Component Of Polycystic Ovary Syndrome Research Articles

The prevalence, phenotype and cardiometabolic risk of polycystic ovary syndrome in treatment-naïve transgender people assigned female at birth.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women of reproductive age. We aimed to investigate the prevalence and phenotypic characteristics of PCOS in testosterone treatment-naïve transgender people assigned female at birth (AFAB), as well as to determine whether cardiometabolic risk factors vary based on the presence of PCOS and its components. Evaluation of 112 testosterone treatment-naïve transgender adults AFAB for PCOS and its individual components, including androgen excess, ovulatory dysfunction and polycystic ovarian morphology (PCOM). In our cohort, 79.5% of transgender individuals AFAB had at least one component of PCOS. The prevalence of PCOS was 38.4% (43/112). Phenotype C was the most common phenotype (17.8%), followed by phenotype B (10.7%). Transgender individuals AFAB with at least one component of PCOS had higher blood pressure (BP) measurements and higher fasting plasma glucose levels compared to those with none. Sixty-one subjects (54%) had hyperandrogenism (HA), with 20 (17.9%) having HA without other components of PCOS. When compared to those without HA, transgender individuals AFAB with HA had higher body mass index (BMI), BP, triglyceride and lower HDL-cholesterol levels. PCOS and androgen excess appear to be prevalent among transgender people AFAB. Transgender individuals AFAB with HA or PCOS may exhibit an unfavorable cardiometabolic risk profile compared to those without any PCOS component. Assessment of androgen excess and the specific components of PCOS at baseline could inform long-term management.

Hirsutism and Polycystic Ovarian Morphology are the Most Frequent Components of Polycystic Ovary Syndrome in Women with Type 1 Diabetes

Polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. In Mexico, its prevalence in patients with type 1 diabetes (T1D) is unknown. To evaluate the clinical and biochemical characteristics of patients with T1D with and without PCOS. A cross-sectional study was conducted to evaluate women of reproductive age with T1D for the diagnosis of PCOS using the criteria of the European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine. Clinical information was obtained from clinical records, and we recorded anthropometric variables and performed a laboratory test during the follicular phase. The estimated glucose disposal rate and visceral adiposity index were also calculated to assess insulin resistance. Subsequently, participants were evaluated based on the presence or absence of PCOS. Thirty-nine percent of patients with T1D had PCOS. The most frequent components of PCOS were polycystic ovary morphology (58.5%), clinical hyperandrogenism (41.5%), oligomenorrhea (29.2%), and biochemical hyperandrogenism (19.5%). Patients with PCOS used more insulin per day (1.04 ± 0.33 vs. 0.71 ± 0.29 IU/kg/d, p=0.003), had lower fasting glucose (116.4 ± 59.79 vs. 161.16 ± 63.9 mg/dl, p=0.029) and higher right ovarian volume (11.36 [8.64-15.89] vs. 6.9 [5.55-8.77] cm3, p=0.005) and Ferriman-Gallwey scores (9.06 ± 2.05 vs. 7.12 ± 3.15 points, p=0.035) compared to patients without PCOS. The frequency of insulin resistance and metabolic syndrome in women with PCOS was 37.5 and 18.8%, respectively. PCOS is a very heterogeneous entity, with a high frequency in women with T1D.

Ovarian volume is more closely related to the different manifestations of polycystic ovary syndrome than follicle number per ovary.

