Polycystic ovary syndrome (PCOS), a disease that usually emerges during adolescence, is characterized by hormonal imbalance and ovarian dysfunction. The prevalence can vary between 5.6 to 21.3% in women and 6% in adolescent girls. This discrepancy is related to the population studied and the diagnostic criteria used. The underlying pathophysiology of PCOS is not fully understood, but it can lead to a number of co-morbidities, including hypertension, diabetes, dyslipidemia, and also, mental health disorders. Clinical and preclinical data indicate neuroendocrine involvement with dysfunction in gamma-Aminobutyric acid (GABA) signaling and neuronal androgen receptors that might reduce hypothalamic sensitivity and lead to an impairment of estradiol and progesterone feedback. Based on these assumptions, the aims of this paper are to review the association of PCOS and psychotic disorders in order to address the burden of women comorbid for both conditions.

Polycystic Ovary Syndrome (PCOS) is an endocrine disease. PCOS afflicts 5 to 10 % of women of reproductive age. The symptoms are: amenorrhea, oligomenorrhea, hirsutism, obesity, infertility, chronic hyperandrogenic anovulation and acne.

In the 1930s, Stein and Leventhal added amenorrhoea to anovulatory dysfunctional uterine bleeding among the known clinical manifestations of the polycystic ovary syndrome (PCOS). Whatever the menstrual pattern, infrequent or absent ovulation with symmetrical enlargement of the ovaries is now a familiar abnormality in women of reproductive age. Diagnosis of PCOS has developed from just the clinically obvious to an appreciation, through ultrasound imaging of the ovaries and endocrine testing, of its subtler forms. Today's clinicians will identify PCOS on the ultrasound image of many small follicles apparent in the periphery of both ovaries, on raised serum unbound testosterone assays, on exaggeration of serum LH levels with the start of pulsatile GnRH therapy, and on follicular overresponsiveness to injections of FSH. Once among the most treatable causes of infertility, ovulation-induction for PCOS remained unsophisticated while microsurgery and assisted conception dissolved frontiers for other causes of infertility. Whereas we now have the benefit of high technology embryo cryostorage to cope with embarrassingly high yields of PCOS oocytes, we still need to explain why, the bigger the ovaries, the more likely (we have long known it to be) that PCOS can be cured simply by reducing ovarian mass. Some cases of PCOS are hereditary and most seem constitutionally determined. PCOS is so common that the questions must be asked, Are we appreciating an extreme of normal? Could the milder forms of PCOS have--or could PCOS have had--evolutionary usefulness?

The aim of this cross-sectional study, that included 146 polycystic ovary syndrome (PCOS) patients, was to evaluate the prevalence, severity and pattern of cutaneous manifestation in Jordanian women with PCOS, as well as their correlation with hormonal abnormalities. A thorough complete cutaneous examination, hormonal assays (Luteinizing hormone [LH], follicle stimulating hormone [FSH], prolactin, total testosterone, free testosterone, dehydroepiandrosterone sulfate) and pelvic ultrasonography were done. The most common cutaneous features of PCOS were acne vulgaris (75.3%) followed by hirsutism (59.6%) then seborrhea (43.2%) and androgenetic alopecia (42.5%). Patients who had acne vulgaris presented at a younger age than patients who did not. Patients who had androgenetic alopecia and stria were older than patients with no such features. Moreover, all cutaneous manifestations of PCOS, except for acne, were associated with higher body mass index (BMI). Elevated LH:FSH ratio of more than 2:1 was the most common hormonal abnormality, followed by increased LH and total testosterone. Acne, hirsutism, androgenetic alopecia, seborrhea, acanthosis nigricans and skin tags are common cutaneous manifestations among Jordanian patients with PCOS. The existence of one or more of these features, especially in overweight and obese patients, should alert the physician towards the possibility of having PCOS.

