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1
Bützow, Tarja. "Gonadotropins and metabolic features in the pathophysiology and treatment of polycystic ovary syndrome." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/butzow/.
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Patterson, Moneka Angilene. "Polycystic Ovary Syndrome Treatment." ScholarWorks, 2017. https://scholarworks.waldenu.edu/dissertations/4319.
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Polycystic ovary syndrome (PCOS) is an endocrine system disorder that affects women of reproductive age. If not treated properly, PCOS can lead to infertility. Lack of proper treatment of PCOS may also result in medical complications such as diabetes or heart disease. The rural clinic where this project took place did not have a mandatory guideline for treatment of PCOS; therefore, no standardized method of diagnosis or treatment of PCOS existed. The purpose of this project, guided by the IOWA evidence-based practice model, was to educate providers on the evidence-based guideline for diagnosis and treatment of PCOS outlined by the Endocrine Society Taskforce. The guideline was selected after a comprehensive literature review and was used to develop an educational program that was provided to 5 nurse practitioners, the medical director and staff. A pre-test post-test design was used to determine if the participants understood the content from the guideline that was presented. Results showed that the researcher-developed test administered to participants yielded scores of 74 on the pre-test and increased after the education program with all participants scoring 100 on the post-test. The guideline used for the education was then presented to the clinic for implementation with the assistance of the medical director's support. The project provided an evidence-based guideline for diagnosing and treating PCOS and raised awareness of PCOS among all staff in a rural clinic where many patients with PCOS are treated. Positive social change may result as providers are better prepared to deliver evidence-based care for PCOS and as infertility and complications of untreated PCOS are reduced.
3
Morin-Papunen, L. (Laure). "Insulin resistance in polycystic ovary syndrome." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514257405.
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Abstract
The polycystic ovary syndrome, described first as the association
of bilateral polycystic ovaries and amenorrhoea, oligomenorrhoea,
hirsutism and obesity, was later shown to be a complex metabolic syndrome.
The first purpose of this study was to investigate the occurrence
of hyperinsulinaemia and the severity of insulin resistance and
glucose tolerance disorders in polycystic ovary syndrome by means of
the oral glucose tolerance test and the euglycaemic hyperinsulinaemic
clamp. The next goal was to investigate whether women with polycystic
ovary syndrome would benefit from insulin-sensitising drugs, and
in particular to compare the effects of metformin and a contraceptive
pill containing ethinyl oestradiol and cyproterone acetate. Altogether,
81 women with polycystic ovary syndrome and 34 healthy control subjects
were involved in the study.
Marked impairment of insulin sensitivity in obese subjects
with polycystic ovary syndrome, including a decrease of both cellular
oxidative and non-oxidative utilisation of glucose, and a slight non-significant
decrease of insulin sensitivity in non-obese subjects was observed.
Both non-obese and obese subjects with polycystic ovary syndrome
exhibited increased abdominal obesity compared with the controls,
confirming the fact that obesity, in particular abdominal obesity,
is an important contributor in the development of insulin resistance
in this syndrome.
Metformin alleviated hyperandrogenism by essentially decreasing
ovarian, but not adrenal androgen secretion. The improvement of
hyperandrogenism and ovarian function seemed to be mediated by the
improvement of hyperinsulinaemia, which resulted itself from subtle
improvements in both hepatic insulin extraction and insulin sensitivity.
Metformin decreased abdominal obesity and the release of free fatty
acids from adipose tissue, and improved ovarian cyclicity and fertility.
The transient decrease in serum leptin levels observed may have
some role in the improvement of ovarian function. The contraceptive
pill significantly improved hyperandrogenism and hirsutism, and
it slightly affected glucose metabolism. Thus, it could be the treatment
of choice in women with hirsutism problems and no fertility hopes.
Metformin could be the drug of choice for women with polycystic
ovary syndrome who wish to conceive. Because of its beneficial metabolic
effects, the value of metformin in reducing the risk of cardiovascular
diseases in polycystic ovary syndrome needs to be further studied.
4
Cho, Li Wei. "Cardiometabolic aspects of polycystic ovary syndrome." Thesis, University of Hull, 2008. http://hydra.hull.ac.uk/resources/hull:5826.
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Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting 6-7% of the population. It is characterised by chronic anovulation and hyperandrogenism with the clinical manifestation of oligomenorrhoea, hirsutism and acne. A ten to twenty fold increased risk for type 2 diabetes in PCOS patients compared to weight matched female control subjects makes the syndrome of high socioeconomic importance. The use of differing diagnostic criteria makes the comparison of studies on PCOS difficult until harmonisation through the Rotterdam consensus in 2004. Despite being removed from the diagnostic criteria by the the Rotterdam consensus, the LH/FSH ratio is still widely used as one of the diagnostic criteria for PCOS. Therefore to determine the usefulness of the LH/FSH ratio in the diagnosis of PCOS, I have conducted a study as described in chapter two and showed that an elevated LH to FSH ratio was as commonly found in normal women as those with PCO, and therefore of no diagnostic value. In January 2004, the European Society for Human Reproduction and Embryology (ESHRE) and the American Society for Reproductive Medicine (ASRM) co-sponsored the Rotterdam polycystic ovary syndrome consensus workshop that published diagnostic guidelines, building on the consensus statement of the National Institutes of Health 1990. The Rotterdam criteria for the diagnosis of PCOS states 2 of the 3 features needs to be present to make the diagnosis, and with the exclusion of other aetiologies (congenital adrenal hyperplasia, androgen-secreting tumors, Gushing's syndrome). These features include (l)Oligo- or anovulation (2)Clinical and/or biochemical signs of hyperandrogenism and (3)Polycystic ovaries (either 12 or more follicles measuring 2-9 mm in diameter, or an ovarian volume of > 10 cm³ ). Following the introduction of this guideline, the diagnosis of PCOS in patients recruited for studies on PCOS have been standardised. However, the current biochemical test for hyperandrogenism in women is still not ideal, due to the variation in the assay at low values. All three of total testosterone, bioavailable testosterone and free androgen index (FAI) are currently used as markers of hyperandrogenism for the diagnosis of PCOS. In chapter three, I evaluated the variability of each of the three markers as well as their use in the diagnosis and monitoring patients with PCOS and found that FAI is a better diagnostic marker for hyperandrogenism in patients with PCOS, but once the diagnosis is made, all three methods are equally good in monitoring disease progression. It has now been recognised that the diagnosis of metabolic syndrome identifies patients at increased risk of developing cardiovascular disease, and attempts have been made to develop the most convenient and useful criteria for the diagnosis of this condition in clinical practice. With the pathogenesis of metabolic syndrome not well understood, central obesity and insulin resistance are acknowledged as important causative factors. Cardiovascular disease studies in PCOS had so far been inconclusive with some suggesting increased cardiac events among women with PCOS whilst other studies suggesting no increase compared with normal cycling women. This may be attributed to small sample size in studies and variation in characteristics of patients recruited as well as surrogate markers used. C-reactive protein (CRP) had been widely used as a marker of inflammation, endothelial dysfunction and risk of cardiovascular disease in general and in patients with PCOS. However, there had not been any studies on the biovailability of this marker as the potential utility of CRP as a marker of cardiovascular risk may be limited by the magnitude of this variability in both health and disease, since there can be substantial overlap between PCOS and control individuals. In chapter four, the biological variation of high sensitivity CRP in women with PCOS were compared to normal menstruating women. I found that while the mean concentration of CRP was higher in individuals with PCOS compared to healthy controls, the intraindividual variation of CRP was similarly large in both groups. Therefore, the potential utility of CRP as a marker of cardiovascular risk may be limited by the magnitude of this variability in both health and disease, since there can be substantial overlap between PCOS and control individuals. PCOS is associated with a high risk of progression to type 2 diabetes (T2DM) and impaired glucose tolerance. A history of T2DM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects. However, factors underlying the progression of PCOS to T2DM are unclear and may be due to either an increase in the underlying insulin resistance or the progression of beta cell failure. Chapter five described a comparison study between the insulin resistance and beta cell functions in patients with PCOS to that of diet controlled T2DM. I found that the progression from PCOS to the development of T2DM is unlikely to be due to a further increase in insulin resistance (or variability), but rather the progressive failure of pancreatic beta cells with a decrease in insulin production. Having established the effectiveness in the diagnosis of PCOS and its progression, I went on to establish the effectiveness of individual treatments of PCOS. The treatment of patients with PCOS requires that the specific goal(s) of the therapy be first established. Individual goals may include fertility, treatment for hirsutism and/or acne, achieving a regular menstrual cycle, weight reduction and the prevention of the long term consequences associated with PCOS (type 2 diabetes, dyslipidaemia and possibly cardiovascular disease) - or all of the above. Treatments aimed at modifying the long-term consequences on cardiometabolic aspect of PCOS include weight reduction strategies as well as the use of insulin sensitizers. There is currently insufficient data to suggest the superiority of one treatment over another or the use of these medications for treatment of cardiometabolic risks in patients with PCOS. Endothelial dysfunction had been recognised as an early marker for cardiovascular disease and chapter six compared the changes in endothelial function in women treated with either metformin or pioglitazone. I found that pioglitazone significantly improved endothelial function and hs-CRP whereas metformin did not produce significant improvements. Chapter seven evaluates the effects of orlistat, metformin and pioglitazone on metabolic profile and biological variability of IR in women with PCOS. The results showed that only orlistat reduced both IR and its variability significantly, though all three drugs were effective in reducing hyperandrogenism within the 12 week period of the study. These effects with orlistat were coupled with a significantly reduction in total cholesterol through a reduction in LDL. After conducting the above studies and searching through literatures, I found that studies in cardiometabolic risks in women with PCOS had so far shown conflicting results, and this may be due to the heterogeneity within the group. Chapter eight evaluates this heterogeneity particularly between anovulatory and ovulatory women with PCOS, where all subjects met the Rotterdam criteria. Women with anovulatory PCOS were found to have higher mean and biological variability of IR compared to those having an ovulatory cycle, and both were higher than women without PCOS. This suggests that the subset of patients who ovulate may be better protected against future cardiovascular consequences. In conclusion, this thesis demonstrated that LH/FSH ratio is of no use in the diagnosis of PCOS and that free androgen index appeared to be the best diagnostic marker when compared to total testosterone and bioavailable testosterone.
