SEARCH · PubMed Health

Results for “PCOS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources

PubMed1999

Dopamine D3 receptor polymorphism is not associated with the polycystic ovary syndrome.

OBJECTIVE: To determine if a polymorphism of the dopamine D3 receptor gene (2 allele), which has been reported previously to be associated with polycystic ovary syndrome (PCOS) in a population of United States Hispanic women, is associated with the disorder in the southeastern United States. DESIGN: Prospective case-control study. SETTING: University reproductive endocrinology laboratory and outpatient clinic. PATIENT(S): Consecutive patients of non-Hispanic white race diagnosed with PCOS (n = 152) and healthy controls (n = 96). INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Patient and control dopamine D3 receptor genotypes, with the 1 allele representing the wild type and the 2 allele denoting a highly prevalent polymorphism. RESULT(S): No difference was noted in the distribution of the three dopamine D3 receptor genotypes (i.e., 1:1, 1:2, and 2:2) among PCOS patients as compared with controls. Furthermore, in contrast to a previous report, the 2:2 genotype was not more prevalent among PCOS patients than among controls. CONCLUSION(S): Our population of non-Hispanic white women from the southeastern United States did not demonstrate an association between a dopamine D3 receptor polymorphism and PCOS.

Adult↗

PubMed1999

Role of the mutations Trp8 => Arg and Ile15 => Thr of the human luteinizing hormone beta-subunit in women with polycystic ovary syndrome.

OBJECTIVE: To evaluate the clinical significance of LH in the form of a mutant beta-subunit in women with polycystic ovary syndrome (PCOS). DESIGN: Prospective, controlled study. SETTING: University hospital. PATIENT(S): Thirty healthy women and 30 women with PCOS. INTERVENTION(S): Clinical, ultrasonographic, and hormonal findings were used to define PCOS. Nucleotide mutations within codons 8 and 15 in the LH beta-subunit gene (Trp8 => Arg and Ile15 => Thr) were analyzed with the use of polymerase chain reaction and subsequent restriction fragment length polymorphism. MAIN OUTCOME MEASURE(S): Serum levels of gonadotropins, androgens, E2, and prolactin were determined, and the results of restriction fragment length polymorphism were analyzed. RESULT(S): Five women in the control group and one woman in the PCOS group were found to be affected by the LHbeta gene mutations. No difference was observed in serum androgen and E2 levels between the affected women and 25 healthy women who were homozygous for the wild-type LH. However, women whose serum LH levels were < or = 5.1 mIU/mL had a higher risk of having mutant LH. CONCLUSION(S): The frequency of LH mutations in women with PCOS is similar to that in healthy women. The presence of the variant does not cause any significant change in serum levels of androgens and E2.

Adult↗

PubMed1999

Classification of polycystic ovary syndrome into three types according to response to human corticotropin-releasing hormone.

OBJECTIVE: To evaluate disturbances of the hypothalamic-pituitary-adrenal axis in women with polycystic ovary syndrome (PCOS). DESIGN: Retrospective cohort study. SETTING: Yokohama City University, Yokohama, Japan. PATIENT(S): Sixty women with PCOS and 19 women with normal menstruation. INTERVENTION(S): Administration of human corticotropin-releasing hormone (hCRH), dexamethasone suppression testing, and stimulation of ovulation with clomiphene citrate. MAIN OUTCOME MEASURE(S): Plasma cortisol and ACTH levels, plasma androstenedione and DHEAS levels, and ovulation rates. RESULT(S): In women with PCOS, plasma ACTH and cortisol levels were significantly higher and the plasma ACTH level after the administration of hCRH was higher than in controls. Based on the response to hCRH, patients with PCOS could be classified into three categories: those with a normal response to hCRH (group 1), those with an exaggerated response of ACTH to hCRH (group 2), and those with a high basal level of cortisol and a poor response to hCRH (group 3). In groups 2 and 3, DHEAS levels were significantly higher, suppression of androstenedione by dexamethasone was significantly greater, and ovulation rates with clomiphene citrate were significantly lower than in group 1. CONCLUSION(S): This classification provides insight into the underlying cause of PCOS and thus is useful in selecting appropriate treatment.

