Biomarker Profiles in Women with PCOS and PCOS Offspring; A Pilot Study

Daan, Nadine M.P.; Koster, Maria P. H.; Wilde, Marlieke A. de; Dalmeijer, Gerdien W.; Evelein, Annemieke M. V.; Fauser, Bart C.J.M.; Jager, Wilco de

doi:10.1371/journal.pone.0165033

Cited by 72 publications

(58 citation statements)

References 53 publications

(60 reference statements)

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“…Though some information shows Th17 of PCOS is decreasing in animal models [74,75], in human PCOS, evidence focuses on the expansion of proinflammatory Th17 subset not only in the blood but also kidneys [75]; however, the reason is obscure. In this condition, IL-6 may inhibit TNFα production and also effectively drive angiogenesis, thus promoting the formation of blood vessels and increases the concentration of the folliclestimulating hormone [76]. It is confirmed that a significant difference in the Th17/Th2 ratio, with a bias toward Th17, is common among patients with PCOS [77].…”

Section: Mediators Of Inflammationmentioning

confidence: 92%

Immunophenotypic Profiles in Polycystic Ovary Syndrome

Pang

et al. 2020

Mediators of Inflammation

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Polycystic ovary syndrome (PCOS) a long-known endocrinopathy and one of the most common endocrine-reproductivemetabolic disorders in women, which can lead to infertility. Although the precise etiology remains unclear, PCOS is considered as a complex genetic trait, with a high degree of heterogeneity. Besides, hormones and immune cells, including both innate and adaptive immune cells, are reportedly a cross talk in PCOS. Chronic low-grade inflammation increases autoimmune disease risk. This proinflammatory condition may, in turn, affect vital physiological processes that ultimately cause infertility, such as ovulation failure and embryo implantation. Here, we review the accumulating evidence linking PCOS with inflammatory status providing an overview of the underlying hormone-mediated dysregulation of immune cells. We mainly focus on the correlational evidence of associations between immune status in women and the increased prevalence of PCOS, along with the specific changes in immune responses. Further recognition and exploration of these interactions may help elucidate PCOS pathophysiology and highlight targets for its treatment and prevention.

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Section: Mediators Of Inflammationmentioning

confidence: 92%

Immunophenotypic Profiles in Polycystic Ovary Syndrome

Pang

et al. 2020

Mediators of Inflammation

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“…Reactive oxygen species-induced (ROS-induced) oxidative stress (OS) is a known activator of nuclear factor kappa-light-chain-enhancer of activated B cells (NF k B), inducing inflammatory responses [5]. Polycystic ovary syndrome (PCOS) is associated with chronic low-grade inflammation as demonstrated by elevated circulating inflammatory agents [32]. Obesity and hyperandrogenism stimulate chronic low-grade inflammation in polycystic ovarian syndrome women [32].…”

Section: Discussionmentioning

confidence: 99%

“…Polycystic ovary syndrome (PCOS) is associated with chronic low-grade inflammation as demonstrated by elevated circulating inflammatory agents [32]. Obesity and hyperandrogenism stimulate chronic low-grade inflammation in polycystic ovarian syndrome women [32]. It is acceptable to propose that monocytes (MNC) recruited into the polycystic ovaries lead to a local inflammatory response that stimulates cytochrome P450 family 17 (CYP17), the ovarian steroidogenic enzyme, responsible for androgen synthesis [5].…”

Section: Discussionmentioning

confidence: 99%

Relationship between Different Anthropometric Measurements and Interleukin-1β, Interleukin-17, Interleukin-27 and Interleukin-35 Levels for Iraqi Infertile Women with Polycystic Ovary Syndrome

Hantoosh

Zageer

Al-Jumaili

2019

JAMPS

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Aims: The study aimed to study impact of type and amount of body fat distribution on interleukin-1β, interleukin-17, interleukin-27, and interleukin-35 levels and on immunologic infertility. Study Design: The study was carried on infertile polycystic ovarian syndrome women. Place and Duration of Study: The study was performed with study subjects attended consultant clinic of Higher Institute for Infertility Diagnosis and Assisted Reproductive Technologies at AL-Nahrain University in Baghdad/Iraq during the period from February 2016 to April 2016. Materials and Methods: Twenty-six infertile polycystic ovarian syndrome women were enrolled in this study. Body mass index (BMI), waist circumference (WC), and waist to hip ratio (WHR) measurements were calculated to all cases. Serum interleukin-1β (IL-1β), interleukin-17 (IL-17), interleukin-27 (IL-27), and interleukin-35 (IL-35) concentrations were measured on cycle day 2. Results: Significant difference in distribution according to BMI, WC, and WHR (P=0.0001, P=0.0001, P=0.04, respectively). Significant difference in IL-1β concentrations according to WHR (P=0.04). Significant difference in IL-17 concentrations according to BMI, WC, and WHR (P=0.02, P=0.03, P=0.008, respectively). Significant difference in IL-27 concentrations according to WC (P=0.03). Significant difference in IL-35 concentrations according to BMI and WC (P=0.0001, P=0.0001, respectively). Conclusions: Amount and type of body fat distribution considerably affected and altered IL-1β, IL-17, IL-27, and IL-35 concentrations and consequently had a role in immunologic infertility.