5
Yasmin, Ephia. "Metabolic aspects of polycystic ovary syndrome." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.545722.
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6
Baker, Elizabeth. "Illness Perceptions of Polycystic Ovary Syndrome." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5176.
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Polycystic ovary syndrome (PCOS) is a chronic illness that affects approximately five million premenopausal women in the United States and is associated with significant cosmetic, reproductive, metabolic, and psychological consequences. Despite its prevalence, few studies have explored the lived experiences and illness perceptions of women living with PCOS. Identifying illness perceptions of women living with (WLW) PCOS is important, because mounting research suggests that a person's perceptions of their chronic illness and its management determine that person's coping behaviors (e.g., adherence, self-management) and, consequently, illness outcomes.
In this dissertation, the Common Sense Model (CSM) is used as a framework to identify the illness perceptions of PCOS held by WLW the syndrome. As such, this dissertation is the first to test the ecological validity of the CSM in a population of women diagnosed with PCOS. In addition, the relationship between illness perceptions and (1) infertility, a common symptom of the syndrome, and (2) health-related quality of life (HRQoL) is explored. Lastly, this study makes a novel contribution to the literature by describing one of the first samples of WLW PCOS recruited through a social networking site. This includes a discussion of the participant's demographic information, fertility experiences, and HRQoL.
This is a two-phase mixed methods study. Phase one consisted of an online quantitative survey capturing data on 376 participants' demographic information and medical history. Data were also collected on each participant's HRQoL using the SF-36, a generic, well-validated measure of the phenomenon. Of the 376 survey participants, 34 were interviewed via phone or video chat in the fall 2013 and spring 2014 semesters. Quantitative data were downloaded from Qualtrics® and analyzed using SAS statistical software version 9.3. In this analysis, descriptive statistics were generated to describe sample characteristics and SF-36 domain scores were calculated for each participant. In the qualitative analysis, data were analyzed through a series of sorting techniques and transcripts were imported into NVivo 10 and subjected to content analysis.
The mean age of survey participants was 31.8 years (SD=5.8). Respondents were primarily non-Hispanic (92.5%), white (88.3%), straight (94.4%), and married (73.4%) with a college education (64.1%). On average, participants reported living with PCOS for 7.6 years (SD=6.1). Approximately half of the sample reported having biological children (47.9%) and currently trying to conceive (42.1%), and most participants reported a history of infertility (70.7%). In addition, almost half of the total sample reported heights and weights that placed them in the morbidly obese category (BMI>35). Lastly, a history of depression (63.6%) and anxiety (68.6%) was common among participants.
Few survey participants reported their general health as being excellent (2.6%) or very good (27.4%). Similarly, women reported the lowest levels of functioning on the dimension of vitality, meaning that, in general, women reported feeling tired and being low in energy. Conversely, women reported the highest scores on the dimensions of physical functioning and role limitations due to physical health, meaning that, in general, women did not report that their health limited their physical abilities or caused problems with work or other daily activities.
Interview findings suggest that WLW PCOS generally have illness perceptions of the syndrome that are consistent with the domains identified in the CSM. In addition, it was found that, in relation to their illness cognitions, WLW PCOS described the extent to which they felt they had a comprehensive understanding of the syndrome, a phenomenon labeled illness coherence. Similarly, participants identified PCOS as a common condition (i.e. labeled perceived prevalence). Lastly, a number of relationships were identified between illness perceptions and (1) infertility status and (2) HRQoL scores.
Overall, this dissertation identifies a number of implications for patient education, provider education, clinical practice, and policy improvements. Examples include addressing (1) unmet information needs, (2) significant psychological morbidity and unmet mental health needs, (3) breastfeeding challenges and need for breastfeeding support, (4) poor quality of care and low patient satisfaction, and (5) limited access to care - all among women living with PCOS.
7
Lindholm, Åsa Maria. "Metabolic Aspects in the Polycystic Ovary Syndrome." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-120235.
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Vanky, Eszter. "Polycystic ovary syndrome - Metformin treatment in pregnancy." Doctoral thesis, Norwegian University of Science and Technology, Faculty of Medicine, 2005. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-688.
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Lindholm, Åsa Maria. "Metabolic Aspects in the Polycystic Ovary Syndrome." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-120235.
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Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders among women of childbearing age and is associated with a number of metabolic disturbances. It has been hypothesised these women carry an increased risk of developing cardiovascular diseases (CVD) with advancing age. The first aim of this thesis was to establish the prevalence of PCOS-related symptoms in Northern Sweden. The Northern part of the WHO MONICA project was used for this purpose. Based on self-reported menstrual disturbances and hirsutism together with biochemical analyses of free androgen index, the estimated prevalence of PCOS in Northern Sweden was 4.8%, which corresponded with previous prevalence studies. Disturbances in the fibrinolytic system are predictors of future cardiovascular events and measurements of plasminogen activator inhibitor 1 (PAI-1) activity and tissue plasminogen activator (tPA) mass concentration may be used to assess fibrinolytic activity in women with PCOS. From the findings, over-weight women with PCOS had impaired fibrinolysis, especially if they displayed objective biochemical markers of hyperandrogenism. Conversely, lean women with PCOS, displayed no signs of disturbed fibrinolysis. The adipose tissue is an active endocrine organ that produces and releases hormones, pro- and anti-inflammatory cytokines, and chemoattractant cytokines. Proinflammatory molecules produced by adipose tissue can be active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. The findings suggested being overweight, rather than the PCOS diagnosis per se, was the main explanatory variable for elevated adipose tissue inflammation in PCOS patients. Weight reduction is the primary target for intervention in overweight and obese women with PCOS. When this thesis was planned, no placebo-controlled trials on anti-obesity drugs in women with PCOS had been conducted. Sibutramine in combination with lifestyle intervention resulted in significant weight reduction in overweight women with PCOS. In addition to the weight loss, sibutramine appeared to have a beneficial effect on metabolic and cardiovascular risk factors.