Background. Polycystic ovary syndrome (PCOS) is the commonest cause of female infertility. Visceral obesity and insulin resistance are key pathophysiological mechanisms behind PCOS. Women suffering from this syndrome and infertility often seek bariatric surgery hoping that they would be able to conceive postoperatively. Objective. At present, there is no consensus on the role of bariatric surgery in the management of PCOS-associated infertility within the medical community, making it difficult to give specific advice to these women, so a review of the literature was necessary. Results. A detailed review of the literature was performed. Only 6 manuscripts were relevant and contained quantitative data. They demonstrated that bariatric surgery results in postoperative conception rates varying from 33% to 100%. Surgery is also associated with amelioration of menstrual irregularities, hormonal abnormalities, and hirsutism that are associated with PCOS. These studies were retrospective and only had a small number of participants with infertility. Conclusions. Bariatric surgery has been shown to conclusively improve life expectancy, quality of life, and comorbidities like type 2 diabetes and obstructive sleep apnea. However, further research is required to identify whether weight loss surgery results in significant improvement in fertility of women with PCOS and to investigate which operation has the best results.

We aimed to investigate a possible role of the endocrine disruptors phthalates, di-2-ethylhexyl phthalate (DEHP) and mono (2-ethylhexyl) phthalate (MEHP), in polycystic ovary syndrome (PCOS) aetiopathogenesis. We also wished to evaluate the relationship between phthalates and metabolic disturbances in adolescents with PCOS.

This study aims to discuss the prevalence of polycystic ovary (PCO) and Polycystic ovary syndrome (PCOS) in women with epilepsy (WWE) on valproate (VPA), carbamazepine (CBZ), or phenobarbitone (PB), drug naive WWE and women with bipolar affective disorder (BPAD) on VPA.

Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder affecting 5-10% of women in reproductive age. Insulin resistance, dyslipidemia, glucose intolerance, hypertension, and obesity are metabolic disorders accompanying the syndrome. PCOS is a chronic proinflammatory state and the disease is associated with endothelial dysfunction. In diseases with endothelial damage, hearing in high frequencies are mostly effected in early stages. We evaluated extended high frequency hearing loss in PCOS patients.

Polycystic ovary syndrome (PCOS) is the most frequent endocrinopathy in women of reproductive age. It is difficult to treat PCOS because of its complex etiology and pathogenesis. Here, we characterized the roles of gut microbiota on the pathogenesis and treatments in letrozole (a nonsteroidal aromatase inhibitor) induced PCOS rat model. Changes in estrous cycles, hormonal levels, ovarian morphology and gut microbiota by PCR-DGGE and real-time PCR were determined. The results showed that PCOS rats displayed abnormal estrous cycles with increasing androgen biosynthesis and exhibited multiple large cysts with diminished granulosa layers in ovarian tissues. Meanwhile, the composition of gut microbiota in letrozole-treated rats was different from that in the controls. Lactobacillus, Ruminococcus and Clostridium were lower while Prevotella was higher in PCOS rats when compared with control rats. After treating PCOS rats with Lactobacillus and fecal microbiota transplantation (FMT) from healthy rats, it was found that the estrous cycles were improved in all 8 rats in FMT group, and in 6 of the 8 rats in Lactobacillus transplantation group with decreasing androgen biosynthesis. Their ovarian morphologies normalized. The composition of gut microbiota restored in both FMT and Lactobacillus treated groups with increasing of Lactobacillus and Clostridium, and decreasing of Prevotella. These results indicated that dysbiosis of gut microbiota was associated with the pathogenesis of PCOS. Microbiota interventions through FMT and Lactobacillus transplantation were beneficial for the treatments of PCOS rats.

Sestrin2 and beclin1 are two newly found proteins that have essential roles in autophagy. This study attempted to evaluate the plasma concentrations of sestrin2 and beclin1 in women with polycystic ovary syndrome (PCOS) and healthy controls and to explore the clinical value of these proteins as novel biomarkers for PCOS.