17-alpha-Hydroxyprogesterone↗

PubMed1999

Lack of insulin-like growth factor binding protein-3 variation after follicle-stimulating hormone stimulation in women with polycystic ovary syndrome undergoing in vitro fertilization.

OBJECTIVE: To investigate serum and follicular fluid (FF) insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) behavior in superstimulated cycles in patients with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: Department of Obstetrics and Gynecology, University of Naples. PATIENT(S): Thirty-two patients with regular menses and tubal and/or male factor infertility and 21 patients with PCOS undergoing IVF. INTERVENTION(S): The IVF program used leuprolide acetate suppression followed by sequential hMG in the subsequent cycle. After follicular development, hCG administration was followed 34-36 hours later by oocyte retrieval. MAIN OUTCOME MEASURE(S): E2, GH, IGF-I, and IGFBP-3 assayed by RIA and immunoradiometric assay. RESULT(S): The controls and patients with PCOS showed similar increases in E2 and GH titers in response to FSH stimulation. Serum IGF-I did not change in either group and was equivalent in the FF. Patients with PCOS had a higher FF IGFBP-3 titer and did not show the decrease in serum IGFBP-3 levels of the control group after FSH stimulation. CONCLUSION(S): The apparent failure of IGFBP-3 reduction in patients with PCOS alters IGF-I bioavailability. Increased sequestration of IGF-I affects ovarian steroidogenesis and may explain the poor response to gonadotropin stimulation.

Adult↗

PubMed2000

Autonomic and neuroendocrine responses to stress in patients with functional hypothalamic secondary amenorrhea.

OBJECTIVE: To evaluate the ability of women affected by functional hypothalamic secondary amenorrhea (FHSA) or polycystic ovary syndrome (PCOS) to adapt to stress. DESIGN: Controlled clinical study. SETTING: University hospital. PATIENT(S): Thirty-one patients affected by FHSA, 29 patients with PCOS, and 30 eumenorrheic women. INTERVENTION(S): The subjects took the Stroop Color Word (Stroop CW) test and underwent blood sampling. MAIN OUTCOME MEASURE(S): Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and serum cortisol levels. RESULT(S): The healthy controls had better Stroop CW scores than patients with FHSA. Serum cortisol levels significantly increased during Stroop CW with respect to the baseline in patients with FHSA or PCOS but not in the healthy controls. The SBP, DBP, and HR of the controls as well as SBP and DBP of patients with PCOS were significantly higher than those measured in patients with FHSA both at the baseline and during Stroop CW. CONCLUSION(S): Patients with FHSA do not cope as well as healthy patients, and their autonomic response to stress is worse than both controls and patients with PCOS.

Adaptation, Physiological↗

PubMed2001

Prevalence of type 2 diabetes mellitus and impaired glucose tolerance in Asian women with polycystic ovary syndrome.

OBJECTIVES: To determine the prevalence of abnormalities of glucose metabolism in Asian women with polycystic ovary syndrome (PCOS) and to assess the different impacts of the 1985 and 1999 WHO consultations and the ADA criteria for the diagnosis of type 2 diabetes mellitus (DM). METHODS: Eighty-five women with PCOS were consecutively included in the study at the Reproductive Endocrinology Unit, Department of Ob-Gyn, Ramathibodi Hospital, Mahidol University. All women underwent a standard oral glucose tolerance test (OGTT). Fasting insulin and testosterone levels were also measured. RESULTS: Seventy-nine women consented to the OGTT. The prevalence of impaired glucose tolerance (IGT) and type 2 DM was 22.8 and 15.2% with the 1985 WHO criteria, and 20.3 and 17.7% according to the 1999 WHO consultation criteria, respectively. The recommendation of the ADA using the fasting glucose levels could only determine a prevalence of 6.3% for type 2 DM. The fasting insulin and testosterone levels were significantly higher in DM than IGT and normal glucose tolerance (NGT) subgroups. The PCOS women with abnormalities of glucose metabolism had a greater body mass index (BMI), higher fasting glucose and 2-h post-load glucose levels than those with NGT. The prevalence of glucose intolerance significantly increased with BMI. CONCLUSIONS: Similar to other ethnic populations, Asian women with PCOS are at risk of developing IGT and type 2 DM especially if obese. The recommendation of the ADA is not appropriate for the diagnosis of type 2 DM in PCOS women.