10
Gharani, Neda. "The molecular genetics of polycystic ovary syndrome." Thesis, Imperial College London, 2000. http://hdl.handle.net/10044/1/8841.
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Atiomo, William Usinode. "Polycystic ovary syndrome coagulation and metabolic studies." Thesis, University of Plymouth, 1998. http://hdl.handle.net/10026.1/2828.
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The polycystic ovary syndrome (PCOS) is a heterogeneous disorder in women characterised by chronic ovulatory failure, hyperandrogenaemia, and insulin resistance. Some women are completely asymptomatic and others present with extreme menstrual disturbance, severe hirsutism, infertility and recurrent miscarriage. The pathophysiology of PCOS is not completely understood, but it is thought that insulin resistance plays a central role. In normal subjects, non-diabetic obese patients and patients with non-insulin dependent diabetes, insulin resistance is associated with elevated plasminogen activator inhibitor-1 (PAI-1) levels. PAI-1 is a glycoprotein, which inhibits the formation of plasmin (a proteolytic enzyme). Plasmin aids fibrinolysis and extracellular proteolysis. High PAI-1 and low plasmin levels increase the risk of thrombosis and impair extracellular proteolysis required in ovarian follicle growth, ovulation and embryo implantation. This study was designed to determine whether elevated plasminogen activator inhibitor-1 (PAI-1) was associated with the insulin resistance present in PCOS, investigate its possible role in the causation of anovulation and recurrent pregnancy loss in these women and ascertain whether it was an additional thrombotic risk factor so that clinicians and patients could take appropriate measures to reduce this risk In a pilot study, systemic PAI-1 activity was significantly elevated in oligomenorrhoiec women with PCOS. A larger study supported these findings, but demonstrated that obesity was a significant confounding factor, as the increase in PAI-1activity disappeared when standardised for weight. Activated Protein-C (APC) resistance was subsequently tested in these women because of the unexpected finding of an increased prevalence of a positive family history of thrombosis in women with PCOS compared with controls, but there was no increase in the prevalence of APC-resistance in PCOS. In another project, the cellular distribution of PAI-1 protein in human ovaries was described for the first time using immunohistochemistry. It was localised to the granulosa and theca cell compartments in both polycystic and normal ovaries, however there was no significant difference in the intensity of PAI-l staining between both groups on image analysis. PAI-1 messenger RNA expression was also evaluated in these biopsies by in-situ hybridisation, but no signal was detected suggesting that there was either a low overall RNA preservation in the tissues, or an insufficient sensitivity of the cocktail of oligonucleotide probes used. This study did not support the hypothesis that elevated PAI-1 was a feature of PCOS, however the in-situ location of PAI-1 protein was demonstrated for the first time in the human ovary and consistent with a previously suspected role in ovulation. The results did not support a role for PAI-1 in anovulation, recurrent miscarriage or increased thrombosis in PCOS.
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Murdoch, Alison Pamela. "Hypothalamic-pituitary relationships in polycystic ovary syndrome." Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/19176.
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Hresko, M. D. "Polycystic ovary syndrome in the older women." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17619.
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Sahota, Sukhwinder K. "The genetic basis of polycystic ovary syndrome." Thesis, University of Aberdeen, 2000. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU134381.
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Polycystic ovary syndrome (PCOS) affects up to 10% of women of a reproductive age and is a major cause of infertility. It is characterised by polycystic ovaries, hyperandrogenism and chronic anovulation. The disorder is genetically inherited and possibly of polygenic nature. Two methods were employed in the investigation of the genetic basis of PCOS: DD RT-PCR and mutation screening for association based studies. Application of DD RT-PCR on ovarian granulosa cells cells from affected and control women identified twenty-three differentially expressed sequences (B1-23). Of these, B4 was confirmed to be differentially expressed in A PCOS patient by competitive RT-PCR. Similarity searching identified the B4 sequence as the PHEX gene (99% homology). The corresponding PHEX protein is postulated to act as an endopeptidase in phosphate regulation. Its role in the ovary of PCOS patients remains to be elucidated. An association based study indicated reduced risk of PCOS associated with the AA genotype (OR=0.04; P<0.05) of the FSHR G2039A polymorphism in antenatal controls. No difference was seen between PCOS and blood donor control individuals. The 2039A allele confers a novel glycosylation site in the peptide sequence and this may effect processing of the FSHR protein in the endoplasmic reticulum. In addition, a reduced risk of PCOS was associated with the -1944CC genotype (OD=0.3) of the -1994 novel polymorphic site in CYP11a in blood donor controls. These findings suggest that a number of genetic factors may be involved in pathogenesis of PCOS. Their identification will open the potential for direct treatment of the symptoms associated with the disorder, especially infertility, and prophylactic management of those patients most at risk from cardiac disease or NIDDM.
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Koivunen, R. (Riitta). "Endocrine and metabolic changes in women with polycystic ovaries and polycystic ovary syndrome." Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514264266.
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Abstract
The prevalence of the isolated ultrasonographic finding of polycystic
ovaries (PCO) in the Finnish population and among women with a history of
gestational diabetes (GDM) and changes in the present carbohydrate metabolism
were investigated in the present study. One aim of this study was to investigate
the prevalence of the recently discovered variant type LH (v-LH) in PCOS and to
compare patient cohorts from Finland, the Netherlands, the United Kingdom and the
United States of America. In addition, this study attempted to evaluate the
nature of the ovarian streoidogenic response of women with PCOS to exogenously
administered human chorionic gonadotrophin (hCG), human menotrophin (hMG) and
follicle stimulating hormone (FSH). The effect of metformin on ovarian
steroidogenesis was also studied.
The prevalence of PCO was significantly higher in younger (≤ 35
years, 21.6%) than among older women (in ≥ 36 years, 7.8%). The overall
prevalence of PCO
in Finnish women was 14.2%. Women with previous GDM revealed a high prevalence of
PCO (39.4%). The carrier frequency of the v-LHb allele in the entire study
population was 18.5%. The frequency of the v-LH carrier was significantly lower
in obese PCOS subjects in the Netherlands (2.0%) and Finland (4.5%). Women with
previous GDM had impaired insulin sensitivity and β-cell function. They also
had
higher adrenal androgen secretion than the control women. Women with PCO and
previous GDM had marked hyperinsulinemia which was not explained by obesity.
Obese PCOS women achieved peak peripheral serum T concentrations at 48 hours
after a hCG injection, preceded by peak levels of 17-OHP and E2 at 24 hours. In
contrast, all steroids measured in the control women reached their maximum serum
concentrations at 96 hours. HMG stimulated the production of ovarian androgens
more efficiently than a urinary FSH after pituitary suppression with a
gonadotrophin releasing hormone agonist (GnRHa).
In conclusion, the prevalence of PCO is common in healthy Finnish women and
even more common in women with a history of GDM. The ultrasonographic appearance
of PCO may be a predictive factor with regards abnormal glucose tolerance during
and after pregnancy and, these women should therefore be advised as to possible
consequences. The high overall frequency of the v-LH allele in women in general
and its low frequency in obese PCOS patients suggests that v-LH plays a role in
reproductive functions and may counteract the pathogenesis of PCOS in obese
individuals. The differences observed in steroid responses to hCG between normal
and PCOS women might be explained by higher theca cell activity or mass in
polycystic ovaries. Women with PCOS did not show a distinctly exaggerated
steroidogenic response to hMG or FSH administration compared with control women.
FSH administration also resulted in increased A and T production.
16
Marsden, Philippa Jane. "Insulin action and ovarian function in polycystic ovary syndrome." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313272.
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Hu, S. "Cardiovascular function in pregnant women with polycystic ovary syndrome." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1346456/.