Polycystic ovary (PCO), a diagnostic component of polycystic ovary syndrome (PCOS), requires either an ovarian volume (OV) criterion or a follicle number per ovary (FNPO) criterion. This study investigated the association of OV and FNPO criteria with various manifestations of PCOS. This cross-sectional study was conducted at a university hospital among 100 patients newly diagnosed with PCOS (according to the revised Rotterdam criteria). Fasting blood samples were collected to measure glucose, total testosterone (TT), luteinizing hormone (LH), follicle-stimulating hormone (FSH), lipid, insulin, and hemoglobin A1c levels. An oral glucose tolerance test was performed. Transabdominal or transvaginal ultrasound of the ovaries was done, depending on patients' marital status. All investigations were conducted in the follicular phase of the menstrual cycle. OV >10 mL and/or FNPO ≥12 indicated PCO. A homeostasis model assessment of insulin resistance (IR) value ≥2.6 indicated IR, and metabolic syndrome (MS) was defined according to the international harmonization criteria. Seventy-six participants fulfilled the OV criterion, 70 fulfilled the FNPO criterion, and 89 overall had PCO. Both maximum OV and mean OV had a significant correlation with TT levels (<italic>r</italic>=0.239, <italic>p</italic>=0.017 and <italic>r</italic>=0.280, <italic>p</italic>=0.005, respectively) and the LH/FSH ratio (<italic>r</italic>=0.212, <italic>p</italic>=0.034 and <italic>r</italic>=0.200, <italic>p</italic>=0.047, respectively). Mean OV also had a significant correlation with fasting insulin levels (<italic>r</italic>=0.210, <italic>p</italic>=0.036). Multivariate binary logistic regression analysis showed that IR (odds ratio [OR], 9.429; 95% confidence interval [CI], 1.701 to 52.271; <italic>p</italic>=0.010) and MS (OR, 7.952; 95% CI, 1.821 to 34.731; <italic>p</italic>=0.006) had significant predictive associations with OV alone, even after adjustment for age and body mass index. OV may be more closely related to the androgenic and metabolic characteristics of PCOS than FNPO.

Cardiovascular disease risk in women with hyperandrogenism, oligomenorrhea/menstrual irregularity or polycystic ovaries (components of polycystic ovary syndrome): a systematic review and meta-analysis.

Prior meta-analyses indicate polycystic ovary syndrome (PCOS) is associated with cardiovascular diseases (CVDs), but have high statistical heterogeneity, likely because PCOS is a heterogenous syndrome diagnosed by having any two of the three components: hyperandrogenism, oligomenorrhea/menstrual irregularity or polycystic ovaries. Several studies report higher risk of CVDs from individual PCOS components, but a comprehensive assessment of how each component contributes to CVD risk is lacking. This study aims to assess CVD risk for women with one of the PCOS components. A systematic review and meta-analysis of observational studies was conducted. PubMed, Scopus, and Web of Science were searched without restrictions in July 2022. Studies meeting inclusion criteria examined the association between PCOS components and risk of a CVD. Two reviewers independently assessed abstracts and full-text articles, and extracted data from eligible studies. Where appropriate, relative risk (RR) and 95% confidence interval (CI) were estimated by random-effects meta-analysis. Statistical heterogeneity was assessed using the I2 statistic. Twenty-three studies, including 346 486 women, were identified. Oligo-amenorrhea/menstrual irregularity was associated with overall CVD (RR = 1.29, 95%CI = 1.09-1.53), coronary heart disease (CHD) (RR = 1.22, 95%CI = 1.06-1.41), and myocardial infarction (MI) (RR = 1.37, 95%CI = 1.01-1.88) but not cerebrovascular disease. These results were broadly consistent even after further adjustment for obesity. There was mixed evidence for the role of hyperandrogenism in CVDs. No studies examined polycystic ovaries as an independent exposure for CVD risk. Oligo-amenorrhea/menstrual irregularity is associated with greater risk of overall CVD, CHD, and MI. More research is needed to assess the risks associated with hyperandrogenism or polycystic ovaries.

Women's Reproductive Milestones and Cardiovascular Disease Risk: A Review of Reports and Opportunities From the CARDIA Study.

In 1985 to 1986, the CARDIA (Coronary Artery Risk Development in Young Adults) study enrolled 5115 Black or White participants, including 2788 women, aged 18 to 30 years. Over the following 35 years, the CARDIA study amassed extensive longitudinal data on women's reproductive milestones, spanning menarche to menopause. Although not initially conceived as a study of women's health, >75 CARDIA study publications address relationships between reproductive factors and events with cardiovascular and metabolic risk factors, subclinical and clinical cardiovascular disease, and social determinants of health. The CARDIA study was one of the earliest population-based reports to note Black-White differences in age at menarche and associations with cardiovascular risk factors. Adverse pregnancy outcomes, particularly gestational diabetes and preterm birth, have been assessed along with postpartum behaviors, such as lactation. Existing studies have examined risk factors for adverse pregnancy outcomes and lactation, as well as their relationship to future cardiovascular and metabolic risk factors, diagnoses, and subclinical atherosclerosis. Ancillary studies examining components of polycystic ovary syndrome and ovarian biomarkers, such as anti-Müllerian hormone, have facilitated examination of reproductive health in a population-based cohort of young adult women. As the cohort transitioned through menopause, examination of the importance of premenopausal cardiovascular risk factors along with menopause has improved our understanding of shared mechanisms. The cohort is now aged in the 50s to mid-60s, and women will begin to experience a greater number of cardiovascular events as well as other conditions, such as cognitive impairment. Thus, in the next decade, the CARDIA study will provide a unique resource for understanding how the women's reproductive life course epidemiology informs cardiovascular risk, as well as reproductive and chronological aging.