Adult↗

PubMed1998

Glucocorticoid receptors on mononuclear leukocytes in polycystic ovary syndrome.

OBJECTIVE: Many studies have suggested that there is a possible hormonal dysregulation of hypothalamic-pituitary-adrenal (HPA) axis and an increased cortisol clearance in patients with polycystic ovary syndrome (PCOS). Therefore in this study, we have examined the role of glucocorticoid receptor/s (GR) characteristics in the developing of these abnormalities in patients with PCOS. METHOD: For this purpose, the number and affinity of GR in peripheral mononuclear leukocytes (MNL) of 10 patients with PCOS and 10 healthy women (controls) were determined. RESULTS: There were no significant differences in the number (6500+/-1001 sites/cell and 6352+/-1697 sites/cell, respectively; P > 0.05) and affinity (3.93+/-0.89 nM and 4.49+/-0.71 nM, respectively; P > 0.05) of GR between the PCOS patients and the controls. CONCLUSIONS: These results suggest that the alterations in the HPA axis and in the cortisol metabolism observed in PCOS are not related to GR deficiency.

Adult↗

PubMed1998

Serum leptin in obese women with polycystic ovary syndrome is correlated with body weight and fat distribution but not with androgen and insulin levels.

Leptin is a hormone produced in the adipose tissue and its concentrations in peripheral blood are significantly correlated with the amount of body fat. Whether other factors, including the pattern of body fat distribution and several hormones (such as insulin, sex steroids, and glucocorticoids), may be involved in the regulation of circulating blood leptin levels is controversial. Women with the polycystic ovary syndrome (PCOS) are hyperandrogenic and most of them are characterized by hyperinsulinemia, insulin resistance, and obesity, particularly the visceral phenotype. To assess the potential contribution of anthropometric factors, androgens, and insulin in determining leptin levels, we examined their relationship with body-mass index (BMI), visceral (VAT) and subcutaneous (SAT) adipose tissue areas, basal androgen levels, and fasting and glucose-stimulated (AUC) insulin in different groups of obese women with PCOS (n = 23) and of age-matched obese (n = 16) and non-obese (n = 10) otherwise healthy controls. The VAT/SAT ratio was measured as a parameter of body fat distribution. Serum leptin levels were significantly higher in obese PCOS women than in obese and normal-weight healthy controls and, within the controls, in the obese than in the non-obese group. In all women considered together, and in each group separately, leptin concentrations were highly significantly correlated with BMI. In addition, after adjusting for BMI, both VAT and the VAT/SAT ratio were positively and significantly correlated with leptin. Partial correlations with the VAT/SAT ratio remained significant in both the obese PCOS group and in controls considered separately, whereas the correlation with the SAT value was significant only in the control group. After adjusting for BMI, no correlation between leptin, androgens and fasting or stimulated (like AUC) insulin was found. These findings indicate that leptin levels in obese women with PCOS are higher than those observed in obese and non-obese controls. Moreover, they suggest that, other than BMI, the pattern of body fat distribution may be an independent factor related to circulating leptin levels, which, on the contrary, do not appear to be related to either androgen or insulin concentrations.

Adipose Tissue↗

PubMed1999

Metformin-induced resumption of normal menses in 39 of 43 (91%) previously amenorrheic women with the polycystic ovary syndrome.