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An association has been proposed between polycystic ovary syndrome (PCOS) and hypertensive disorders of pregnancy, with an increasing body of evidence indicating that PCOS may have significant implications for pregnancy outcomes and long-term health of a woman and her offspring. Whether PCOS itself or the associated conditions, like obesity and fertility treatment, are responsible for these increased risks is a continuing matter of debate. Ambulatory blood pressure and carotid artery elasticity were therefore prospectively investigated in matched PCOS and control pregnancies. Twenty two PCOS–control subject pairs with singleton pregnancies, matched for age, body mass index, parity and ethnicity, were recruited in the first trimester (T1, 11–13 weeks). Ambulatory blood pressure recording for 24 h and carotid artery ultrasound for elasticity estimation and intima media thickness (IMT) were performed in T1 and in the second (T2, 22–24 weeks) and third (T3, 32–34 weeks) trimesters. In addition, endothelial function was examined using post-occlusive reactive hyperaemia (PORH). At nearly all time points during gestation, ambulatory systolic, diastolic and mean arterial pressures were elevated in PCOS versus control pregnancies. Carotid artery stiffness index was greater and compliance was less in PCOS pregnancies compared with controls. Differences in night-time systolic pressure and carotid artery elasticity were greatest in T3. PCOS also increased the incidence of hypertensive disorders of pregnancy. IMT was also higher in PCOS group in all trimesters of pregnancy but there was no significant difference in PORH results in both groups throughout pregnancy. Pregnant women with PCOS have higher baseline ambulatory blood pressure and impaired arterial elasticity, suggestive of disturbed vascular adaptation to pregnancy. The IMT was also higher in pregnant PCOS women, consistent with the notion of increased cardiovascular co-morbities in PCOS.
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Chedumbarum, Pillay O. D. "The association between polycystic ovary syndrome and endometrial cancer." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19981/.
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HYPOTHESIS: Women suffering from polycystic ovary syndrome have an increased risk of developing endometrial carcinoma. AIM: To determine whether people with polycystic ovary syndrome have an increased risk of developing endometrial carcinoma. BACKGROUND: Endometrial cancer is one of the commonest cancers to occur in women in the Western World and unopposed oestrogen stimulation of the uterus is amongst one of the aetiologies postulated for this condition. It is generally assumed that women with polycystic ovary syndrome are more likely to develop endometrial hyperplasia and carcinoma for the reason mentioned above. The validity of this association has however never been tested. This relationship is investigated within this thesis. METHODS: 1. A case- control study comparing the ovarian morphology of women diagnosed with endometrial carcinoma and those with benign gynaecological conditions. 2. An immunohistochemical study to assess expression of cell cycle and apoptotic proteins (surrogate markers of prognosis) in cases of endometrial carcinoma from women with PCO or from women with normal ovaries. 3. A microarray study of gene expression in the endometrium of cycling and non-cycling women with polycystic ovary syndrome. RESULTS: We found no significant difference in the prevalence of PCO (using this as a marker of PCOS in the absence of information on biochemistry) in the ovaries of patients diagnosed with endometrial cancer compared to women with benign gynaecology disease. Cyclin D1 expression was significantly increased in the endometrial cancers associated with PCO whilst the expression of ki67, Bcl2 and p53 was not significantly different. A total of 101 genes were differentially expressed in the endometrium of women with PCOS with regular cycles, long cycles and simple endometrial hyperplasia. CONCLUSION: Although our numbers were small, these results challenge the assumption that PCOS is a risk factor for endometrial cancer. The raised expression of Cyclin D1 in endometrial cancers associated with PCO suggests that the prognosis for women with PCO is not necessarily better than those without PCO. There were alterations in the expression of genes which affect endometrial function in women with PCOS including those with regular menstrual cycle women. This suggests that the altered hormonal environment has an effect on gene expression at a very early stage which may have an implication on endometrial carcinogenesis.
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Aghilla, Mohamed M. "Inflammation and cardio-metabolic risks in polycystic ovary syndrome." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/50038/.
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Polycystic Ovary Syndrome (PCOS) is the most common reproductive and endocrine disorder in females during their reproductive life. The syndrome is characterized by a constellation of symptoms and signs including menstrual disturbance, hyperandrogenism and polycystic ovaries. Other features of PCOS include obesity, metabolic syndrome, insulin resistance and an increased risk of developing diabetes mellitus and cardiovascular disease. Recently, PCOS has been recognized as a low grade inflammatory condition. Several inflammatory markers have been found to be raised in PCOS, such as interleukin-6, tumour necrosis factor-alpha and Interleukin-18. Low grade inflammation may potentially produce an insulin resistant state and promote the development of atherosclerosis. Insulin sensitzers such as metformin and pioglitazone have been shown to have a favourable effect not only on the symptoms of PCOS, but also on the hormonal and metabolic parameters in those subjects. In my thesis I primarily focussed on IL-18, B cells activating factor (BAFF), and the hepatokine, Fetuin-A, all linked to insulin resistance. IL-18 has a strong affinity towards its natural inhibitor, IL-18 binding protein (BP) and binding of IL-18 to IL-18 BP results in neutralization of IL-18, and consequently reduced free IL-18; the active form of the molecule. I have shown that PCOS women have a higher free IL-18, with hyperinsulinaemia the main factor that determines IL-18 in vitro. Furthermore, I have shown that Pioglitazone treatment for 12 weeks decreased both the total and free IL-18 in PCOS women. The reduction of IL-18 was accompanied by an improvement in IR. On the other hand, metformin treatment for six months failed to improve insulin sensitivity and did not influence IL-18 levels. BAFF, a novel adipokine, was studied in PCOS subjects, and I found lower BAFF levels in this cohort of patients. In vivo, BAFF correlated negatively with androgens, and in vitro work revealed that androstenedione as a negative regulatory factor for BAFF production Fetuin-A also known human protein α2-Heremans-Schmid glycoprotein, is a known natural inhibitor for insulin and abundantly expressed and secreted by the liver; fetuin-A has been suggested to act as a link between obesity, insulin resistance and MS. The circulating levels of Fetuin A are increased in women with PCOS, which is more pronounced when associated with MS. Metformin decreases Fetuin A in vivo, and also decreases both the expression and secretion of Fetuin A from HepG2 cells.
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Blair, S. A. "Cardiovascular and Inflammatory Risk Factors in Polycystic Ovary Syndrome." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527660.
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Lakhani, K. "Arterial wall mechanics in women with polycystic ovary syndrome." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444762/.
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Around 20% women of reproductive age are found to have polycystic ovaries (PCO) during ultrasound examinations and approximately 10% have symptoms of polycystic ovary syndrome (PCOS), which is associated with multiple risk factors for cardiovascular disease. The aim of this thesis was to investigate arterial mechanical properties and responsiveness to vasoactive stimuli in young women with PCOS, PCO and controls, using non-invasive ultrasound techniques. The influence of PCOS-related endocrine and metabolic perturbations on aortic function was investigated in a mifepristone-treated rat model of PCOS. The carotid artery pulsatility index was decreased in PCO and PCOS women and there was a paradoxical vasoconstrictor response to a dilator stimulus in these women relative to controls. Vascular compliance was decreased in the internal carotid artery in PCO and PCOS women PCOS women also exhibited increased intima-media thickness (IMT) of the common carotid and common femoral arteries compared with controls. In the cutaneous microcirculation, the response to the vasodilator acetylcholine (ACh) was depressed in PCOS women, whilst the response to sodium nitroprusside (SNP nitric oxide donor - NO) was unaffected. Mifepristone-treated rats exhibited increased serum luteinising hormone, testosterone, and polycystic ovaries. Ultrasound analysis indicated that aortic diameter and blood flow in vivo were unaffected in treated rats, but aortic compliance was reduced. In-vitro assessment of endothelial and vascular smooth muscle function of rat aorta demonstrated decreased relaxation with ACh, which was not abolished by L-NAME, however, the effect of SNP was greater, a finding which raises the possibility of an alternative dilator mechanism that may be independent of NO system. Since increased IMT, endothelial dysfunction and abnormal reactivity are independent risk factors for cardiovascular disease, these results also provide evidence of preclinical atherosclerotic surrogate markers in women with PCOS and PCO. These findings increase the likelihood of an association between PCOS (and probably PCO) and cardiovascular morbidity and mortality.
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Coulson, Rose-Marie Kate. "Cardiovascular risk in young women with Polycystic Ovary Syndrome." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/74062/.
