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PubMed2003

Screening for Cushing's syndrome in obese women with and without polycystic ovary syndrome.

Obesity and insulin resistance, menstrual abnormalities and clinical and biochemical signs of hyperandrogenism are common features in women with polycystic ovary syndrome (PCOS) and Cushing's syndrome (CS). Further, an overdrive of the pituitary-adrenal axis has been documented in PCOS and this condition is often present in women with CS. For this reason, screening for hypercortisolism is often needed in obese women with polycystic ovaries. The aim of this study was to compare the diagnostic value of different screening tests for CS in a population of obese premenopausal women with PCOS and without PCOS (OB) and in a group of patients with CS. We reviewed retrospectively the case records of 117 obese women of reproductive age (60 PCOS and 57 OB, BMI 25.1-70.1, 13-45 yr) who were screened for CS at our Institution in the years 1995-2001 and turned out to be free of the disease. Data were compared with those of 58 premenopausal obese women with active CS (BMI 25.1-50.2 kg/m2, 18-45 yr). Screening for CS was performed by urinary free cortisol (UFC) (three consecutive 24-h urine collections), cortisol circadian rhythm (blood samples taken at 08:00-17:00-24:00 h), and 1 mg overnight dexamethasone suppression test (DST). A 24:00 h plasma cortisol (MNC) of 207 nmol/l, a UFC of 221 nmol/day and plasma cortisol after DST of 50 nmol/l and 138 nmol/l were taken as cut-off values for the diagnosis of CS. As expected, patients with CS showed elevated basal and post-dexamethasone plasma cortisol and UFC levels (p < 0.001 vs OB and PCOS). PCOS had higher UFC (p < 0.005) but not MNC and post-DST plasma cortisol levels compared to OB. DST showed the greatest specificity and diagnostic accuracy in differentiating CS from PCOS and OB (both p < 0.05 vs MNC and UFC, according to the 138 nmol/l criterion) while MNC and UFC displayed a similar discriminatory value. However, by using a lower threshold (50 nmol/l) as response criterion, there were no diagnostic differences between DST and the other tests. Specificity and diagnostic accuracy of UFC measurement was lower in PCOS than in OB (both p < 0.05) whilst there were no differences between groups for DST and MNC. Similarly, the area under the ROC curve relative to DST, giving an estimate of the inherent diagnostic accuracy of the test, was slightly greater than those of MNC and UFC (z = 0.694 and z = 0.833 for DST vs MNC and UFC, respectively, both p = NS). These results indicate that the 1-mg DST and MNC are unaffected by the presence of PCOS and can be safely used to screen for CS premenopausal obese women with PCOS, while caution should be exercised in interpreting mildly elevated UFC levels in these patients.

Adult↗

PubMed2003

Is hyperprolactinemia associated with insulin resistance in non-obese patients with polycystic ovary syndrome?

Insulin resistance is common in polycystic ovary syndrome (PCOS). Moderate elevations in serum PRL concentration may contribute to insulin resistance in PCOS. The aim of this study was to determine PRL on development of insulin resistance in non-obese hyperprolactinemic patients with PCOS. Ninety-eight non-obese subjects with PCOS and 100 non-obese healthy control were accepted in the study. Serum glucose, lipids, androgens, free androgen index (FAI), gonadotropins, fat mass and percentage, SHBG, and insulin levels were measured. Homeostasis model assessment (HOMA) was used as index of pancreatic beta-cell function and tissue insulin sensitivity. Independent t-test was used in comparison of results. In patients with PCOS, FAI and mean HOMA-(%B) level were higher than in the control group (p<0.0001), whereas mean HOMA-(%S) in subjects with PCOS was lower than in the control group (p<0.0001). Patients with PCOS were divided into subgroups according to their serum prolactin level (< 24 or > or = 24 ng/ml). Although FAI was not different, mean insulin and HOMA-(%B) levels in hyperprolactinemic patients were higher than in normoprolactinemic subjects (p<0.001). HOMA-(%S) in hyperprolactinemic patients with PCOS was lower than in normoprolactinemic patients (p<0.002). In conclusion, PCOS is associated with insulin resistance; non-obese hyperprolactinemic PCOS patients may be more insulin-resistant than normoprolactinemics and there may be an association between hyperprolactinemia and insulin resistance in PCOS.