Objective: To review the potential role and specific impact of statin drugs in women with PCOS. The evidence for this use of statins in PCOS is limited and still under further investigation. Materials and methods: A search was conducted using PubMed, DynaMed and PubMedHealth databases through October 16, 2016 using the terms polycystic ovary syndrome, PCOS, hydroxymethylglutaryl-CoA reductase inhibitors, hydroxymethylglutaryl-CoA, statin, atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin and simvastatin. English-language trials evaluating statins in PCOS were obtained and incorporated if they provided relevant data for providers. Results: We summarize twelve trials involving statins in PCOS. The trials were predominantly 12 weeks to 3 months in length (8 of the 12 trials) and low to moderate dose of statin drugs were used. The majority (10 of 12) of the trials show that statins reduce testosterone levels or other androgen hormones (DHEA-S and androstenedione), half of the trials evaluating LH/FSH ratio show an improvement, and all had positive effects on lipid profiles. Conclusion: Statins show promising improvements in serum levels of androgens and LH/FSH ratios translating to improved cardiovascular risk factors above and beyond simply lowering LDL levels. More investigation is needed to determine if statins can clinically impact women with PCOS long term, particularly those who are young and are not yet candidates for traditional preventative treatment with a statin medication.

Several studies have reported the association between polycystic ovary syndrome (PCOS) and low-grade chronic inflammation to be of uncertain cause: obesity, insulin resistance, or PCOS itself. The aim of the study was to investigate the WBC (white blood cell) count and CRP (C-reactive protein) concentration in women with PCOS and to determine the factors that affect their concentration. The study included 200 women aged 18-40 with PCOS and 105 healthy women as the control group, recruited in the Department of Gynaecological Endocrinology of Medical University in Warsaw from 2016 to 2018. Each patient underwent clinical, biochemical, and ultrasonographic assessments. WBC and CRP were significantly higher in the PCOS group (Z = -2,353, p = 0,019 and Z = -2,453, p = 0,014). WBC positively correlated with serum insulin at 0, 60, and 120 min during the oral glucose tolerance test (INS0: r = 0,221, p = 0,001; INS1: r = 0,194, p = 0,003; INS2: r = 0,022, p = 0,001), testosterone (r = 0,130, p = 0,046), androstenedione (r = 0,212, p = 0,001), and DHEAS (r = 0,178, p = 0,006) and negatively correlated with progesterone (r = -0,204, p = 0,002), estradiol (r = -0,140, p = 0,032), and SHBG (r = -0,308, p < 0,001). CRP positively correlated with insulin concentration in 0, 60, and 120 min during the oral glucose tolerance test (INS0: r = 0,343, p < 0,001; INS1: r = 0,276, p = 0,001; INS2: r = 0,320, p < 001) and negatively correlated with progesterone (r = -0,194, p = 0,030) and SHBG (-0,244, p = 0,005). We also estimated positive correlation between BMI and serum CRP and WBC concentration. Multiple linear regression analysis showed that CRP values are positively associated with BMI (beta = 0,374, p < 0,001) and insulin level (INS1) (beta = 0,282, p = 0,004); and WBC results are negatively associated with SHGB (beta = -0,284, p < 0,001) but positively associated with testosterone (beta = 0,163, p = 0,024) and BMI (beta = 0,157, p = 0,047). PCOS is associated with increased WBC and CRP concentrations. The main predicting factors of increased CRP are BMI and insulin resistance, but there is also a relationship between WBC count in PCOS and androgen concentration itself so that inflammation may be mediated not only through adiposity but also through increased androgen concentration.

Abnormalities in gut microbiota diversity are considered important mechanisms in metabolic disorders in polycystic ovarian syndrome (PCOS). However, the data on the association of these disorders with the PCOS phenotype remain controversial. The objectives of this study were to estimate the alpha diversity of the gut microbiota of healthy women and PCOS patients depending on phenotype. The study participants (184 premenopausal women: 63 with PCOS, 121 without PCOS) were recruited during the annual employment assessment in the Irkutsk Region and the Buryat Republic (Russia) in 2016-2019. For PCOS diagnosis, we used the Rotterdam (2003) criteria and definitions of PCOS phenotypes. Five indexes of alpha diversity (ASV, Shannon, Simpson, Chao, and ACE) were estimated for the gut microbiota in all participants using amplicon metasequencing. As a result, two out of five alpha diversity indexes showed a statistical difference between the non-PCOS and PCOS groups. We did not find a significant difference in the alpha diversity of gut microbiota in the subgroups of women with hyperandrogenic PCOS phenotypes vs non-androgenic phenotype D and the group of women with the presence of only one of the PCOS criteria. Nevertheless, "classic" PCOS phenotypes demonstrated the most significant decrease in alpha diversity compared with healthy women without any signs of PCOS.