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Background: Young women with Polycystic Ovary Syndrome (PCOS) may have increased measures of cardiovascular risk. It is difficult to determine how much of this risk is due to PCOS itself and how much is due to obesity and insulin resistance,which are common in PCOS and are themselves associated with greater cardiovascular risk. Aims and Methods: The study aimed to determine if arterial stiffness, carotid intima-media thickness and diastolic dysfunction were increased in young women with PCOS independently of the effects of obesity. A cross-sectional study of women with PCOS and healthy volunteers aged 16-45 years was undertaken. Subjects had a comprehensive assessment of body composition (including computed tomography assessment of visceral fat), measurements of arterial stiffness (aortic pulse wave velocity; aPWV), common carotid intima-media thickness (ccIMT), diastolic function (longitudinal tissue velocity; e’:a’) and metabolic measures including an oral glucose tolerance test to assess insulin area under the curve (IAUC), a marker of insulin resistance. Results: After adjustment for age and body mass index, PCOS subjects had greater insulin response (IAUC) following glucose challenge (adjusted difference [AD] 35900 pmol min/l, P<0.001), higher testosterone (AD 0.57 nmol/l, P<0.001) and high molecular weight adiponectin (AD 3.01μg/ml, P=0.02) than controls. There were no significant differences in aPWV (AD -0.13m/s, P=0.33), ccIMT (AD - 0.01mm, P=0.13) or e’:a’ (AD -0.01, P=0.86). After adjustment for age, height and central pulse pressure, aPWV and e’:a’ were associated with log visceral fat and IAUC. After adjusting for log visceral fat, the relationships between aPWV or e’:a’ and IAUC were only party attenuated. There was no relationship between cardiovascular measures and adiponectin or testosterone. Conclusions: Insulin resistance and central obesity are associated with subclinical dysfunction in young women, but a diagnosis of PCOS does not appear to confer additional risk at this age.
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Dilaver, Nafi Mehmet. "The role of anti-Mullerian hormone in the ovary : relevance to polycystic ovary syndrome." Thesis, St George's, University of London, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.719152.
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Anti-Mullerian hormone (AMH) is secreted by granulosa cells (GC) in the ovary and is produced in much higher amounts by GCs in women with polycystic ovary syndrome (PCOS). The aim of this project was to examine the role of AMH in the normal ovary and thereby understand the consequences for follicle development of greater concentrations found in women with PCOS. Human granulosa-luteal cells (GLCs), human theca tissue and KGN cells were used to investigate the effect of AMH on GC growth and apoptosis. Furthermore, the relationship between AMH and the essential gonadotrophins of folliculogenesis, i.e. FSH and LH were investigated. AMH signalling was also investigated in GLCs from women with and without PCOS. In addition, the effect of AMH on whole genome expression in GLCs from women with normal ovaries and PCOS was determined. AMH inhibited GC proliferation but did not appear to do this via apoptosis. AMH also had a differential effect on SMAD proteins in normal and PCOS cells. Interestingly, AMH increased inhibitory SMADs 6 & 7 and decreased pSMAD 1/5/8 in PCOS cells compared to basal levels. Finally, AMH had a significant differential effect on the transcriptome profile of cells from women with normal ovaries and PCOS. In summary, a differential effect of AMH in cells from women with normal ovaries and PCOS has been demonstrated, with evidence to speculate that the inhibitory role of AMH in the ovary may be due to an effect on the cell cycle.
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Tan, Bee Kang. "Adipokines and the Metabolic Aspects of the Polycystic Ovary Syndrome." Thesis, University of Warwick, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490677.
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Polycystic Ovary Syndrome (PCOS) is the most common endocrine disorder amongst women of reproductive age associated with a number of adverse metabolic sequealae. These women have an increased risk of insulin resistance and hyperinsulinemia, an increased risk of glucose intolerance and type 2 diabetes mellitus, dyslipidemia, subclinical atherosclerosis and vascular dysfunction, independent of BMI. With the epidemic of obesity, the PCOS phenotype is becoming ever more so prevalent and represents a clear and present health issue that needs to be addressed urgently. The studies describe for the first time the expression of visfatin and Retinol-Binding Protein 4 (RBP4) as well as adiponectin receptors, in corresponding sc and om human adipose tissues at both mRNA and protein levels. Also, it was shown that there was significant upregulation of visfatin and RBP4 as well as adiponectin receptors gene expression and protein in both these adipose tissue depots in overweight women with PCOS, including significantly higher circulatin visfatin and RBP4 levels, compared with matched controls. Furthermore, in isolated sc adipocytes, visfatin and RBP4 mRNA as well as adiponectin receptor(s) expression was significantly higher in age, BMI and WHR matched overweight PCOS women. Leptin was found to regulate om adipose tissue visfatin protein production and secretion, exhibiting a 'biphasic' response with a peak at leptin 10-9 M; a dose which is of physiological relevance in both mice and humans; returning to baseline with higher doses of leptin. This was true even in experiments conducted with C57BLIKs db/db mice, which lacked the membrane bound long leptin receptor (OB-Rb); thus highlighting the possible role of the membrane bound short leptin receptor (OBRa) in leptin induced visfatin protein production. Also, the apparent diminished response to higher doses of leptin with respect to visfatin production may be partly explained by the concurrent significant increase in the secretion of the soluble leptin receptor (SLR) at higher doses ofleptin. Binding ofleptin with SLR decreases the bioavailability of leptin to membrane bound leptin receptors and as a consequence, attenuates leptin's biological actions. Finally, when omental adipose tissues were subjected to leptin treatment in the presence of inhibitors of MAPK and PI3K, there was a significant decrease in leptin induced visfatin protein production and secretion. The MAPK and PI3K signalling pathways are known to functionally signal through both the short (OB-Ra) as well as the long (OB-Rb) leptin receptors. Leptin and visfatin may therefore playa coordinated role in various bodily functions, for example adipogenesis. Furthermore, the studies provide novel evidence that testosterone and 17~-estradiol increase both AdipoRl and AdipoR2 mRNA and protein levels; also, that 17~-estradiol significantly increases RBP4 secretion and up-regulates RBP4 mRNA expression and protein levels in human sc and om adipose tissue explants. Finally, HEK-293 cells were found to be suitable to further study and clarify the signalling pathways of both AdipoRl and AdipoR2. The temporal differences observed with respect to the activation ofAMPK between globular adiponectin and full length adiponectin forms the basis of further studies looking into the regulation of glucose and lipid metabolism, the molecular causes of diabetes and atherosclerosis, and the development of anti-diabetic and anti-atherosclerotic drugs.
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Tang, Thomas Man Hay. "The use of metformin for women with polycystic ovary syndrome." Thesis, University of Leeds, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485775.
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Pellatt, Laura Jane. "Metformin treatment in polycystic ovary syndrome : single drug, triple benefit?" Thesis, St George's, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511953.
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Barber, T. "Polycystic ovary syndrome: The role of the genes and obesity." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489409.
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There is a frequent concurrence of obesity and polycystic ovary syndrome (PCOS). To confirm the mechanistic link between these two common conditions, the studies detailed in this thesis have employed both genetic and physiological approaches.
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Edmund, Sara J. "Motivating Weight Loss Among Obese Women with Polycystic Ovary Syndrome." Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/228437.
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The purpose of the study was to evaluate the feasibility of utilizing an existing web based weight loss program and the effectiveness of the program in increasing self efficacy and motivation for weight loss among obese women with PCOS. There is consensus among many infertility experts that weight loss should be the first line of therapy for infertility and PCOS among obese women desiring pregnancy. Web based interventions have been effective in other areas of health behavior change. However, there have been no studies to evaluate use of a web-based weight loss program with the targeted population. Bandura's Social Cognitive Theory provides the basis for the contention that self efficacy is a major factor in self regulation. Another factor is motivation, which enhances self efficacy, thus creating behavior change. A sample of nine women participated in the one group pretest/posttest study measuring self efficacy, motivation and web site visits. BMI was calculated based on self-reported height and weight at baseline and after four weeks as a secondary outcome. There were significant increases in both self-efficacy and motivation for weight loss. Feasibility measures were not met at 90%. Eight of nine participants decreased their BMI. These results support utilization of currently available, free, online weight loss programs for this population.
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Chavez-Ross, Maria Alexandra. "Follicle selection dynamics in the mammalian ovary." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391766.