Adult↗

PubMed2004

Serum adiponectin in women with polycystic ovarian syndrome and its relation to clinical, metabolic and endocrine parameters.

UNLABELLED: Several studies have demonstrated that low levels of serum adiponectin are present in obesity, insulin resistance, hypertension and hyperlipidemias. The aim of our study was to determine whether serum adiponectin level is different between patients with polycystic ovarian syndrome (PCOS) and control subjects. We also investigated relationships between various cardiovascular risk factors, levels of serum adiponectin and other hormones, such as androstendione, testosterone, estradiol, DHEAS, sex hormone binding globulin (SHBG), and leptin. We also analysed the correlation between serum adiponectin and free androgen index. Ninety-one women with clinical diagnosed PCOS and 53 healthy control subjects, carefully matched by body mass index (BMI) and age, were enrolled in the study. The fasting blood samples were obtained and all participants underwent an oral 75 g glucose tolerance test. The prevalences of impaired glucose tolerance (IGT), hypertension and hypertriglyceridemia were higher in the PCOS group. PCOS women had increased androgen concentrations and higher free androgen index and decreased level of serum SHBG. Lower serum adiponectin concentrations were observed among cases than in controls (median 13.7 microg/ml vs 17.8 microg/ml, p<0.001) despite being matched by BMI. In the PCOS group adiponectin levels correlated significantly with: BMI (r=-0.32, p=0.002), waist circumference (r=-0.32, p=0.003), waist-to-hip ratio (WHR, r=-0.38, p=0.001), triglycerides (r=-0.31, p=0.007), SHBG (r=0.30, p=0.003) and free androgen index (r=-0.29, p=0.02). In contrast, the adiponectin level does not appear to be related to total testosterone, DHEAS and leptin levels. The adiponectin and SHBG levels were found to be decreased in PCOS women with IGT compared to PCOS women with normal glucose tolerance, but after adjustment by BMI or WHR, the differences were no longer statistically significant. To exclude a possible confounding effect due to a higher prevalence of IGT in the PCOS group, this comparison was repeated for the subgroup of 58 PCOS women and 48 control women after excluding those with IGT. Neither adiponectin nor SHBG were significantly different between those subgroups. Multiple regression analysis revealed that serum adiponectin concentrations were best predicted by WHR, free androgen index and presence of IGT when all patients were considered. In PCOS subjects, the only independent predictor of adiponectin concentrations was glucose tolerance status. CONCLUSIONS: Lower adiponectin levels were observed in PCOS group than in control women, and these differences were probably due to higher prevalence of IGT in these cases.

Adiponectin↗

PubMed2006

Polycystic ovary syndrome in men: Stein-Leventhal syndrome revisited.

Polycystic ovary syndrome (PCOS), also referred to as Stein-Leventhal syndrome, is one of the most common endocrinopathies. It is characterized by hyperandrogenism, hyperinsulinemia, central obesity, polycystic ovaries, and anovulation. However, some of these manifestations, including the polycystic ovaries, are neither specific for the disorder, nor found in all affected individuals. PCOS appears to be due to one or more primary defects in the upstream gonadotropin/androgen and/or insulin pathway, with the polycystic ovaries being one of many downstream manifestations. Yet, the pathophysiology of PCOS is not completely elucidated. Since the primary defect underlying PCOS may be an upstream endocrine and/or metabolic disturbance, rather than a defect in the ovaries themselves, we hypothesize that this aberration can also arise in men and that the absence of polycystic ovaries in men with other stigmata of the disorder should not eliminate the diagnosis. Our hypothesis is supported by the observation that a genetic susceptibility to PCOS exists, and that PCOS-type manifestations are not limited to women. Indeed, male relatives may suffer from insulin resistance, obesity, diabetes mellitus, and cardiovascular disease. Therefore, recognition of this syndrome in men is important, since pharmacologic treatments identified for women with PCOS may alleviate metabolic problems related to insulin resistance and its sequelae in men with a similar underlying defect. We suggest that first-degree relatives of patients with PCOS should be examined not only for phenotypic features characteristic of PCOS but also for biochemical evidence of hyperinsulinemia and hyperandrogenism. In addition to examining these individuals for obesity, the women should be evaluated for hirsutism and the men should be screened for early-onset male-pattern alopecia and excess hairiness. Serologic evaluation should included the ratio of fasting levels of glucose to insulin, a glucose tolerance test, the free testosterone level and the sex hormone-binding globulin level. Finally, both male and female first-degree relatives of patients with PCOS should be tested for the underlying molecular defect(s) of this condition, once it is identified. As new treatments for PCOS emerge, e.g. insulin-sensitizing drugs, it will be important to determine if these treatments have beneficial effects on the metabolic symptoms and complications in all afflicted patients, regardless of gender.