Polycystic ovary syndrome (PCOS) is a common disorder in women of reproductive age. This study investigated the effects of L-carnitine on the clinical and laboratory findings of women with PCOS.

Polycystic ovary syndrome (PCOS) is one of the most common hormonal disorders, occurring in 5-10% women in reproductive ages. Despite a long history of studies on PCOS, its etiology is still unknown. Oxidative stress is now recognized to play a central role in the pathophysiology of many different disorders, including PCOS. Although intracellular reactive oxygen species (ROS) production and propagation are controlled by highly complex antioxidant enzymatic and non-enzymatic systems, understanding of mechanisms that oxidative stress is important to develop strategies for prevention and therapy of PCOS. This article reviews the literature data related to the mechanisms of oxidative stress in PCOS.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age. Chemerin has recently been discovered as a novel adipokine associated with obesity and metabolic syndrome. Excessive autophagy activity and overexpression of autophagy-related genes in follicular granulosa cells are important mechanisms of PCOS. This study aimed to investigate the effect of chemerin on autophagy in PCOS.

The objective of the present study was to examine some factors involved in follicular development of women with polycystic ovary syndrome (PCOS). Women with PCOS showed increased levels of serum luteinizing hormone (LH) but decreased follicular production of progesterone and estradiol by pre-ovulatory follicles. The mRNA expression corresponding to steroidogenic acute regulatory protein (StAR), and 20alpha-hydroxysteroid dehydrogenase (20α-HSD) was increased, while that corresponding to cytochrome P450 aromatase (P450arom) was decreased in PCOS follicles as compared to controls. No changes in the mRNA expression for 3beta-hydroxysteroid dehydrogenase 2 (3β-HSD2), cytochrome P450 side-chain cleavage (P450scc), cytochrome P450 17 alpha hydroxylase/lyase (P450c17), cyclooxygenase 2 (COX2), and transcription factors (GATA-4 and GATA-6) were found. We conclude that despite the hyper-luteinized environment of PCOS follicles, these follicles produce lower levels of progesterone and estradiol, and that this is characterized by increased degradation of progesterone and decreased estradiol synthesis. Our data demonstrate that the synthesis of prostaglandin F2α (PGF2α) may be affected in PCOS-follicles and that the transcription factors GATA-4 and GATA-6 are present in PCOS-follicles but they are not involved in the abnormal transcription observed in the steroidogenic enzymes.

Increased body iron is associated with insulin resistance. Hepcidin is the key hormone that negatively regulates iron homeostasis. We hypothesized that individuals with insulin resistance have inadequate hepcidin levels for their iron load.

Polycystic ovary syndrome (PCOS) is a complex disorder with heterogenous phenotypes and unclear etiology. A recent phenotypic clustering study identified metabolic and reproductive subtypes of PCOS. We hypothesize that the heterogeneity of PCOS manifestations reflects different mechanistic pathways and can be identified using a genetic approach. We applied k-means clustering to categorize the genome-wide significant PCOS variants into clusters based on their associations with selected quantitative traits that likely reflect PCOS etiological pathways. We evaluated the association of each cluster with PCOS-related traits and disease outcomes. We then applied Mendelian randomization to estimate the causal effects between the traits and PCOS. Three categories of variants were identified: adiposity, insulin resistant, and reproductive. Significant associations were observed for variants in the adiposity cluster with body mass index (BMI), waist circumference and breast cancer, and variants in the insulin-resistant cluster with fasting insulin, glucose values, and homeostatic model assessment of insulin resistance (HOMA-IR). Sex hormone binding globulin (SHBG) has strong association with all three clusters. Mendelian randomization suggested a causal role of BMI and SHBG on PCOS. No causal associations were observed for PCOS on disease outcomes.

Polycystic ovary syndrome (PCOS) is a complex multifactor disorder and genetic factors have been implicated in its pathogenesis. Our previous genome-wide association study (GWAS) had identified allele frequencies in several single nucleotide polymorphisms (SNPs) in gene USP34 (Ubiquitin-Specific Protease 34) were significantly different between PCOS cases and controls. This study was aimed to replicate the previous results in another independent cohort.