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“…These latter findings suggest that 437 the NIH and Rotterdam diagnostic criteria do not identify biologically distinct subtypes of 438 PCOS. There have been previous efforts to subtype PCOS using unsupervised clustering (25)(26)(27)(28), 439 but no subsequent investigation into the biologic relevance of the resulting subtypes. 440…”

Section: Subtypes In Pcos Families 398mentioning

confidence: 99%

Phenotypic clustering reveals distinct subtypes of polycystic ovary syndrome with novel genetic associations

Dapas¹,

Lin²,

Nadkarni

et al. 2019

Preprint

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AD) 20 ghayes@northwestern.edu (MGH) 21 22 DISCLOSURE STATEMENT: The authors have nothing to disclose. 23 metabolic subtype (KCNH7/FIGN, P=1.0×10 -8 ). We have previously reported that rare 47 variants in DENND1A, a gene regulating androgen biosynthesis, were associated with PCOS 48 quantitative traits in a family-based whole genome sequencing analysis. We classified the 49 reproductive and metabolic subtypes in this family-based PCOS cohort and found that the 50 subtypes tended to cluster in families and that carriers of rare DENND1A variants were 51 significantly more likely to have the reproductive subtype of PCOS. Limitations of our study 52 were that only PCOS cases of European ancestry diagnosed by NIH criteria were included, 53 the sample sizes for the subtype GWAS were small, and the GWAS findings were not 54 replicated. 55 56 Conclusions 57In conclusion, we have found stable reproductive and metabolic subtypes of PCOS. Further, 58 these subtypes were associated with novel susceptibility loci. Our results suggest that these 59 subtypes are biologically relevant since they have distinct genetic architectures. This study 60 demonstrates how precise phenotypic delineation can be more powerful than increases in 61 sample size for genetic association studies. 62 63Understanding the genetic architecture of complex diseases is a central challenge in 64 human genetics (1-3). Often defined according to arbitrary diagnostic criteria, complex 65 diseases can represent the phenotypic convergence of numerous genetic etiologies (4)(5)(6)(7)(8). 66Recent studies in type 2 diabetes support the concept that there are disease subtypes with 67 distinct genetic architecture (7,8). Identifying and addressing genetic heterogeneity in 68 complex diseases could increase power to detect causal variants and improve treatment 69 efficacy (9). 70Polycystic ovary syndrome (PCOS) is a highly heritable, complex genetic disorder 71 affecting up to 15% of reproductive-age women worldwide, depending on the diagnostic 72 criteria applied (10). It is characterized by a variable constellation of reproductive and 73 metabolic abnormalities (Fig 1). It is the leading cause of anovulatory infertility and a major 74 risk factor for type 2 diabetes (T2D) in women (11). Despite these substantial morbidities, 75 the etiology(ies) of PCOS remains unknown (12). Accordingly, the commonly-used 76 diagnostic criteria for PCOS, the National Institutes of Health (NIH) criteria (13) and the 77 Rotterdam criteria (14,15), are based on expert opinion, rather than mechanistic insights, and 78 are designed to account for the diverse phenotypic presentations of PCOS. The NIH criteria 79 require the presence of hyperandrogenism (HA) and chronic oligo/anovulation or ovarian 80 dysfunction (OD) (13). The Rotterdam criteria include polycystic ovarian morphology 81 (PCOM) and require the presence of at least two of these three key reproductive traits, 82 resulting in three different affected phenotypes: HA and OD with or without PCOM, also 83 known as NIH PCOS, as w...

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Biomarker Profiles in Women with PCOS and PCOS Offspring; A Pilot Study

Cited by 72 publications

References 53 publications

Immunophenotypic Profiles in Polycystic Ovary Syndrome

Immunophenotypic Profiles in Polycystic Ovary Syndrome

Relationship between Different Anthropometric Measurements and Interleukin-1β, Interleukin-17, Interleukin-27 and Interleukin-35 Levels for Iraqi Infertile Women with Polycystic Ovary Syndrome

Phenotypic clustering reveals distinct subtypes of polycystic ovary syndrome with novel genetic associations

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