Female↗

PubMed1999

Serum leptin as an additional possible pathogenic factor in polycystic ovary syndrome.

OBJECTIVES: Recent data raised the possibility that high leptin levels may contribute to infertility in some women with PCOS. DESIGN AND METHODS: To assess changes in leptin levels and its relationship to some hormonal changes (insulin, testosterone, SHBG, FSH, LH, and prolactin) associated with PCOS in obese (n = 27) and nonobese (n = 18) patients when compared to obese and nonobese normal controls (n = 20). RESULTS: Leptin concentration were significantly higher in PCOS than in controls, p < 0.05, with 81% sensitivity and 50% specificity. Whereas, high serum insulin levels were found in obese and nonobese women with PCOS, high serum leptin, FAI together with reduced SHBG were found in obese rather than nonobese PCOS women. Moreover, hyperleptinemia in PCOS women was not correlated to hyperinsulinemia (r = -0.13 and -0.4 in obese and nonobese PCOS women, respectively). In the patient's group correlation analysis between fasting serum leptin and different studied variables showed some correlation with body mass index (BMI) only (r = 0.413) suggesting that high leptin levels could be a characteristic of the obese PCOS. However, multiregression analysis showed that together with testosterone, leptin can successfully predict the presence or absence of PCOS. CONCLUSION: The potential significance of leptin for the pathophysiology of PCOS will await direct studies of the effects of exogenous leptin and/or its inhibitors on the reproductive axis of women, including those with PCOS.

Adolescent↗

PubMed2005

Role of ovary and adrenal glands in hyperandrogenemia in patients with polycystic ovary syndrome.

Ovary is the main source of the hyperandrogenism in polycystic ovary syndrome (PCOS). Adrenal glands may also be involved in the pathogenesis of the development of PCOS. To investigate this possibility and to find out if buserelin test is able to distinguish PCOS patients from the patients with idiopathic hirsutism (IH), ACTH and buserelin tests were performed in 29 women with PCOS, 21 women with IH, and 20 control subjects (CS). We also aimed to determine the role of dysregulation of 17 hydroxylase in the development of PCOS. Basal and stimulated dehydroepiandrosterone sulfate (DHEA-S) and stimulated cortisol (F) levels after ACTH administration were significantly higher in PCOS group than in IH and CS groups (p<0.0001 and p<0.05, respectively). PCOS patients also possessed significantly higher basal and stimulated 17-hydroxyprogesterone (17-OH P) levels, including the peak levels (p<0.02), during buserelin testing when compared with IH patients and CS. There was no significant correlation between the ACTH-stimulated and the buserelin-stimulated peak 17-OH P values. In conclusion, significantly higher basal and ACTH-stimulated levels of F and DHEA-S in PCOS compared with controls and patients with IH, reflect that adrenal hyperactivity also plays a role in hyperandrogenemia seen in PCOS. Because of the lack of the correlation between ACTH-stimulated and buserelin-stimulated 17-OH P levels, it is hard to say that adrenal hyperactivity seen in PCOS is the result of the dysregulation of cytochrome P450c17-alpha enzyme. Our results suggest that buserelin test which is an GnRH analogue could distinguish at least some of the patients with PCOS from the other patients presenting with the common symptoms of hyperandrogenemia.

Adrenal Glands↗

PubMed2005

Genetic determinants of insulin action in polycystic ovary syndrome.

