842 of the luteinizing hormone receptor; rs6165, rs6166, rs2268361, and rs2349415 of the follicle-stimulating hormone receptor; and rs2002555 of the anti-müllerian hormone receptor. The limitations most affecting the results of these studies include small sample sizes, heterogeneous study populations, lack of generalizability due to ethnicity, and lack of control or adjustment for confounders. It is necessary to develop a standardized study protocol and separate polycystic ovary syndrome patients based on phenotype in order to obtain stronger results in the future.

No description available.

PCO(S) är ett tillstånd som påverkar äggstockarna. Tillståndet gör det lättare att gå upp i vikt och många som har diagnosen har en övervikt. Syftet med uppsatsen är att få en bild av hur personer med PCO(S) och övervikt bemöts i svensk hälso- och sjukvård. Den frågeställning som behandlas i uppsatsen är "Hur bemöts personer med PCO(S) och övervikt i svensk hälso- och sjukvård?". Undersökningen utfördes med hjälp av en webbenkät som delades i Facebook-gruppen "Vi med PCO(S) i Norden". 13 frågor utformades och de flesta baserades på tidigare forskning. 11 frågor hade fasta svarsalternativ och 2 frågor var öppna. 89 personer svarade på enkäten. Majoriteten av respondenterna upplevde ett dåligt bemötande i hälso- och sjukvården. En stor del upplevde att de själva behövde vara pålästa om PCO(S) för att få ett bra bemötande. Många av respondenterna efterfrågade mer påläst vårdpersonal och önskade att få bli behandlade med respekt och utan fördomar. Det framkom också att många föredrog om övervikt bara togs upp av vårdpersonal om det var relevant till vårdbesöket och många föredrog också att bli tillfrågade om ett samtycke att diskutera övervikt innan detta togs upp. Det framkom också att en del av deltagarna bytt vårdgivare till följd av dåligt bemötande samt att vissa undvikt att söka vård för att de varit rädda för ett dåligt bemötande relaterat till deras vikt. Patientgruppen verkar extra utsatt för dåligt bemötande och det antas att patientgruppen får lägga ner mycket extra tid på sin vård.

BACKGROUND: Polycystic ovarian syndrome (PCOS) is one of the most common endocrine dysfunction problems among women of the reproductive age, with a global prevalence of 4-20%, causing 430,000 associated DALYs. Initial treatment of PCOS is mainly focused on diet and exercise and, if left untreated, PCOS can lead to many complications including, but not limited to, diabetes, metabolic syndrome, cardiovascular disease and endometrial cancer. In India, one out of five women are found to have PCOS with the numbers increasing with every year, according to a 2015 study done by Metropolis Healthcare. Some studies done in other parts of the country have shown that there is very limited knowledge about PCOS. Currently there is no data about the knowledge, attitudes and practices about PCOS in Kerala, India, which is an area known to have the highest rates of diabetes in India as well as an area having a high rate of infertility. PROPOSED PROJECT AND SIGNIFICANCE: This study is proposed to assess the knowledge, attitudes and practices of PCOS among women of reproductive age (18-45 years) in urban and rural areas of Thrissur, Kerala, India. This will help in understanding if there are any barriers to treatment and highlight the best preventive measures, as well as treatment strategies in this population, that might reduce its health burden. CONCLUSION: This will be a pilot study assessing perceptions of PCOS in Kerala, India. If this study demonstrates a low understanding of PCOS as shown in other parts of India, this will provide help in understanding the reasons why the prevalences of PCOS as well as diabetes and infertility, are increasing in the state of Kerala.

Abstract Introduction The degradation of plastic waste into smaller micro- and nanoplastic (MNPs) molecules has led to widespread distribution of these particles and accumulation in the environment, making human exposure inevitable. This can result in, or exacerbate, pathological conditions leading to immune dysfunction, neurodegenerative diseases, and infertility. Yet few studies have examined the effects of nanoplastics (NPs) on human health, especially the reproductive system. Reproductive toxicity of plastic particles has been mostly studied in males with most studies investigating microplastics. Therefore, the present study aims to assess the reproductive health consequences of NPs exposure in females by quantifying serum estradiol and progesterone, examining estrous cyclicity, and assessing ovarian reserve (number and quality of follicles) which is a key indicator of female fertility. Materials & Methods The present study was carried out in female mice (C57BL/6) exposed orally to water (control) or one of two solutions containing different concentrations of Polystyrene nanoplastics (PS-NPs; 100 µg/l or 1000 µg/l in water. Exposure occurred daily for 29 days, and vaginal lavage samples were collected for the last 15 days of the exposure phase to check for change in estrous cyclicity. Mice were euthanized at the end of the study and their blood samples and reproductive tissues were collected. Ovaries were fixed in 10% formalin, embedded in paraffin wax, serially sectioned at 5 µm thickness, and stained with hematoxylin and eosin (H&E) for microscopy and follicle analysis. ELISA was also performed to quantify the progesterone and estradiol serum levels. Results There was a significant increase in the estrous cycle length in the high dose (1000 µg/l) PS-NPs exposure group compared to control (5.53±.25 days vs 4.7±0.23 days, P=0.02). Moreover, there was a significant decrease in serum progesterone levels in the high-dose exposure group compared to control (mean difference=1.64 pg/ml, standard error of difference (SED)=0.64, P=0.03). Additionally, it was shown that PS-NPs exposure significantly reduced antral follicles’ diameter in both the low dose (238.61±19.01 µm vs 167.35±19.01 µm, P=0.03) and high dose exposure groups compared to the control group with the higher dose showing a more pronounced reduction in antral follicle' size (238.61±19.01 µm vs 131.95±19.01 µm, P=0.001). Conclusion Oral PS-NPs exposure in female mice appears to induce toxicity by reducing antral follicles size, increasing the estrous cycle length, and decreasing progesterone levels which may result in anovulation and different reproductive issues, such as infertility and polycystic ovary syndrome (PCOS). The effect of PS-NPs on infertility along with NPs’ mechanism of action in female reproductive system should be investigated in future studies. / Thesis / Master of Science (MSc) / Plastics in the environment break down into smaller particles called micro- and nanoplastics. These plastic particles are pollutants present in the aquatic and terrestrial environments entering every level of the food chain and ultimately reaching humans, yet few studies have examined the effects of nanoplastics on human health. A recent World Health Organization (WHO) report on nanoplastics has stressed the urgent need for toxicological studies to assess potential human health effects. Therefore, this study examined the effect of nanoplastics on the female reproductive system. This study was carried out in female mice exposed orally to a solution containing a vehicle control (water) and two different concentrations of nanoplastics (100 and 1,000 µg/l). Exposure occurred daily for a period of 29 days. At the conclusion of the study the mice were humanly euthanized with their blood and reproductive tissues collected for laboratory analysis. Results showed that nanoplastics exposure resulted in irregular reproductive cycle in mice along with a decrease in antral follicle size and progesterone levels which are indicators of anovulation and can lead to disorders, such as infertility and polycystic ovary syndrome (PCOS) which should be further investigated in future studies.