In 43 amenorrheic women with polycystic ovary syndrome (PCOS), 31 (74%) with fasting hyperinsulinemia (> or =20 microU/mL), our aim was to determine whether Metformin (Bristol-Myers Squibb, Princeton, NJ), which reduces hyperinsulinemia, would reverse the endocrinopathy of PCOS, allowing resumption of regular normal menses. A second aim was to assess the effects of weight loss versus other Metformin-induced effects on ovarian function, and to determine if there were different responses to Metformin between those who lost weight and those who did not. A third aim was to assess associations between PCOS, 4G/5G polymorphism in the promoter sequence of the plasminogen activator inhibitor-1 gene (PAI-1 gene), and PAI activity (PAI-Fx). Of the 43 women, 40 (93%) had normal fasting blood glucose and 37 had normal hemoglobin A1C (HgA1C); onlythree (7%) had type 2 diabetes mellitus. Metformin (1.5 to 2.25 g/d) was given for 6.1+/-5.1 months (range, 1.5 to 24), to 16 patients for less than 3 months, to 12 for 3 to 6 months, and to 15 for at least 6 months. On Metformin, 39 of 43 patients (91%) resumed normal menses. The percentage of women resuming normal menses did not differ among treatment duration groups (P<.1) or among dose groups (P>.1). The body mass index (BMI) decreased from 36.4 + 7 Kg/m2 at study entry to 35.1+/-6.7 on Metformin (P=.0008). Of 43 patients, 28 (67%) lost weight (1 to 69 pounds), with nine (21%) losing at least 12 pounds. On Metformin, the median fasting serum insulin decreased from 26 microU/mL to 22 (P=.019), testosterone decreased from 61 ng/dL to 47 (P=.003), and estradiol increased from 41 pg/mL to 71 (P=.0001). Metformin-induced improvements in ovarian function were independent of weight loss (testosterone decrease, P<.002; estradiol increase, P<.0004). The change in response variables on Metformin did not differ (P>.05) between those who lost weight and those who did not, excepting Lp(a), which increased 4 mg/dL in those who lost weight and decreased 9 mg/dL in those who did not (P = .003). The change in response variables on Metformin did not differ among the five quintiles of weight loss, excepting fasting glucose (P<.05), which increased 6 mg/dL in those who lost the least weight on Metformin versus those in the 60th to 80th percentile for weight loss, in whom glucose decreased 33 mg/dL. Although the pretreatment fasting serum insulin was not significantly correlated with testosterone (r=.24, P=.13) or androstenedione (r=.27, P=.09), on Metformin, the change in insulin correlated positively with the change in testosterone (r=.35, P=.047) and with the change in androstenedione (r=.48, P=.01). Patients were more likely than normal controls (83% v 64%, P=.016) to be heterozygous or homozygous for 4G polymorphism of the PAI-1 gene and were also more likely to have high PAI-Fx (> or =22 U/mL, 28% v3%, chi(2)=10.1, P=.001). Metformin reduces the endocrinopathy of PCOS, allowing resumption of normal menses in most (91%) previously amenorrheic women with PCOS.

Adult↗

PubMed2003

Depression in women with polycystic ovary syndrome: clinical and biochemical correlates.

BACKGROUND: We assessed the prevalence of mood disturbance among women with prospectively documented polycystic ovary syndrome (PCOS). METHODS: Thirty-two women with PCOS completed the Center for Epidemiological Studies-Depression Rating Scale (CES-D). Clinical and biochemical characteristics were assessed. RESULTS: Sixteen women had CES-D scores indicative of depression. Depression was associated with greater insulin resistance (P=0.02) and higher body mass index (P=0.05). Women receiving oral contraceptives for the treatment of PCOS were less depressed than patients not receiving treatment (P=0.03). LIMITATIONS: Possible selection bias, use of a screening tool alone without further diagnostic evaluation of depression, small samples size and lack of direct comparison with an age matched control group, should be considered in interpretation of these results. CONCLUSION: Findings suggest a high prevalence of depression among women with PCOS, and an association between depression and PCOS markers.

Adult↗

PubMed1999

Polycystic ovary syndrome and ovarian autoimmunity--assessment of ovarian antibodies by EIA.