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Barnard, Louise. "Neuropsychological functioning and psychological wellbeing in women with polycystic ovary syndrome." Thesis, University of Leeds, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432639.
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Rajkhowa, Madhurima. "Insulin resistance in polycystic ovary syndrome mechanisms and the metabolic consequences." Thesis, Keele University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242286.
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Udiawar, Maneesh. "Cardiometabolic and neuroimaging correlates of cognitive function in polycystic ovary syndrome." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/103000/.
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Background: Polycystic ovary syndrome (PCOS) is a disorder characterized by insulin resistance and hyperandrogenism, which leads to an increased risk of type 2 diabetes in later life. Androgens and insulin signalling affect brain function but little is known about brain structure and function in younger adults with PCOS. Aims and Methods: To establish whether young women with PCOS display altered white matter microstructure and cognitive function. Eighteen individuals with PCOS (age, 31 ± 6 y; body mass index [BMI] 30 ± 6 kg/m2) and 18 control subjects (age, 31 ± 7 y; BMI, 29 ± 6 kg/m2), matched for age, IQ, and BMI, underwent anthropometric and metabolic evaluation, diffusion tensor MRI, a technique especially sensitive to brain white matter structure, and cognitive assessment. Cognitive scores and white matter diffusion metrics were compared between groups. White matter microstructure was evaluated across the whole white matter skeleton using tract-based spatial statistics. Associations with metabolic indices were also evaluated. Results: PCOS was associated with a widespread reduction in axial diffusivity (diffusion along the main axis of white matter fibres) and increased tissue volume fraction (the proportion of volume filled by white or grey matter rather than cerebrospinal fluid) in the corpus callosum. Cognitive performance was reduced compared with controls (first principal component, t = 2.9, P = .007), reflecting subtle decrements across a broad range of cognitive tests, despite similar education and premorbid intelligence. In PCOS, there was a reversal of the relationship seen in controls between brain microstructure and both androgens and insulin resistance.
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Fruhling, Caroline Davis. "Sport Participation History Among Young Females Diagnosed with Polycystic Ovary Syndrome." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1555519666452497.
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McCook, Judy G., Beth A. Bailey, Stacey L. Williams, Sheeba Anand, and Nancy E. Reame. "Differential Contributions of Polycystic Ovary Syndrome (PCOS) Manifestations to Psychological Symptoms." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/7172.
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The purpose of this study was to investigate the relative contributions of previously identified Polycystic ovary syndrome (PCOS) manifestations (infertility, hirsutism, obesity, menstrual problems) to multiple psychological symptoms. Participants were 126 female endocrinology patient volunteers diagnosed with PCOS who completed a cross-sectional study of PCOS manifestations and psychological symptoms. Participants had significantly elevated scores on nine subscales of psychological symptoms. Menstrual problems were significantly associated with all symptom subscales as well as the global indicator, while hirsutism and obesity were significantly related to five or more subscales. After controlling for demographic factors, menstrual problems were the strongest predictor of psychological symptoms. Findings suggest features of excess body hair, obesity, and menstrual abnormalities carry unique risks for adverse psychologic symptoms, but menstrual problems may be the most salient of these features and deserve particular attention as a marker for psychological risk among women with PCOS.
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Tomatis, Virginia Beatriz. "Effects of green tea and coffee polyphenols on cardiometabolic function in polycystic ovary syndrome." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709141.
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Tyndall, Victoria. "Androgens and the ovary." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5591.
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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.
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Hedström, Helena. "GABA-steroid effects in healthy subjects and women with polycystic ovary syndrome." Doctoral thesis, Umeå universitet, Obstetrik och gynekologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-49375.
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Background: The progesterone metabolite allopregnanolone is involved in several clinical conditions in women, e.g. premenstrual dysphoric disorder. It is a very potent GABA-steroid with GABA-A receptor effects similar to other GABA-agonists, e.g. benzodiazepines, and it causes sedation. An objective way to examine effects on the GABA-A receptor in humans is to measure saccadic eye velocity (SEV), which is reduced by GABA-agonists, e.g. allopregnanolone. Animal studies suggest that allopregnanolone is involved in the regulation of gonadotropin secretion via the GABA-A receptor, but this has not been studied in humans. Polycystic ovary syndrome (PCOS) is the most common endocrine disturbance among women of fertile age (5–10%), characterized by polycystic ovaries, menstrual dysfunction, hyperandrogenity, and 50% have obesity. Studies have shown higher allopregnanolone levels in overweight people. PCOS women have increased levels of androstanediol, an androgen metabolite which is an GABA-A receptor agonist. Tolerance often occurs when persons are exposed to high levels of GABAergic modulators. It has not been studied whether GABA-A receptor sensitivity in PCOS women is changed. Another progesterone metabolite, isoallopregnanolone, is the stereoisomere of allopregnanolone but has not been shown to have any GABA-A receptor effect of its own. Instead it has often been used to control steroid specificity to allopregnanolone. Aims: To compare the effects of allopregnanolone and isoallopregnanolone on gonadotropin secretion. To compare allopregnanolone levels, GABA-A receptor sensitivity to allopregnanolone and effects on gonadotropin secretion in both cycle phases and PCOS conditions. To examine pharmacokinetics and pharmacodynamic properties for isoallopregnanolone. Method: In the follicular phase healthy women were examined for the effect of allopregnanolone or isoallopregnanolone on gonadotropin secretion. PCOS women and healthy women in both cycle phases were given allopregnanolone and the differences in effects on SEV were examined, as well as changes in serum levels of gonadotropins and allopregnanolone at baseline and during the test day. Pharmacokinetics and GABA-A receptor sensitivity using SEV were explored for isoallopregnanolone in healthy women. Results: Allopregnanolone decreases gonadotropin serum levels in healthy controls in both cycle phases, but has no effect on gonadotropin secretion in women with PCOS. PCOS women have higher baseline serum levels of allopregnanolone than follicular phase controls, but lower levels than luteal phase controls. PCOS women show greater reduction in SEV to allopregnanolone than controls. Isoallopregnanolone has no effect on gonadotropin secretion. There is an effect of isoallopregnanolone on SEV, explained by a metabolism of isoallopregnanolone into allopregnanolone. Conclusion: There are significant differences in the GABA-A receptor response to a GABA-steroid in different endocrine conditions in women of fertile age examined with saccadic eye velocity. The GABA-steroid allopregnanolone decreases gonadotropin serum levels in healthy women but not in PCOS women. The lack of effect on gonadotropins by isoallopregnanolone suggests an involvement of the GABA-A receptor.
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Gaasenbeek, Michelle Lynn. "Candidate gene analysis of the CYP11A1 genomic region and polycystic ovary syndrome." Thesis, Imperial College London, 2005. http://hdl.handle.net/10044/1/7571.
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Fridström, Margareta. "Endocrine and therapeutic aspects of infertile women with the polycystic ovary syndrome /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3175-5/.
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Katz, Jonathan Richard. "Production and interconversion of steroid hormones in obesity and polycystic ovary syndrome." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398202.
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Barry, John Anthony. "Exploration of biological causes of psychological problems in polycystic ovary syndrome (PCOS)." Thesis, City University London, 2011. http://openaccess.city.ac.uk/11666/.
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Background: Polycystic ovary syndrome (PCOS) affects up to 10% of women, and is characterised by elevated testosterone (T) levels. Women with PCOS have higher scores than healthy women on a range of measures of psychological problems. Objective: To test the hypotheses that: 1/ The female fetus in a PCOS pregnancy experiences elevated T levels; 2/ T causes mood disturbance in women with PCOS. 3/women with PCOS show more signs of mood disturbance typical of symptoms of reactive hypoglycaemia than healthy controls. Design: Mainly between-groups cross-sectional studies. Also two meta-analyses. Setting: The research took place mainly in two London gynaecology clinics, University College London Hospital (UCLH) and the Royal Free Hospital, Hampstead (RFH). Some of the research was conducted online, and at three other gynaecology and fertility clinics. Participants: Participants were recruited from hospital clinics, support groups for women with PCOS, or the internet. Most participants were women aged 18-40. Outcome Measures: Testosterone; psychometric measures of mood disturbance. Results: 1/ Elevated T was found in the umbilical cord blood of the female fetus in PCOS pregnancies; 2/ Mood problems in PCOS were not directly caused by T. 3/ Women with PCOS showed higher levels of mood problems typical of hypoglycaemia than controls. Conclusions: The findings suggest the female fetus in a PCOS pregnancy may be exposed to relatively high levels of T. Mood problems in adults with PCOS are possibly caused by the direct effects of low blood glucose and indirect effects of T (e.g. obesity) than direct effects of T. Further research using the gold-standard biochemical assessment methods is required for any replications of these findings.