INTRODUCTION: Insulin resistance is associated with both type 2 diabetes (T2 D) and polycystic ovary syndrome (PCOS). There is an association of T2 D with several polymorphisms in candidate genes related to insulin resistance. However, there is limited information about the association of these polymorphisms with PCOS. METHODS: 57 non-diabetic women with PCOS and a control group of 567 healthy non-diabetic women underwent an oral glucose tolerance test (OGTT). They were genotyped for the polymorphisms Gly972Arg in IRS-1, Gly1057Asp in IRS-2, SNP 43, 44, and 45 in CAPN10, Pro12Ala in PPAR(gamma)2, C-512 T in FOXC2, and T45 G in adiponectin. RESULTS: Women with PCOS had higher 2-h blood glucose levels (6.5 +/- 0.2 vs. 6.0 +/- 0.06 mmol/l, p = 0.03) compared to control women, higher fasting insulin (79 +/- 7 vs. 53 +/- 2 pmol/l, p = 0.02), and a lower insulin sensitivity estimated from the OGTT (12.4 +/- 1.1 vs. 19.1 +/- 0.5 U, p = 0.0001). More homozygous G allele carriers of the T45 G polymorphism in the adiponectin gene were found in women with PCOS compared to controls (13.2 % vs. 2.6 %, p = 0.008). In women with PCOS, G-allele carriers had lower fasting insulin levels than TT carriers (61 +/- 9 vs. 88 +/- 10, p = 0.02) in contrast to controls (p = 0.03 for interaction genotype x PCOS). The other polymorphisms were distributed equally among women with PCOS and controls (all p > 0.5). SUMMARY: We found a higher prevalence of the T45 G polymorphism in the adiponectin gene in women with PCOS compared to controls. This was not associated with a more insulin resistant phenotype in PCOS, however. Other frequent polymorphisms in genes related to insulin resistance and type 2 diabetes showed no association with PCOS.

Adiponectin↗

PubMed2003

Does ovarian blood flow distinguish between ovulatory and anovulatory patients with polycystic ovary syndrome?

OBJECTIVE: The purpose of this study was to determine whether parameters of ovarian blood flow distinguish between women with polycystic ovary syndrome (PCOS) who ovulate and those who are anovulatory. STUDY DESIGN: This was a prospectively enrolled trial, carried out as a cross-sectional comparison of 12 ovulatory patients with PCOS and 20 matched subjects with classic PCOS and 10 healthy control subjects. Hormonal parameters and ovarian blood flow by color flow Doppler imaging were obtained in the early follicular phase. RESULTS: Characteristic elevations in luteinizing hormone (LH) and androgens were found in both groups with PCOS compared with control groups. Women with anovulatory PCOS had high insulin levels and lower Quantitative Insulin-Sensitivity Check Index (QUICKI) values compared with women with ovulatory PCOS, although both groups had values that were different from healthy control subjects (P<.01). Ovarian volume was similar in the two groups with PCOS, but pulsatility and resistance indices were lower in anovulatory PCOS (P<.01) compared with ovulatory PCOS and control subjects, who had similar findings. Insulin correlated negatively with the resistance index and QUICKI correlated positively (r=0.653, P<.01). There was a negative correlation between the resistance index and unbound testosterone (r=-0.5, P<.05). CONCLUSION: These data suggest that differences in ovarian blood flow in anovulatory versus ovulatory women with PCOS and that hormonal factors, including insulin resistance, may influence this relationship. The alterations in blood flow in anovulatory PCOS may contribute toward or result from anovulation.

Adult↗

PubMed1997

Endocrine abnormalities in ovulatory women with polycystic ovaries on ultrasound.