There are conflicting reports of an association of ovarian antibodies, detected by immunofluorescence, with polycystic ovary syndrome (PCOS). The objective of this study was to evaluate the association of ovarian autoimmunity with PCOS. A validated immunoassay for ovarian antibodies was used to assess serum from women with PCOS and with menopause and normal cycling women as controls. The frequency of ovarian antibodies was similar (25%) among the controls and PCOS. Thus, unlike the association of ovarian antibodies detected with this test in patients with unexplained infertility and premature menopause, the prevalence of ovarian antibody in patients with PCOS is not significantly different to controls.

Aged↗

PubMed2003

Valproic acid fails to induce polycystic ovary syndrome in female rats.

PURPOSE: Valproic acid (VPA) treatment in female patients is suggested to be associated with the occurrence of a variety of endocrine side effects that include many characteristic symptoms of polycystic ovary syndrome (PCOS). The aim of our study was to prospectively measure whether VPA treatment was associated with the presentation of PCOS symptoms in rats, as well as determine whether this model could be used to examine the underlying mechanism by which these effects are induced. METHODS: Normal estrus-cycling female rats (n=22) were treated perorally three times daily with VPA (300 mg/kg/day), divalproex sodium (DVS) (330 mg/kg/day), or phosphate-buffered saline for a minimum of 30 days. PCOS-associated symptoms (estrus cycle, weight, estradiol and testosterone levels, aromatase activity, and ovarian morphology) were assessed at baseline, mid-, and endpoint. RESULTS: There was no significant difference in the mean number of days animals were in proestrus-estrus or metestrus-diestrus between the three groups. All groups of animals gained weight during the study and there were no appreciable differences in mean weight gain or leptin between groups. Total serum estradiol or testosterone levels and ovarian aromatase activity were not significantly different between the groups. The number of corpora lutea was not significantly different between the groups; however, cystic follicles were present in 50% of the drug-treated animals compared to 25% of saline-treated animals. CONCLUSIONS: VPA and DVS treatment were associated with a higher proportion of animals developing cystic follicles but did not mimic the VPA-induced PCOS that is observed in women. Thus, it appears that the rat has limited usefulness for modeling VPA-induced symptoms associated with PCOS.

Animals↗

PubMed2001

Polycystic ovary syndrome: the new millenium.

Our understanding of Polycystic Ovary Syndrome (PCOS) has been hampered by varying diagnostic criteria, and ignorance of the etiology of the syndrome. PCOS women are uniquely insulin resistant and obesity aggravates this underlying predisposition to insulin resistance. Diagnostic criteria which focus on hyperandrogenism and/or menstrual irregularity are more likely to identify insulin resistant women, than such criteria as abnormal gonadotropin secretion or ovarian morphology. The lack of a clear etiologic mechanism to the syndrome has led to a multitude of symptom-oriented treatments with few therapies improving all aspects of the endocrine syndrome of PCOS. Improving insulin sensitivity has become established as a baseline treatment strategy in PCOS. There are, however, few randomized controlled trials of adequate power to provide an evidence based guide to treatment in PCOS.

Cardiovascular Diseases↗

PubMed1999

Insulin action in the polycystic ovary syndrome.

Research on insulin action in PCOS has been intensive after the identification of insulin resistance as a feature of the syndrome in 1980. It is now clear that PCOS is a metabolic as well as a reproductive disorder and an important cause of type 2 diabetes mellitus in women. The cellular and molecular mechanisms of insulin resistance in PCOS are distinct from those in other insulin resistance syndromes. Elucidating these mechanisms promises to provide considerable insight into insulin receptor signal specificity. Conversely, insulin resistance is now known to have an important role in the pathogenesis of the reproductive disturbances of PCOS. It is thought that one or several genetic defects may cause both the insulin resistance and reproductive abnormalities characteristic of PCOS.

Androgens↗

PubMed2000

Insulin-lowering medications in polycystic ovary syndrome.