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McCook, Judy G., Nancy E. Reame, and Samuel S. Thatcher. "Health-Related Quality of Life Issues in Women with Polycystic Ovary Syndrome." Digital Commons @ East Tennessee State University, 2005. https://dc.etsu.edu/etsu-works/7174.
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Objective: To evaluate the influence of obesity, fertility status, and androgenism scores on health-related quality of life in women with polycystic ovary syndrome (PCOS).
Design: Cross-sectional, correlational.
Setting: Private reproductive endocrinology practice in two southeast U.S. cities.
Participants: Convenience sample of 128 women with PCOS, half of whom were attempting to conceive in addition to being treated for PCOS. Most were White (97%), married (78%), with a mean age of 30.4 years (SD ± 5.5).
Main Outcome Measures: The Health-Related Quality of Life Questionnaire (PCOSQ) for women with polycystic ovary syndrome. A laboratory panel and clinical measures, including body mass index, waist-to-hip ratio, and degree of hirsutism.
Results: The most common health-related quality of life concern reported by women with PCOS was weight, followed in descending order by menstrual problems, infertility, emotions, and body hair.
Conclusions: The psychological implications of PCOS are easily underestimated and have been largely ignored. Nursing has a pivotal role in recognizing these concerns and implementing therapy to improve quality of life in women with PCOS.
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Greenwell, Audry, Judy G. McCook, Stacey Williams, Sheeba Anand, and Beth Bailey. "Polycystic Ovary Syndrome: Morbidity Issues and the Psychosocial Impact on Infertile Women." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/7186.
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Objective: Polycystic ovary syndrome (PCOS) is a multidimensional endocrine disorder and the leading female infertility. PCOS is characterized as a clustering of clinical concerns, which include hyperandrogenism, obesity, and menstrual abnormalities/infertility. These characteristics were examined with regard to their impact on women's psychosocial concerns and health related quality of life. Design: Cross-sectional, correlational Setting: Private endocrinology practice in the rural Southeastern U.S. Participants: The study sample consisted of 126 women with PCOS. Methods: Convenience sampling yielded 126 subjects who met the diagnosis for PCOS, underwent laboratory testing and physical assessment, completed psychological and quality of life survey instruments and were included in data analysis. Results: Results of multiple regression analyses, controlling for demographic covariates, were completed on markers of hyperandrogenism, obesity and current fertility intent. Findings revealed hirsutism was significantly related to increased symptoms of anxiety and somatization and decreased quality of life among women with PCOS, while elevated androgen levels were significantly related to decreased quality of life. Current fertility intent significantly impacted symptoms related to interpersonal sensitivity, anxiety, psychoticism, and the global symptom severity index. Specifically, women not currently trying to conceive had higher levels of these psychological symptom outcomes. Conclusion/Implications for nursing practice: Women with PCOS are at elevated risk for psychological distress, and psychological symptoms appear to increase with increasing severity of PCOS symptoms. Women not currently trying to conceive appear to be at higher risk for psychological distress and lower quality of life.
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Lord, J. M. "The role of visceral fat in polycystic ovary syndrome - The central issue?" Thesis, Exeter and Plymouth Peninsula Medical School, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700627.
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Nicholas, Susan L. "Risk reduction strategies for assisted conception in women with polycystic ovary syndrome." Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/12467/.
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Superovulation in assisted conception can create Ovarian Hyperstimulation Syndrome (OHSS). Morbidity and even mortality that can occur with OHSS should be avoided by using the lowest risk and safest treatment strategy. Women with Polycystic Ovary Syndrome (PCOS) are at high risk of over response due to the ample number of antral follicles capable of responding to stimulation. Diagnosis of PCOS is based on a collection of subjective symptoms, signs and laboratory investigations. Anti-Mullerian Hormone (AMH), produced by the granulosa cells of the antral follicles, is elevated in women with PCOS. In a consecutive series of women presenting to an infertility clinic, the finding of increased AMH in those with PCOS was confirmed. Furthermore, AMH was shown to correlate with anovulation and hyperandrogenism. A single AMH value is interchangeable with any of the Rotterdam diagnostic criteria. Proposed values are 29pmol/L for polycystic ovarian morphology and 45pmol/L for either anovulation or hyperandrogenism using the generation II assay. Metformin has been shown to reduce the risk of OHSS in an agonist IVF cycle. The antagonist cycle is recommended for those at high risk of over-response. In a randomised double-blinded placebo controlled trial on 153 recruited patients; metformin was shown to have no effect on the incidence of OHSS in an antagonist cycle. There was no improvement in clinical pregnancy or live birth rate. The trial highlighted the discrepancy in clinical outcome between a White Caucasian and South Asian population. Avoidance of superovulation is an attractive option offered by in vitro maturation (IVM). A pilot study of 30 IVM cycles proved that immature oocytes can mature and fertilise in vitro at similar published rates. Unfortunately, no clinical pregnancies were created despite adequate transferred embryo quality. Although no incidence of OHSS, IVM appears to have been superseded by alternative approaches with replicable higher pregnancy rates.
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Smith, Rebecca. "The role of functional variants in the aetiology of polycystic ovary syndrome." Thesis, Smith, Rebecca (2017) The role of functional variants in the aetiology of polycystic ovary syndrome. Honours thesis, Murdoch University, 2017. https://researchrepository.murdoch.edu.au/id/eprint/38196/.
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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting reproductive aged women, as well as being the leading cause of anovulatory infertility. The syndrome is characterised by hyperandrogenism, anovulation, an overabundance of preovulatory follicles within the ovary and insulin resistance. Sufferers also have an increased risk of developing type 2 diabetes, obesity, endometrial cancer, and mental health sequalae.
It is well understood that PCOS has a genetic component with a heterogeneous mode of inheritance, as is evident from familial and population studies. However, despite the discovery of a number of risk alleles via genome wide association studies (GWAS), the genetic aetiology of the syndrome remains largely unknown. An alternative approach to GWAS for identifying mutations involved in genetic diseases is via whole exome sequencing. This method detects functional variants (i.e. mutations occurring in protein coding genes) that are present within the exome and are segregating within affected families. Therefore, undertaking exome sequencing on PCOS patients has the potential to identify genetic lesions involved in the aetiology of the syndrome.
The overarching aim for this project was to increase understanding of the aetiology of PCOS by identifying functional variants within families afflicted with PCOS using exome sequencing. To achieve this, bioinformatic analysis was performed on exome sequencing data files collected before the commencement of this project by the Keogh Institute. The functional variant rs143321413 within the eukaryotic elongation factor kinase 2 (EEF2K) gene was identified within one of the exome sequenced families affected by PCOS. The possible functional role of the rs143321413 variant was then investigated using an in vitro model system. This was done by producing mammalian expression vectors containing wildtype and mutant EEF2K sequences. These vectors were then transfected into a human embryonic kidney cell line containing the SV40 large T antigen (HEK293FT cells). Protein was extracted and a co-immunoprecipitation was performed to determine whether rs143321413 impacts the ability of EEF2K to bind to its substrate. Lastly, exome sequencing was also carried out on additional women affected by PCOS who were newly recruited throughout this project to identify new functional variants for future study.
The main finding from this thesis was the discovery of the novel rs143321413 variant, which has the potential to be involved with PCOS. Mammalian expression vectors containing both wildtype EEF2K and mutant EEF2K sequences were successfully created. Additionally, optimisation of the protocol was accomplished for transfection reactions to induce expression of these vectors within HEK293FT cells.Both of these experimental achievements will aid in the future research of rs143321413 and by extension PCOS. Finally, two additional variants were identified within the data from the newly exome sequenced individuals, that have the potential to be involved in aetiology of PCOS.