Association of insertion/deletion polymorphism of angiotensin converting enzyme gene with metabolic components of polycystic ovary syndrome

Background: Polycystic ovary syndrome (PCOS) has taken the prime position as an endocrine disease in women of reproductive age and is estimated to affect 2.2–22.5% worldwide and in Indian women it ranges from 9% to 12%. The primary defects that cause PCOS still remains unknown. A lot of genetic factors not excluding polymorphisms and mutations of multiple genes have been linked with PCOS, exact mechanisms which might be the cause of PCOS are yet unknown. Angiotensin converting enzyme (ACE) and its yields are related with angiogenesis of ovarian epithelium, restoration of meiosis, steroidogenesis, and follicular growth. Aims and Objectives: The present study was aimed to establish the association of ACE insertion/deletion (I/D) polymorphism in PCOS patients and to assess the influence of this polymorphism on the metabolic components of PCOS. Materials and Methods: Genomic DNA was extracted from blood obtained from 100 patients with PCOS and 100 healthy controls following ethical guidelines. DNA was amplified by polymerase chain reaction (PCR) using I/D distinct allele primers. PCR products were assessed after being exposed to gel electrophoresis. Results were analyzed in respect to biochemical parameters. Results: The allelic frequency and genotypic distribution of the ACE gene polymorphism is associated with PCOS in women. The concentrations of testosterones as well as luteinizing hormone/follicle stimulating hormone ratio among the distinct genotypes were significantly different. The presence of “D” allele in a population more likely to be associated with formation of polycystic ovary and hyperandrogenism was observed. Conclusion: The data suggest that ACE I/D polymorphism and PCOS pathology are unassociated. However, aggravation of clinical symptoms of PCOS can be linked to the steroidogenesis which, in turn, is associated with the polymorphism.

Substituting serum anti-Müllerian hormone for polycystic ovary morphology increases the number of women diagnosed with polycystic ovary syndrome: a community-based cross-sectional study.