Polycystic-appearing ovaries (PAO) on ultrasound have been described in a variety of endocrinopathies and also occur in ovulatory women. By some investigators this is merely referred to as 'PCO' (polycystic ovaries). Although there is controversy in this regard, we do not consider women with PAO/PCO who have no known endocrine disturbance to have polycystic ovary syndrome (PCOS) and therefore prefer not to use the term 'PCO' which is often equated with PCOS. We studied 15 ovulatory women with normal-appearing (NAO) ovaries on ultrasound and 15 matched ovulatory women with PAO/PCO. Compared to ovulatory women, 25 other women were studied who were considered to have PCOS. Of these, 15 were overweight and 10 were of normal weight. All the PCOS women had serum concentrations of luteinizing hormone (LH), testosterone, unbound testosterone, androstenedione and dihydroepiandrosterone sulphate (DHEAS) which were significantly higher (P < 0.01) than values in the normal women, regardless of ovarian morphology. These values were similar in the two groups of ovulatory women with NAO and PAO/PCO. Fasting insulin was elevated in women with PCOS with increased body weight (P < 0.01) and was higher than in ovulatory women with NAO and PAO/PCO and than in women of normal weight with PCOS. Serum insulin-like growth factor (IGF)-I and binding protein (BP)-3 were similar in all groups but serum IGFBP-1 was significantly (P < 0.01) lower in those women with PCOS with increased body weight, compared to all other groups. Compared to values in ovulatory women with NAO, serum IGFBP-1 was also significantly (P < 0.05) lower in women with PAO/PCO and those women with PCOS of normal weight. These lower values were similar in women with PAO/PCO and in normal weight women with PCOS. On an individual basis, an elevation of at least one serum androgen value was found in 33% of women with PAO/PCO. These data confirm that increased body weight accentuates the metabolic alterations in PCOS, but suggest that subtle endocrine disturbances, similar to those that are found in PCOS, may be uncovered in up to a third of ovulatory women with PAO/PCO. It appears that a disturbance of the IGF/IGFBP-1 axis is common and apparently closely associated with alterations in ovarian morphology.

Adult↗

PubMed1997

Heterogeneity in beta cell activity, hepatic insulin clearance and peripheral insulin sensitivity in women with polycystic ovary syndrome.

The aim of this study was to evaluate the impact of reduced peripheral insulin sensitivity, beta cell hypersecretion and reduced hepatic insulin clearance in the hyper-insulinaemia of lean and obese PCOS patients. A total of 35 women with polycystic ovary syndrome (PCOS) and 10 lean normo-ovulatory controls underwent an oral glucose tolerance test and an euglycaemic-hyper-insulinaemic clamp study. PCOS patients were classified into four groups according to their BMI and insulin secretion (normo-lean; normo-obese; hyper-lean; hyper-obese), and results were compared between groups and with the controls. All the PCOS groups showed significantly higher insulin secretion than controls; there were no differences in insulin response to glucose load between lean and obese normo- and hyper-insulinaemic patients. Secretion of c-peptide was greater in PCOS groups than controls. All the hyper-insulinaemic PCOS patients had lower values of hepatic insulin clearance, independent of BMI, when compared either with controls (P < 0.001) or with PCOS normo-insulinaemic women (P < 0.01). Normo- and hyper-insulinaemic obese patients had similar total body glucose utilization (M value), which was lower than in lean PCOS subjects and controls. Our results suggest that evaluation of insulin resistance alone does not fully characterize the PCOS population; differences in liver metabolism of insulin are present in obese insulin resistant subjects and in lean patients with normal insulin sensitivity when divided into normo- and hyper-insulinaemic subgroups. Insulin resistance and hyper-insulinaemia may represent two distinct features of the insulin disorder in PCOS: the former appear to reflect the presence of obesity, while the latter may be a primary feature of PCOS.

Adolescent↗

PubMed2004

Serum and adipocyte resistin in polycystic ovary syndrome with insulin resistance.

BACKGROUND: The aim of this study was to investigate the relationship between resistin and insulin resistance in patients with polycystic ovary syndrome (PCOS). METHODS: We compared serum resistin levels in 17 PCOS women and 10 lean, healthy, age-matched non-PCOS women and also compared levels of insulin receptor (IR), phosphatidylinositol-3 kinase (PI3-kinase), glucose transporter 4 (GLUT4) protein and resistin mRNA in adipocytes isolated from the omental adipose tissue of five of the PCOS patients and five age- and weight-matched, non-PCOS controls, to look for local defects in insulin action in PCOS. RESULTS: The PCOS group was hyperinsulinaemic and displayed an impaired insulin response in a 75 g oral glucose tolerance test and an abnormal homeostasis model insulin resistance index. Serum resistin levels were similar in PCOS patients and controls; however, resistin mRNA levels were 2-fold higher in adipocytes from PCOS patients. No correlation was found between serum resistin levels and either the BMI or testosterone levels. Western blot analysis showed that adipocyte levels of insulin receptor, PI3-kinase, and GLUT4 were respectively decreased by 56, 39.4 and 54% in PCOS patients compared with controls. CONCLUSIONS: These results suggest that overexpression of the resistin gene in adipocytes may be a local determinant factor in the pathogenesis of PCOS.