Introduction The degradation of plastic waste into smaller micro- and nanoplastic (MNPs) molecules has led to widespread distribution of these particles and accumulation in the environment, making human exposure inevitable. This can result in, or exacerbate, pathological conditions leading to immune dysfunction, neurodegenerative diseases, and infertility. Yet few studies have examined the effects of nanoplastics (NPs) on human health, especially the reproductive system. Reproductive toxicity of plastic particles has been mostly studied in males with most studies investigating microplastics. Therefore, the present study aims to assess the reproductive health consequences of NPs exposure in females by quantifying serum estradiol and progesterone, examining estrous cyclicity, and assessing ovarian reserve (number and quality of follicles) which is a key indicator of female fertility. Materials & Methods The present study was carried out in female mice (C57BL/6) exposed orally to water (control) or one of two solutions containing different concentrations of Polystyrene nanoplastics (PS-NPs; 100 µg/l or 1000 µg/l in water. Exposure occurred daily for 29 days, and vaginal lavage samples were collected for the last 15 days of the exposure phase to check for change in estrous cyclicity. Mice were euthanized at the end of the study and their blood samples and reproductive tissues were collected. Ovaries were fixed in 10% formalin, embedded in paraffin wax, serially sectioned at 5 µm thickness, and stained with hematoxylin and eosin (H&E) for microscopy and follicle analysis. ELISA was also performed to quantify the progesterone and estradiol serum levels. Results There was a significant increase in the estrous cycle length in the high dose (1000 µg/l) PS-NPs exposure group compared to control (5.53±.25 days vs 4.7±0.23 days, P=0.02). Moreover, there was a significant decrease in serum progesterone levels in the high-dose exposure group compared to control (mean difference=1.64 pg/ml, standard error of difference (SED)=0.64, P=0.03). Additionally, it was shown that PS-NPs exposure significantly reduced antral follicles’ diameter in both the low dose (238.61±19.01 µm vs 167.35±19.01 µm, P=0.03) and high dose exposure groups compared to the control group with the higher dose showing a more pronounced reduction in antral follicle' size (238.61±19.01 µm vs 131.95±19.01 µm, P=0.001). Conclusion Oral PS-NPs exposure in female mice appears to induce toxicity by reducing antral follicles size, increasing the estrous cycle length, and decreasing progesterone levels which may result in anovulation and different reproductive issues, such as infertility and polycystic ovary syndrome (PCOS). The effect of PS-NPs on infertility along with NPs’ mechanism of action in female reproductive system should be investigated in future studies. / Thesis / Master of Science (MSc) / Plastics in the environment break down into smaller particles called micro- and nanoplastics. These plastic particles are pollutants present in the aquatic and terrestrial environments entering every level of the food chain and ultimately reaching humans, yet few studies have examined the effects of nanoplastics on human health. A recent World Health Organization (WHO) report on nanoplastics has stressed the urgent need for toxicological studies to assess potential human health effects. Therefore, this study examined the effect of nanoplastics on the female reproductive system. This study was carried out in female mice exposed orally to a solution containing a vehicle control (water) and two different concentrations of nanoplastics (100 and 1,000 µg/l). Exposure occurred daily for a period of 29 days. At the conclusion of the study the mice were humanly euthanized with their blood and reproductive tissues collected for laboratory analysis. Results showed that nanoplastics exposure resulted in irregular reproductive cycle in mice along with a decrease in antral follicle size and progesterone levels which are indicators of anovulation and can lead to disorders, such as infertility and polycystic ovary syndrome (PCOS) which should be further investigated in future studies.