Can serum anti-Müllerian hormone (AMH) replace polycystic ovary morphology (PCOM) determined by ultrasound as a diagnostic component of polycystic ovary syndrome (PCOS)? Despite good correlations between serum AMH and PCOM, the use of a high serum AMH as a proxy for PCOM resulted in the reclassification of PCOS in 5% of study participants, with the main effect being more women identified, although some women previously classified as having PCOS were no longer classified as such. AMH has been proposed as an alternative to PCOM as a diagnostic component of PCOS. Previous studies are limited by poorly defining PCOS, use of infertile women as comparators, measurement of hormones by immunoassay that lack precision in the female range, low-resolution ovarian ultrasound and inconsistent handling and storage of serum samples. This is an Australian cross-sectional study of 163 non-healthcare-seeking women. Serum AMH was measured by both the Ansh picoAMH assay and the Beckman Coulter Access 2 (BA2) assay, in parallel with androgens measured by liquid chromatography-tandem mass spectrometry, in blood samples of women, not pregnant, breast feeding or using systemic steroids, who also underwent high-resolution ovarian ultrasound. PCOS was determined by the Rotterdam criteria with PCOM defined by the Androgen Excess-PCOS Taskforce recommendation of ≥25 follicles in at least one ovary. Cut-off serum concentrations that best identified women as having PCOM were identified by receiver operator characteristic (ROC) curves. A total of 163 women, mean (SD) age 32.5 (5.5) years, who provided a blood sample and had both ovaries visualized on ultrasound were included in the analysis. Women with isolated PCOM had higher median (range) Ansh AMH and BA2 AMH concentrations than those with no PCOS characteristics [56.9 pmol/l (34.6, 104.2) versus 18.7 (3.2, 50.9), P = 0.002 and 38.5 pmol/l (22.2, 100.2) versus 16.7 (3.5, 38.9), P = 0.002, respectively]. An AMH ≥ 44.0 pmol/l, suggested by the ROC curve, identified 80.6% of women with PCOM, falsely identified 15.2% of women without PCOM as having PCOS and had a positive predictive value of 55.6%. The negative predictive value was 94.9%. An AMH BA2 assay cut-off of ≥33.2 pmol/l provided a sensitivity of 80.6%, a specificity of 79.5% and a positive predictive value for PCOM of 48.1%. The negative predictive value was 94.6% for PCOM. When serum AMH was used in the place of PCOM as a diagnostic criterion for PCOS, the Ansh assay resulted in an additional seven women classified as having PCOS and no longer classified one woman as having PCOS. For the BA2 assay, eight additional and two fewer women were classified as having PCOS. Overall, both assays resulted in six more women being classified as having PCOS. Women with functional hypogonadotrophic hypogonadism were not excluded and may have been misclassified as having an oligo-amenorrhoea-PCOM phenotype. As study participants were predominantly Caucasian/White, our findings cannot be generalized to women of other ethnicities. Although serum AMH reflects the number of developing ovarian follicles, the absolute values vary between assays and specific reference ranges for individual assays are required. Irrespective of the assay used, replacing PCOM with serum AMH to diagnose PCOS in a community-based sample altered the number of women classified as having or not having PCOS. Consequently, although overall the risk of women being identified as having PCOS would be increased, some women would no longer be classified as having this condition. The study was supported by the Norman Beischer Research Foundation and the Grollo-Ruzzene Foundation. S.R.D. is an NHMRC Senior Principal Research Fellow (Grant No. 1135843). S.R.D. reports unrelated support that includes grants from the NHMRC Australia, personal fees for educational activities from Besins Healthcare, Abbott Chile, BioFemme and Pfizer Australia, personal Advisory Board/consultancy fees from Theramex, Abbott Laboratories, Astellas, Mayne Pharmaceuticals, Roche Diagnostics, Lawley Pharmaceuticals and Que Oncology and has received institutional grant funding from Que Oncology and Ovoca research. The other authors declare no conflicts of interest. N/A.

2013-P: Lifestyle Intervention, Metformin, and Acarbose Treatments Differentially Impact Liver Fat Content, Serum Lipids, and Hormone Profiles in Obese Polycystic Ovary Syndrome Patients with Impaired Glucose Tolerance

Introduction: Polycystic ovary syndrome (PCOS) is often associated with obesity, insulin resistance, abnormal glucose tolerance, lipid metabolic disorders, and fatty liver. It remains unknown how current therapies impact these different components of PCOS. Objective: We aim to evaluate the effects of lifestyle intervention (low calorie diet, LCD), metformin and acarbose treatment on fat mass, insulin sensitivity, hormone profiles, liver fat content and lipids profile in obese PCOS patients with impaired glucose tolerance (IGT). Methods: In a 12-week, randomized, open tag prospective clinical trial, we recruited thirty obese PCOS patients, and randomly divided them into three groups: LCD, metformin, and acarbose group. Body weight, adipose tissue distribution, and serum sex hormone levels were measured before and after treatment. MRI was used to measure the liver fat content (LFC) and abdominal fat mass (AFM); Insulin sensitivity and beta-cell function were evaluated by OGTT and two-step hyperglycemic clamp; Serum free fatty acids (FFAs) were measured by GC-MS. Results: In all three groups, AFM and insulin secretion were significantly decreased as measured by MRI, OGTT and glucose clamp, respectively. LCD significantly improved the insulin sensitivity as determined by HOMA-IR, disposition index, and matsuda index. Metformin significantly improved hyperandrogenism. Interestingly, we found only acarbose significantly decreased triglyceride, FFAs, and LFC. Conclusion: All treatment modalities were effective in the treatment of PCOS women with obesity and IGT, only acarbose significantly decreased the triglyceride and FFAs, and ameliorated the LFC, suggesting that acarbose is an effective agent that could be used in PCOS patients with IGT and fatty liver. Disclosure S. Li: None. Y. Wang: None. J. Cai: None. W. Liu: None. H. Yin: None. T. Tao: None.