Adipocytes↗

PubMed2005

Uterine effects of metformin administration in anovulatory women with polycystic ovary syndrome.

BACKGROUND: Metformin has been shown to improve fertility in anovulatory patients with polycystic ovary syndrome (PCOS), inducing not only a high ovulation and pregnancy rate but also reducing the incidence of miscarriages. The aim of the present study was to evaluate the uterine effects of metformin in patients with PCOS who ovulated under metformin. METHODS: Thirty-seven non-obese primary infertile anovulatory patients with PCOS and another 30 age- and body mass index-matched healthy women (control group) were studied. PCOS patients were treated with metformin (850 mg twice daily) for 6 months, whereas the control group did not receive any treatment. In these PCOS patients who ovulated whilst under metformin treatment (PCOS group) and in controls, uterine, sub-endometrial and endometrial blood flow, and endometrial thickness and pattern were evaluated using serial ultrasonographic assessments. RESULTS: Before treatment, uterine, sub-endometrial and endometrial blood flows were significantly lower in patients with PCOS than in the control group. All indexes of uterine vascularization were significantly improved in the PCOS group with metformin treatment and were not different from the controls. Nor was any difference in endometrial thickness and pattern detected between PCOS and control groups. After grouping the data of PCOS patients who ovulated under metformin for cycles with favourable/unfavourable reproductive outcome, no difference in any parameter was observed. CONCLUSIONS: Metformin improves all surrogate markers of endometrial receptivity in PCOS patients, without difference between patients who had favourable or unfavourable reproductive outcome.

Adult↗

PubMed2006

Indices of low-grade chronic inflammation in polycystic ovary syndrome and the beneficial effect of metformin.

BACKGROUND: Women with polycystic ovary syndrome (PCOS) have an increased prevalence of insulin resistance (IR) and related disorders. Elevated serum levels of cellular adhesion molecules (CAMs) reflect low-grade chronic inflammation and have been associated with several insulin-resistant states. The objective of this study is to investigate whether soluble inflammatory markers [soluble intercellular adhesion molecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sE-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1) and C-reactive protein (CRP)] are altered in PCOS and to further elucidate the effect of metformin treatment on their levels. METHODS: Two young populations were studied [62 women with PCOS and 45 normal women of similar age, BMI and waist-to-hip ratio (WHR)]. Plasma levels of sICAM-1, sVCAM-1, sE-selectin and high-sensitivity CRP (hsCRP) were measured in both groups. Additionally, the effect of metformin on these molecules was investigated in 22 women with PCOS who accepted to metformin protocol (1700 mg daily for a 6-month period). RESULTS: In the total population studied, plasma levels of hsCRP (mg/l), sICAM-1 (ng/ml) and sE-selectin (ng/ml) were higher in the PCOS group compared with those in controls (hsCRP 1.31 +/- 0.22 versus 0.92 +/- 0.27, P = 0.014, sICAM-1 301.21 +/- 24.80 versus 209.86 +/- 17.05, P = 0.025, sE-selectin 57.37 +/- 4.08 versus 45.67 +/- 4.62, P = 0.045, respectively). sVCAM-1 (ng/ml) did not differ statistically among the two groups (P = 0.896). A significant reduction in hsCRP and sVCAM-1 was achieved after 6 months of metformin administration: PCOS pretreatment hsCRP 1.92 +/- 0.60 versus PCOS post-treatment hsCRP 0.52 +/- 0.26, P = 0.005; PCOS pretreatment sVCAM-1 668.09 +/- 98.38 versus PCOS post-treatment sVCAM-1 365.82 +/- 99.77, P = 0.039. CONCLUSION: These findings imply the presence of chronic inflammation in women with PCOS. Metformin decreases the levels of plasma inflammatory indices. Further investigation is required to determine whether these findings may prove to be of clinical significance for PCOS patients.

Adult↗

PubMed1995

High incidence of embryo transfer cancellations in patients with polycystic ovarian syndrome.