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Maruthini, Deivanayagam. "Follicle and oocyte metabolism in women with polycystic ovary syndrome undergoing assisted conception." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.545703.
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Javed, Zeeshan. "Novel interventional therapies to improve cardiovascular risk in women with polycystic ovary syndrome." Thesis, University of Hull, 2018. http://hydra.hull.ac.uk/resources/hull:16518.
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Introduction: Polycystic ovary syndrome (PCOS) is associated with a diverse range of endocrine, metabolic and cardiovascular risk factors. Low vitamin D in PCOS is associated with multiple cardiovascular risk factors and vitamin D replacement therapy has been suggested as a promising alternative for the prevention and treatment of PCOS. Empagliflozin; a sodium-glucose cotransporter 2 (SGLT2) inhibitor, has been shown to have several favourable effects on inflammatory and cardiovascular risk factors in both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) patients and could potentially be a treatment option in women with PCOS. Methods: The first study was a randomized, double-blind, placebo-controlled trial with an objective to determine the effect of vitamin D supplementation on liver fibrosis markers. Forty overweight and obese women with PCOS were randomization to either vitamin D 3200 IU daily or placebo for 3 months. The second trial was a randomised open-label parallel study to look at the effects of empagliflozin versus metformin on hormonal, metabolic and cardiovascular risk factors in women with PCOS. Forty overweight and obese women with PCOS were randomization to either empagliflozin 25mg or metformin 1500mg daily for 3 months. Results: For vitamin D treatment, there were significant reductions in individual liver fibrosis markers [hyaluronic acid (HA), N-terminal pro-peptide type-III pro-collagen (PIIINP), tissue inhibitor of metalloproteinase-1 (TIMP-1)] and their cumulative enhanced liver fibrosis (ELF) score was associated with a significant improvement in alanine aminotransferase (ALT) levels in patients randomized to vitamin D, whereas there were no changes in any of these parameters in the placebo group. There were no changes in free androgen index (FAI), insulin resistance (Homeostasis model assessment-insulin resistance; HOMA-IR), other anthropometric, inflammatory and body composition parameters in either group. There were no significant changes in endothelial microparticles (EMPs) in the vitamin D group as compared to the placebo group. In the second study, there were significant reductions in anthropometric and body composition parameters in patients randomized to empagliflozin while patients on metformin had significant increases in these parameters as compared to baseline. Between groups comparisons at the end of the study showed that the percentage reductions in anthropometric and body composition parameters were statistically significant in the empagliflozin group as compared to the metformin group. There was significant reduction in total testosterone levels in the metformin group only but not in the empagliflozin group. There were no significant changes in FAI, HOMA-IR, reactive hyperaemic index (RHI), fasting lipids and other hormonal and metabolic markers in both the groups. However, there were significant increases in cluster of differentiation 54 (CD54) and cluster of differentiation 62 (CD62) microparticles in the empagliflozin group and cluster of differentiation (CD106) microparticles in both the empagliflozin and metformin groups. Conclusions: Direct beneficial effects of vitamin D supplementation on markers of hepatic fibrosis were seen in overweight and obese women with PCOS shown by a reduction in the ELF score and its constituent liver fibrosis markers (HA, PIIINP, TIMP-1). However, vitamin D supplementation did not improve endothelial function as suggested by no significant changes in EMPs in the vitamin D group as compared to the placebo group. In the second trial, empagliflozin improved anthropometric and body composition indices after three months of treatment. However, there was significant increase in CD54 and CD62 microparticles after empagliflozin and CD106 microparticles after both empagliflozin and metformin treatments suggesting that the effects of empagliflozin and metformin could be partly mediated through modulation of endothelial function. This research work suggests both vitamin D and SGLT2 inhibition (empagliflozin) as potential treatment options in women with PCOS for improving future cardiovascular risk.
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Borgen, Silvia Sini-Laulu. "Exploiting molecular genetic diagnoses of polycystic ovary syndrome to achieve better patient outcome." Thesis, Borgen, Silvia Sini-Laulu (2018) Exploiting molecular genetic diagnoses of polycystic ovary syndrome to achieve better patient outcome. Honours thesis, Murdoch University, 2018. https://researchrepository.murdoch.edu.au/id/eprint/52163/.
Full textAbstract:
Polycystic ovary syndrome (PCOS) is an endocrinopathy that affects 5% to 10% of women. It is the most common reproductive disorder in women and is characterised by menstrual irregularity, hyperandrogenism, and polycystic ovarian morphology. This disorder also involves a major risk factor for non-insulin dependent diabetes, hypertension, and cardiovascular disease.
While PCOS is believed to have a complex genetic component, the exact nature of this component remains largely unknown. However, Genome Wide Association Studies (GWAS) and exome sequencing have begun to generate statistically significant and replicable data from which more specific investigations can be launched. PCOS related variants highlighted by these methods can then be the subject of functional studies that seek to identify the functional role that these variants may be involved in. The efficient uncovering of variants, including exomic identification and functional characterisation of the genetic lesions, can aid genetic diagnosis of PCOS, which in turn will help achieve better patient outcomes and provide the basis for targeted therapies.
The focus of this study was that efficient genetic diagnosis of PCOS will be assisted by an increased understanding of the aetiology of PCOS gained via exome sequencing identification of related individuals and functional characterisation of variants. To this end, related individuals with clinically defined PCOS were recruited and exome sequencing carried out to uncover putative causal mutations.
In addition, a functional study of growth differentiation factor-9 (GDF9) was conducted due to its role in folliculogenesis and female fertility, as well as its proximity to a PCOS linked variant (rs13164856) identified via a GWAS. A single 1-bp deletion mutation (783celC) in GDF9 was targeted, as this deletion is known to cause primary ovarian insufficiency. The possible functional role of this GDF9 variant was then tested using an in vitro model. This was achieved by creating mammalian expression vectors containing the wildtype and mutant sequences.
The primary achievement of this thesis was the uncovering of causal putative mutations shared between first-degree relatives suffering from PCOS. This data will potentially aid in uncovering the aetiology of PCOS. Functional characterisation of the GDF9 mutation was unsuccessful due to failure of overexpression of the GDF9 mutant construct.
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Piltonen, T. (Terhi). "Age-related androgen secretion in healthy women and in women with polycystic ovary syndrome." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514274369.
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Abstract
The number of ovarian follicles declines with age resulting in a significant decrease of fertility by the age of 40. However, the age when follicle loss starts to affect ovarian endocrine function is not well recognized. The purpose of the present study was to investigate age-related ovarian/adrenal androgen secretion, which is crucial for estrogen biosynthesis in healthy women and in women with polycystic ovarian syndrome (PCOS). Another aim of the study was to compare the usefulness of different serum markers in assessing ovarian aging and in diagnosing polycystic ovaries (PCOs) and PCOS.
The human chorionic gonadotropin (hCG) test was used to study the endocrine potential of ovaries/adrenals. The ovarian capacity to secrete and synthesize androgens was found to be decreased as early as at the age of 30 in regularly menstruating women. In women with PCOS, both basal and hCG-stimulated androgen levels were about 50% higher than in healthy women and they remained high until late reproductive age. Similarly to regularly menstruating women, the androgen secretion capacity in PCOS subjects decreased with age, and estradiol concentrations remained unchanged until the age of 44 years. Adrenal androgen synthesis was not changed during hCG-tests. Since serum antimüllerian hormone (AMH) and follicle stimulating hormone (FSH) levels were changed significantly after the age of 25 years in regularly menstruating women, they may be considered as useful serum markers reflecting the ovarian aging process. In women with PCOS, AMH levels were continuously 2- to 3-fold higher than in healthy women possibly reflecting high follicle number in these women.
A decline in ovarian endocrine function before the age of 30 is one of the first signs of ovarian aging. However, in women with PCOS ovarian androgen secretion capacity is markedly increased and remain high throughout the reproductive years. The results of the present studies also indicate that LH/hCG does not play a role in adrenal androgen synthesis, since LH/hCG did not stimulate adrenal androgen synthesis. The measurement of AMH is a useful tool to estimate ovarian aging process as well as to diagnose PCOs/PCOS.