Chronic combined hyperandrogenemia and western-style diet in young female rhesus macaques causes greater metabolic impairments compared to either treatment alone.

Does developmental exposure to the combination of hyperandrogenemia and western-style diet (WSD) worsen adult metabolic function compared to either treatment alone? Young female rhesus macaques treated for 3 years, beginning at menarche, with combined testosterone (T) and WSD have increased weight gain and insulin resistance compared to controls and animals treated with either T or WSD alone. Hyperandrogenemia is a well-established component of polycystic ovary syndrome (PCOS) and can be observed in peripubertal girls, indicating a potential pubertal onset of the disease. Obesity is often associated with hyperandrogenemia in peripubertal girls, and overweight girls appear to be at higher risk for the development of PCOS later in life. Juvenile (2.5- year old) female rhesus macaques were divided into four groups (n = 10/group): control animals receiving cholesterol implants and a control diet with 15% of calories derived from fat (C), animals receiving T implants (mean serum levels: 1.35 ± 0.01 ng/ml) and a control diet (T), animals receiving a cholesterol implant and a WSD with 36% of calories derived from fat (WSD) and animals receiving a T implant and a WSD (T + WSD). Animals were maintained on the treatments for 36 months and were 5.5 years old at study completion. Metabolic testing consisted of body measurements including weight, dual-energy X-ray absorptiometry scans, activity monitoring, and glucose tolerance testing at zero months and at least once every 12 months for the remainder of the study. Indirect calorimetry and serum hormone assays were performed following 36 months of treatment. Body weight and fat mass gain were significantly increased in T + WSD at 24 and 36 months of treatment compared to the other three groups. Log transformed fasting insulin and Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) were significantly increased in T + WSD animals at 3 years of treatment compared to all other groups. T-treatment caused a greater rate of decline in activity after 18 months, while food intake and metabolic rate were largely unaffected by treatments. Variability was present in the metabolic parameters measured; however, this is similar to the heterogeneity observed in human populations. Chronic hyperandrogenemia beginning at puberty may exacerbate metabolic dysfunction in women consuming a WSD and account for the increased rates of obesity and insulin resistance observed in PCOS patients. Counseling of female patient populations with elevated androgens about the potential benefit of consuming a lower fat diet could improve long-term metabolic health outcomes. Eunice Kennedy Shriver National Institute of Child Health & Human Development P50HD071836 and Oregon National Primate Center Grant P51 OD011092. The authors have no competing conflict of interests to disclose.

Impact of hypovitaminosis D on clinical, hormonal and insulin sensitivity parameters in normal body mass index polycystic ovary syndrome women

Earlier data on the relationship of 25 hydroxyvitamins (25OHD) levels with various components of polycystic ovary syndrome (PCOS) has been conflicting. We studied 122 normal body mass index (BMI) women with PCOS (cases) and 46 age and BMI-matched healthy women (controls) and assessed the impact of serum 25OHD levels on clinical, biochemical and insulin sensitivity parameters in these lean Indian women with PCOS. The mean age and BMI of the cases and controls were comparable. Mean serum 25OHD levels respectively were 10.1 ± 9.9 and 7.9 ± 6.8 ng/ml with 87.7% and 91.1% vitamin D (VD) deficient. No significant correlation was noted between 25OHD levels and clinical, biochemical and insulin sensitivity parameters except with the total testosterone levels (p = 0.007). Also, no significant difference in these parameters was observed once the PCOS women were stratified into various subgroups based on the serum 25OHD levels. We conclude that VD deficiency being common in normal BMI Indian women with or without PCOS does not seem to alter the metabolic phenotype in these women.