This study was aimed at assessing the outcome of in-vitro fertilization (IVF) and embryo transfer in patients with polycystic ovarian syndrome (PCOS). The results of IVF and embryo transfer in PCOS patients (PCOS group, 78 cycles of 26 patients) were compared with those of a control group (423 cycles in 202 patients without male factor; age and ovarian stimulation protocol were matched). Although the pregnancy rate per transfer was not different in the two groups of patients (25 versus 34%, PCOS versus control group), the PCOS group had a significantly lower pregnancy rate per follicle aspiration (19 versus 31%, P < 0.05). A notable result was a significantly higher incidence of embryo transfer cancellations in the PCOS group (22 versus 8%, P < 0.01), which resulted from unpredictable failure of either oocyte recovery or fertilization. The incidence of unexplained complete failure of fertilization was significantly higher in the PCOS group (18 versus 5%, P < 0.01). These results may reflect a reduced quality of the oocytes in the PCOS group, and there was a subgroup of PCOS patients who repeatedly produced poor results of treatment. Although the ovarian stimulation regimen best suited to PCOS patients remains to be determined, special care should be taken during ovarian stimulation, especially when the PCOS patients had experienced unexplained failure of oocyte recovery or fertilization in the previous treatment cycle(s).

Adult↗

PubMed2006

Severe endothelial dysfunction in young women with polycystic ovary syndrome is only partially explained by known cardiovascular risk factors.

OBJECTIVE: We aimed to assess whether metabolic abnormalities can explain endothelial dysfunction and associated cardiovascular disease risk (CVDr) in polycystic ovary syndrome (PCOS). Endothelial function, a recognized composite marker of CVDr, may be reduced in PCOS and can be precisely and noninvasively assessed by cardiovascular magnetic resonance (CMR). PATIENTS: Fourteen women with anovulatory PCOS (age [mean +/- SD] 33 +/- 4 years) and 13 controls (age: 33 +/- 6 years) with similar body mass index and regular menses. METHODS: Endothelium-dependent (flow-mediated dilatation - FMD) and -independent (glyceryl trinitrate - GTN) changes in the brachial artery area were measured using CMR in women with PCOS and controls. Arterial function was assessed twice, in the early follicular phase and mid cycle in controls and after an interval of 2 weeks in PCOS subjects. Fasting lipids, glucose, insulin and sex hormones were measured at the first visit. RESULTS: FMD was greatly reduced in women with PCOS compared to controls (-1%vs 5% and 2%vs 12%, P < 0.01) without differences in GTN responses. Risk factors were more prevalent in PCOS women and displayed significant linear relationships with FMD. PCOS status was the strongest predictor of FMD. Linear regression between PCOS and FMD remained significant after correction for all CVD risk markers linked to the metabolic syndrome. CONCLUSION: PCOS is associated with changes in CVD risk markers and pronounced endothelial dysfunction. However endothelial dysfunction with PCOS is only partly explained by recognized CVD risk markers.

Adult↗

PubMed1992

Which hormone tests for the diagnosis of polycystic ovary syndrome?

OBJECTIVE: To assess the frequency of abnormal values for hormone measurements commonly used in the biochemical diagnosis of polycystic ovary syndrome (PCOS). DESIGN: Hormone measurements in 63 unselected women with clinical and ultrasound diagnosis of PCOS attending gynaecological and general endocrine clinics in a District General Hospital were compared with those from a group of 20 normal ovulatory controls in the early follicular phase of their cycles. MEASUREMENTS: Serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), LH/FSH ratio, total testosterone, derived free testosterone, sex hormone binding globulin, androstenedione, and dehydroepiandrosterone (DHEA) were measured by radioimmunoassays. LH and FSH measured by two different assays. RESULTS: The mean serum LH and LH/FSH ratio were significantly (P less than 0.01) higher in the women with PCOS compared with the normal group, but these two measurements were in the abnormal range for only 35% and 41-44%, respectively. Absolute gonadotrophin values were significantly different using the two assay methods, which employed the same reference preparation as standard. Mean serum total testosterone concentration was significantly higher in the PCOS group and was the most frequently (70%) abnormal biochemical marker for PCOS. Sex hormone binding globulin (SHBG) did not differ significantly between the two groups but showed a negative correlation with body mass index in women with PCOS. The combination of SHBG and testosterone to derive a free testosterone value did not further aid the biochemical diagnosis of PCOS. Androstenedione was significantly higher in the PCOS group than in the control group, with a frequency of 53%. There was no significant difference in DHEA-S between the two groups. CONCLUSION: When typical ovarian ultrasound appearances plus the clinical features of oligomenorrhea and/or hirsuitism were used to define PCOS total testosterone was the best single hormonal marker of the condition. Testosterone, androstenedione or LH, either alone or in combination, were raised in 86% of women with PCOS and these should be the definitive hormonal tests. Using LH/FSH ratio as a biochemical criterion for diagnosis of PCOS should be abandoned because of its low sensitivity. To be of value the normal range for all hormones should be precisely defined in a group of regularly ovulating women in the early follicular phase of the cycle for the assay used in each laboratory.