A growing body of evidence suggests that serum hyperinsulinemia contributes to the excess ovarian androgen secretion observed in women with PCOS. As a group, women with PCOS are hyperinsulinemic and insulin resistant when compared with weight-matched normal women, but not all PCOS subjects display clear metabolic defects. The small studies using insulin-sensitizing drugs have demonstrated conclusively that a reduction in serum insulin levels is associated with a reduction of ovarian androgen secretion in PCOS, providing further evidence that hyperinsulinemia contributes to hyperandrogenism by increasing ovarian androgen secretion and reducing SHBG. The improvement of serum androgen levels with multiple different drug classes with different mechanisms of actions suggests an effect mediated by reduction in circulating insulin levels rather than a direct ovarian effect of the drugs. Although the studies published to date have increased understanding of the pathophysiologic mechanisms of PCOS, before these drugs can be recommended as first-line therapy for women, longer term clinical trials are needed to compare their safety and efficacy with other established therapies, such as oral contraceptive pills and antiandrogens. Because of the potential direct and unique beneficial effects of these medications on metabolism, studies must be performed to evaluate their efficacy in combination with other therapies, especially oral contraceptives. It is likely that subsets of patients who cannot tolerate traditional medications will be better managed with insulin sensitizers as first-line therapy; however, to date, the optimal way to identify these subjects is unknown. Whether therapy should be limited to subjects with documented hyperinsulinemia also remains unknown.

Diazoxide↗

PubMed2001

Polycystic ovary syndrome, hyperandrogenism, and insulin resistance.

Results from recent basic and clinical research investigations have greatly improved our understanding of insulin resistance in general and insulin resistance associated with PCOS in particular. With this understanding has come the possibility of using new methods to treat PCOS. This is particularly true when discussing the use of insulin-sensitizing drugs. Caution must be exercised in using these drugs because of unforeseen acute or remote adverse side effects. Postulated relationships among PCOS, hyperandrogenism, and insulin resistance do not completely solve the endocrinologic mystery of the patient with PCOS. For example, how does the partial destruction of the ovary (e.g., wedge biopsy or ovary drilling by laser or cautery), which does not affect insulin resistance, result in ovulatory cycles? Why does the administration of excessive exogenous insulin in the case of the insulin-dependent diabetic fail to cause hyperandrogenism? Certainly, much remains to be learned about the reproductive endocrine disturbance we now call PCOS.

Female↗

PubMed2001

The role of the adrenal cortex in polycystic ovary syndrome.

Adrenal androgen excess affects approximately 25% of PCOS patients. The exact etiology of this excess in PCOS patients is unclear. Some evidence that adrenal androgen excess may be a genetic trait. The adrenal androgen response to ACTH is highly individualized, and the relative response seems to be constant over time. In addition, there is a strong familial component to adrenal androgen levels in normal individuals and PCOS patients. It is possible that the tendency to overproduce adrenal androgens is an inherited risk factor for the development of PCOS. Overall, few hyperandrogenic patients actually have isolated deficiencies of 3 beta-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11-hydroxylase. The ovarian hormonal secretion in PCOS can affect adrenal androgen secretion and metabolism, although this factor accounts for only part of this abnormality. More likely, the adrenal androgen excess results from a generalized hyperresponsiveness of the adrenal cortex to ACTH, but without an increase in CRH or ACTH sensitivity. Although glucocorticoid administration may improve the ovulatory function of these patients, the results are modest and cannot be predicted by the circulating androgen levels.

Adrenal Cortex Diseases↗

PubMed2001

Obesity and weight loss in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) and obesity are common and complicated disorders that are influenced by genetic and environmental factors. Obesity is a prominent feature of PCOS; at least 50% of patients with PCOS are obese. Obesity appears to exert an additive, synergistic effect on the manifestations of PCOS, independently impacting insulin sensitivity, risk for diabetes, and adverse cardiovascular profile. There is evidence for the benefit of weight reduction in the management of PCOS in the obese patient. Weight loss remains a primary intervention in treatment of this disorder.

Female↗