Cystatin C, a novel cardiometabolic risk marker in women with polycystic ovary syndrome

Objective: To investigate the impact of urinary albumin excretion (UAE) and cystatin C on the metabolic components of polycystic ovary syndrome (PCOS).Methods: Seventy-five women with PCOS were divided into two groups according to metabolic syndrome as MetS + and MetS−. Clinical, metabolic and renal parameters were compared between the groups. Correlation analyses were performed between cystatin C, microalbuminuria and clinical and metabolic parameters in women with PCOS.Results: Waist/hip ratio (WHR), body mass index, LDL cholesterol, triglyceride, total cholesterol, cystatin C, UAE were significantly higher in the MetS + group compared with the MetS − one. HDL cholesterol was significantly higher in the MetS − group than the MetS + one. The UAE positively correlates with LDL cholesterol, triglyceride and total cholesterol levels. Cystatin C positively correlates with UAE, WHR, LDL cholesterol, triglyceride, total cholesterol levels.Conclusions: Evaluating UAE and cystatin C may be important for the detection of target subjects at high risk for future metabolic syndrome and cardiovascular disease.

Comparison of 25-hydroxyvitamin D and Calcium Levels between Polycystic Ovarian Syndrome and Normal Women.

Given the relationship of vitamin D deficiency with insulin resistance syndrome as the component of polycystic ovary syndrome (PCOS), the main aim of this study was to compare serum level of 25hydroxyvitamin D [25(OH)D] between PCOS patients and normal individuals. A cross sectional study was conducted to compare 25(OH)D level between117 normal and 125 untreated PCOS cases at our clinic in Arash Hospital, Tehran, Iran, during 2011-2012. The obtained levels of 25(OH)D were classified as follows: lower than 25 nmol/ml as severe deficiency, between 25-49.9 nmol/ml as deficiency, 50-74.9 nmol/ml as insufficiency, and above 75 nmol/ml asnormal. In addition, endocrine and metabolic variables were evaluated. Among PCOS patients, our findings shows 3(2.4%) normal, 7(5.6%) with insufficiency, 33(26.4%) with deficiency and 82(65.6%) with severe deficiency, whereas in normal participants, 5(4.3%) normal, 4(3.4%) with insufficiency, 28(23.9%) with deficiency and 80(68.4%) with severe deficiency. Comparison of 25(OH)D level between two main groups showed no significant differences (p= 0.65). Also, the calcium and 25(OH)D levels had no significant differences in patients with overweight (p=0.22) and insulin resistance (p=0.64). But we also found a relationship between 25(OH)D level and metabolic syndrome (p=0.01). Furthermore, there was a correlation between 25(OH)D and body mass index (BMI) in control group (p=0.01), while the C-reactive protein (CRP) level was predominantly higher in PCOS group (p<0.001). Although the difference of 25(OH)D level between PCOS and healthy women is not significant, the high prevalence of 25(OH)D deficiency is a real alarm for public health care system and may influence our results.

Prospective association of polycystic ovary syndrome with coronary artery calcification and carotid-intima-media thickness: the Coronary Artery Risk Development in Young Adults Women's study.

To study the independent associations of polycystic ovary syndrome (PCOS), and its 2 components, hyperandrogenism and anovulation, with coronary artery calcification (CAC) and carotid artery intima-media thickness (IMT). At the year 20 of the Coronary Artery Risk Development in Young Adults (CARDIA) study, a population-based multicenter cohort of young adults, women (mean age, 45 years) with information on menses and hirsutism in their twenties were assessed for CAC (n=982) and IMT (n=988). We defined PCOS as women who had both irregular menses and hyperandrogenism (n=55); isolated oligomenorrhea (n=103) as women who only had irregular menses; and isolated hyperandrogenism (n=156) as women who had either hirsutism or increased testosterone levels. Logistic regressions and general linear models were used to estimate the associations between components of PCOS and subclinical CVD. The prevalence of CAC was 10.3% overall. Women with PCOS had a multivariable adjusted odds ratio of 2.70 (95% confidence interval, 1.31-5.60) for CAC. Women with either isolated oligomenorrhea or isolated hyperandrogenism had no increased risk of CAC when compared with unexposed women. Women with PCOS had significantly increased bulb and internal carotid-IMT measurements; however, no significant differences were noted in bulb or internal carotid artery IMT among women with either isolated oligomenorrhea or isolated hyperandrogenism when compared with unexposed women. There were no differences in common carotid-IMT among the 4 study groups. In this study, women with PCOS, manifested as both anovulation and hyperandrogenism, but not women with one of these manifestations alone, were at increased risk for the development of subclinical CVD.