Androstenedione↗

PubMed2000

Evidence for association between polycystic ovary syndrome and premature carotid atherosclerosis in middle-aged women.

Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder characterized by obesity, hyperandrogenism, and insulin resistance. An adverse lipid profile has also been observed in PCOS-affected women, suggesting that these individuals may be at increased risk for coronary heart disease at a young age. The objective of the present study was to evaluate subclinical atherosclerosis among women with PCOS and age-matched control subjects. A total of 125 white PCOS cases and 142 controls, aged >/=30 years were recruited. Collection of baseline sociodemographic data, reproductive hormone levels, and cardiovascular risk factors was conducted from 1992 to 1994. During follow-up (1996 to 1999), these women underwent B-mode ultrasonography of the carotid arteries for the evaluation of carotid intima-media wall thickness (IMT) and the prevalence of plaque. A significant difference was observed in the distribution of carotid plaque among PCOS cases compared with controls: 7.2% (9 of 125) of PCOS cases had a plaque index of >/=3 compared with 0.7% (1 of 142) of similarly aged controls (P=0.05). Overall and in the group aged 30 to 44 years, no difference was noted in mean carotid IMT between PCOS cases and controls. Among women aged >/=45 years, PCOS cases had significantly greater mean IMT than did control women (0.78+/-0.03 versus 0.70+/-0.01 mm, P:=0. 005). This difference remained significant after adjustment for age and BMI (P:<0.05). These results suggest that (1) lifelong exposure to an adverse cardiovascular risk profile in women with PCOS may lead to premature atherosclerosis, and (2) the PCOS-IMT association is explained in part by weight and fat distribution and associated risk factors. There may be an independent effect of PCOS unexplained by the above variables that is related to the hormonal dysregulation of this condition.

Age Factors↗

PubMed2003

Subcutaneous adipose tissue pattern in lean and obese women with polycystic ovary syndrome.

The new optical device, Lipometer, permits the noninvasive, quick, safe, and precise measurement of the thickness of subcutaneous adipose tissue (SAT) layers at any given site of the human body. Fifteen anatomically well-defined body sites from neck to calf describe the SAT topography (SAT-Top) like an individual "fingerprint." SAT-Top was examined in 33 women with polycystic ovary syndrome (PCOS), in 87 age-matched healthy controls and in 20 Type-II diabetic women. SAT-Top differences of these three groups were described, and, based on a hierarchical cluster analysis, two distinctly different groups of PCOS women, a lean (PCOS(L)) and an obese (PCOS(O)) cluster, were found. For visual comparison of the different types of body fat distribution, the 15-dimensional body fat information was condensed to a two-dimensional factor plot by factor analysis. For comparison of the PCOS like body fat distribution with the "healthy" fat pattern, the (previously published) SAT-Top results of 590 healthy women and men (20-70 years old) and 162 healthy girls and boys (7-11 years old) were added to the factor plot. PCOS(O) women showed a SAT-Top pattern very similar to that of women with Type-II diabetes, even though the diabetic women were on average 30 years older. Compared with their healthy controls, SAT-Top of these PCOS(O) patients was strongly skewed into the android direction, providing significantly decreased leg SAT development and significantly higher upper body obesity. Compared with healthy women, PCOS(L) patients had significantly lower total SAT development (even though height, weight, and body mass index did not deviate significantly), showing a slightly lowered amount of body fat in the upper region and a highly significant leg SAT reduction. This type of fat pattern is the same as found in girls and boys before developing their sex specific body fat distribution. We conclude that women with PCOS develop an android SAT-Top, but compared in more detail, we found two typical types of body fat distribution: the "childlike" SAT pattern in lean PCOS patients, and the "diabetic" body fat distribution in obese PCOS women.

Adipose Tissue↗