The prevalence of autoimmune thyroiditis is not increased in women with polycystic ovary syndrome after adjustment for family predisposition.

Purpose: Several studies suggest a linkage between PCOS and autoimmunity with a high frequency of chronic autoimmune thyroiditis (AIT) reported in PCOS patients, however, this subject remains controversial. The aim of this study was to investigate the prevalence of AIT in PCOS women and identify parameters that would serve as independent predictors of AIT.

Methods: Two hundred fifty seven (257) PCOS patients according to the NIH criteria and one hundred forty three (143) controls, women with normal menstrual cycles and without clinical or biochemical hyperandrogenism, were recruited for the study.

The effect of anti-TNF therapy on thyroid function in patients with inflammatory bowel disease.

The aim of this study was to investigate for first time the thyroid function in patients with inflammatory bowel disease (IBD) and the potential effect of anti-TNF (tumor necrosis factor) therapy. We evaluated 41 patients with IBD (25M/16F, 36.5 ± 11.

Adrenal hyperandrogenism does not deteriorate insulin resistance and lipid profile in women with PCOS.

Objective: The aim of this study was to investigate the impact of adrenal hyperandrogenism on insulin resistance and lipid profile in women with polycystic ovary syndrome (PCOS).

Patients And Methods: We studied 372 women with PCOS according to the NIH criteria. 232 age- and BMI-matched women served as controls in order to define adrenal hyperandrogenism (DHEA-S >95th percentile).

Polycystic ovary syndrome (PCOS) and endocrine disrupting chemicals (EDCs).

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of unclear etiopathogenesis that is likely to involve genetic and environmental components synergistically contributing to its phenotypic expression. Endocrine disrupting chemicals (EDCs) and in particular Bisphenol A (BPA) represent a group of widespread pollutants intensively investigated as possible environmental contributors to PCOS pathogenesis. Substantial evidence from in vitro and animal studies incriminates endocrine disruptors in the induction of reproductive and metabolic aberrations resembling PCOS characteristics.

Impact of androgen and dietary advanced glycation end products on female rat liver.

Background/aims: Advanced glycation end products (AGEs) have been related to a wide range of liver disorders including hyperandrogenic states such as the Polycystic Ovary Syndrome (PCOS). The aim of the present study is to evaluate the potential impact of dietary glycotoxins exposure and androgen excess on hepatic histology and biochemistry in an androgenized female rat model.

Methods: The study population consisted of 80 female Wistar rats, divided in 3 groups, a group of prepubertal (Group A, n=30) and adult rats (Group B, n=20) that were androgenized via subcutaneous implantation of dihydrotestosterone-containing pellets as well as a group of adult non-androgenized rodents (Group C, n=30).

Current perspectives on the health risks associated with the consumption of advanced glycation end products: recommendations for dietary management.

Advanced glycation end products (AGEs) constitute a complex group of compounds produced endogenously during the aging process and under conditions of hyperglycemia and oxidative stress. AGEs also have an emerging exogenous origin. Cigarette smoke and diet are the two main exogenous sources of AGEs (glycotoxins).

Endocrine disruptors and polycystic ovary syndrome: a focus on Bisphenol A and its potential pathophysiological aspects.

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of unknown etiology that may arise from a combination of a number of underlying genetic interactions and predispositions with environmental factors. Endocrine disruptors and, in particular, Bisphenol A may represent one of the many underlying causes of the syndrome as they are experimentally linked to metabolic and reproductive derangements resembling PCOS-related disorders. Exposure to endocrine-disrupting chemicals may act as an environmental modifier to worsen symptoms of PCOS in affected females or to contribute to the final phenotype of the syndrome in genetically predisposed individuals.

Reduced ovarian glyoxalase-I activity by dietary glycotoxins and androgen excess: a causative link to polycystic ovarian syndrome.

Glyoxalase detoxification system composed of glyoxalase (GLO)-I and GLO-II is ubiquitously expressed and implicated in the protection against cellular damage because of cytotoxic metabolites such as advanced glycation end products (AGEs). Recently, ovarian tissue has emerged as a new target of excessive AGE deposition and has been associated with either a high AGE diet in experimental animals or hyperandrogenic disorders such as polycystic ovarian syndrome (PCOS) in humans. This study was designed to investigate the impact of dietary AGEs and androgens in rat ovarian GLO-I activity of normal nonandrogenized (NAN, group A, n = 18) and androgenized prepubertal (AN) rats (group B, n = 29).

Endocrine disruptors and polycystic ovary syndrome (PCOS): elevated serum levels of bisphenol A in women with PCOS.

Context: Bisphenol A (BPA) is a widespread industrial compound used in the synthesis of polycarbonate plastics. In experimental animals, neonatal exposure to BPA results in a polycystic ovary-like syndrome (PCOS) in adulthood. A bidirectional interaction between androgens and BPA levels has been disclosed.

In overweight/obese but not in normal-weight women, polycystic ovary syndrome is associated with elevated liver enzymes compared to controls.

Objective: To investigate liver enzymes in a cohort of women with Polycystic Ovary Syndrome (PCOS) and controls divided according to body mass index (BMI) and their association with features of the syndrome.

Design: Eighty-three PCOS women and 64 healthy women were studied. Patients and controls were subdivided into two groups, a lean subgroup (BMI <25kg/m(2)) and an overweight/obese subgroup (BMI >25kg/m(2)).

Does polycystic ovary syndrome start in childhood?

Polycystic Ovary Syndrome (PCOS), the most frequent endocrinopathy in reproductive-aged women, represents a multifactorial nosologic entity considering its pathogenesis and clinical repercussions. PCOS is characterized mainly by hyperandrogenemia and anovulation, while insulin resistance has been established as a key player in the pathophysiology of the syndrome. The natural course of PCOS appears to originate in fetal life and factors of the intrauterine environment have been incriminated in the early pathogenesis of the syndrome.