High-sensitivity C-reactive protein (hs-CRP) levels and its relationship with components of polycystic ovary syndrome in Indian adolescent women with polycystic ovary syndrome (PCOS)

C-reactive protein (CRP) is a risk marker for type 2 diabetes mellitus and cardiovascular diseases. In polycystic ovary syndrome (PCOS), limited data are available on high-sensitivity C-reactive protein (hs-CRP) levels and its relationship with components of PCOS especially in Indian women. The objective was to determine serum hs-CRP concentration in adolescent women with and without PCOS and to assess possible correlations of serum hs-CRP levels with components of PCOS in Indian women. One hundred and sixty women with PCOS and sixty non-PCOS women having normal menstrual cycles were included. Clinical assessment included anthropometry, Ferriman–Gallwey (FG) score and blood pressure (BP) measurement. Laboratory evaluation included estimation of T4, TSH, LH, FSH, total testosterone, prolactin, cortisol, 17OHP, hs-CRP, lipid profile, and insulin, and glucose after 2-h oral glucose tolerance test. Homeostasis Model Assessment Insulin resistance index (HOMA-IR) and Quantitative Insulin Sensitivity Check Index (QUICKI) and glucose intolerance was calculated. FG score, LH, FSH, total Testosterone, HOMA-IR and QUICKI were significantly different among women with or without PCOS (p < 0.01). Although hs-CRP levels showed a higher trend in women having PCOS, there was no significant difference between the groups (p > 0.05). A significant and positive correlation was found between hs-CRP and body mass index (BMI) (r = 0.308, p < 0.01) among PCOS group. The results in Indian adolescent women suggest that hs-CRP levels may not per se be associated with PCOS, rather can be related to fat mass in this subset of subjects.

The Effect of Chromium Supplementation on Polycystic Ovary Syndrome in Adolescents

BackgroundPolycystic ovary syndrome (PCOS) is a common condition. Treatment with chromium has been shown to improve insulin sensitivity in adults with PCOS. Treatment of adolescents with PCOS remains a challenge. ObjectiveTo investigate the effect of chromium supplementation on the various components of polycystic ovary syndrome in adolescent girls. Patients and MethodsThirty-five adolescent girls with PCOS were enrolled. History of menstrual irregularities was recorded. All underwent physical examination for presence of acne, scoring of hirsutism, and calculation of body mass index. Pelvic ultrasonography was done and serum free testosterone was measured in all subjects. All subjects received 1000 μg chromium picolinate for 6 months followed by re-evaluation. ResultsMean (SD) age was 15.5 (1) years (range: 14-17 y). No significant change in BMI standard deviation score (SDS) with chromium supplementation was noted (1.9 (0.7) SDS vs 2 (0.7) SDS, P = .638). The number of patients with oligo/amenorrhea decreased with treatment (29/35 (83%) versus 11/35 (31%), P < .001). Significant reduction in mean ovarian volume (P < .001), total follicular count (P < .034), and free testosterone (P< .002) was observed. No significant improvement in acne or hirsutim was noted. ConclusionSupplementation with chromium to adolescents with PCOS is a promising treatment option.

Elevated androgens during puberty in female rhesus monkeys lead to increased neuronal drive to the reproductive axis: a possible component of polycystic ovary syndrome

Hyperandrogenemia is associated with several clinical disorders in which both reproductive dysfunction and metabolic changes may coexist [i.e. polycystic ovary syndrome (PCOS), obesity and congenital adrenal hyperplasia]. Moreover, there is growing evidence that the elevated levels of circulating androgens in obese girls may lead to an increased neuroendocrine drive to the reproductive axis, similar to that associated with PCOS. To test whether androgen exposure in the childhood and adolescent period could lead to pubertal alterations in LH secretory patterns, female rhesus monkeys received subcutaneous testosterone implants prepubertally beginning at 1 year of age, maintaining a 3.7-fold increase (P = 0.001) in circulating testosterone levels over cholesterol-implant controls (n = 6/group) into the post-pubertal period. In early adulthood, pulsatile secretion of LH was measured over 12 h during the early follicular phase of a menstrual cycle, and responsiveness of the pituitary to gonadotrophin-releasing hormone was determined. In addition, ultrasounds were performed to assess ovarian morphology and glucose tolerance testing was performed to assess insulin sensitivity. The timing of menarche was similar between groups. Testosterone-treated animals had a significantly greater LH pulse frequency during the early follicular phase compared with controls (P = 0.039) when measured at 5 years of age. There was a larger LH response to GnRH when testosterone-treated animals were 4 years of age (P = 0.042), but not when the animals were 5 years old (P = 0.57). No differences were seen in insulin sensitivity or ovarian morphology, and the groups showed similar rates of ovulation in early adulthood. Exposure to increased levels of androgens over the course of pubertal development appears to trigger physiological changes in the neural drive to the reproductive axis that resemble those of obese hyperandrogenemic girls in early adulthood and are characteristic of PCOS.

Hyperandrogenism, ovulatory dysfunction, and polycystic ovary syndrome with valproate versus lamotrigine

To evaluate development of components of polycystic ovary syndrome (PCOS) and PCOS in women with epilepsy initiating valproate or lamotrigine therapy. Female individuals with epilepsy and regular menstrual cycles were eligible for this prospective study. Participants were randomized to 12 months of valproate (n = 225) or lamotrigine (n = 222) therapy. Serum androgen levels were measured every 3 months. Urinary pregnanediol glucuronide levels were measured weekly for two 3-month periods. The primary end point was development of PCOS components (ie, hyperandrogenism or ovulatory dysfunction). A post hoc analysis was conducted in women more than 2 years after menarche (177 lamotrigine, (HA) 186 valproate) to exclude OD the confounding effect of puberty. More women in the valproate group than the lamotrigine group developed (OD) in the prospective (54% valproate, 38% lamotrigine; p = 0.010) and the post hoc (HA) analyses (36% valproate, 23% lamotrigine; p = 0.007). More women in the valproate group than the lamotrigine group developed PCOS (9 vs 2%; p = 0.007). Development of HA was more frequent with OD valproate than lamotrigine among those initiating treatment at age younger than 26 years (44% valproate, 23% lamotrigine; p = 0.002) but was similar if treatment was started at age 26 years or older (24% valproate, 22% lamotrigine). Development of HA occurred more frequently with valproate than lamotrigine, especially if medication was started at age younger than 26 years.

Insulin sensitivity does not differentiate by hirsutism in non-obese women with polycystic ovary syndrome

Hirsutism is one of the component of polycystic ovary syndrome. According to the Rotterdam Consensus has concluded that principially obese women with polycystic ovary syndrome (PCOS) should be evaluated for the metabolic syndrome. The aim of the present study was to investigate the insulin sensitivity in PCOS women with and without hirsutism regardless of obesity. Clinical characteristics, sex hormones and fasting glucose and insulin levels of fifty-eight women with PCOS were analyzed. Hirsutism has been evaluated through the Ferriman-Gallwey (FG) map scoring system. Twenty-two women (38%) were hirsute. They were not any significant difference between hirsute and nonhirsute women for their sex steroids and insulin sensitivity (P>0.05). There were no correlation among sex steroids, WHR and insulin sensitivity in relation to FG score in the subgroup with hirsutism (P>0.05). Our study suggests that normal weight and overweight women with hirsutism can have normal insulin sensitivity and normal levels of circulating androgens in PCOS women.

Is insulin resistance an essential component of PCOS?: The influence of confounding factors.

Insulin resistance is often considered a regular component of polycystic ovary syndrome (PCOS). Many interventional studies assume a state of insulin resistance in all patients. However, the evidence is based on small samples that are often insufficient to adjust for significant confounding factors. Moreover, several studies have not confirmed differences in insulin sensitivity between women with PCOS and healthy controls, especially in non-obese patients. This debate article provides an overview of the data published regarding the presence of abnormal or normal insulin sensitivity in PCOS. In conclusion, available data offer evidence that a substantial subgroup of women with PCOS have insulin sensitivity comparable with healthy controls if matched carefully for potential confounding factors.