Ovarian Hyperandrogenism Research Articles

Correlations of Insulin Resistance and Serum Testosterone Levels with LH:FSH Ratio and Oxidative Stress in Women with Functional Ovarian Hyperandrogenism.

Functional ovarian hyperandrogenism (FOH) is a form of polycystic ovary syndrome (PCOS) characterized by elevated circulating levels of androgens derived from the ovary. Insulin resistance (IR) is the most common etiological factor in women with FOH. IR causes the generation of increased oxidative stress (OS) and diminished antioxidant status. OS is directly correlated with both IR and testosterone levels, which consequently contribute to endocrine and biochemical alterations in FOH women. In the current study, elevations in total testosterone, free testosterone and luteinizing hormone (LH) levels accompanied by a decrease in follicle stimulating hormone (FSH) level leading to higher LH:FSH ratio were the prominent endocrine changes observed in women with FOH. A significant increase in fasting blood levels of glucose and insulin, as well as an elevated IR were also seen in FOH women, as compared to their age matched controls. Women with FOH have higher pro-oxidant and lower anti-oxidant levels in blood than their age matched controls. In FOH women, elevations in LH:FSH ratio and OS are correlated more with hyperandrogenemia than with IR. Of the androgens, free rather than total testosterone has better positive correlations with elevated LH:FSH ratio and OS, and hence, the former is a better predictive marker for the development of biochemical PCOS in women with FOH.

Obesity-Induced Infertility and Hyperandrogenism Are Corrected by Deletion of the Insulin Receptor in the Ovarian Theca Cell

Women with polycystic ovary syndrome (PCOS) exhibit elevated androgen levels, oligoanovulation, infertility, and insulin resistance in metabolic tissues. The aims of these studies were to determine the role of insulin signaling in the development and function of ovarian theca cells and the pathophysiologic effects of hyperinsulinism on ovarian function in obesity. We disrupted the insulin receptor (IR) gene specifically in the theca-interstitial (TI) cells of the ovaries (Cyp17IRKO). No changes in reproductive development or function were observed in lean Cyp17IRKO female mice, suggesting that insulin signaling in TI cell is not essential for reproduction. However, when females were fed a high-fat diet, diet-induced obesity (DIO) wild-type (DIO-WT) mice were infertile and experienced increased circulating testosterone levels, whereas DIO-Cyp17IRKO mice exhibited improved fertility and testosterone levels comparable to those found in lean mice. The levels of phosphorylated IRS1 and CYP17 protein were higher in the ovary of DIO-WT compared with DIO-Cyp17IRKO or lean mice. Ex vivo studies using a whole ovary culture model demonstrated that insulin acts independently or additively with human chorionic gonadotropin to enhance androstenedione secretion. These studies reveal the causal pathway linking hyperinsulinism with ovarian hyperandrogenism and the infertility of obesity.

Diagnosis of Polycystic Ovary Syndrome: AMH in combination with clinical symptoms

We assessed the utility of using anti-Müllerian hormone (AMH) and clinical features of polycystic ovary syndrome (PCOS), polycystic ovarian morphology (PCOM), oligo/amenorrhea (OA), and hyperandrogenism (HA) for diagnosing PCOS, and compared their diagnostic accuracy with those of classical diagnostic systems. A total of 606 females were admitted to a university hospital with menstrual irregularities or symptoms of hyperandrogenism were enrolled in this cross-sectional study. Fasting blood samples were collected. Pelvic and/or abdominal ultrasonography and clinical examination were performed. Patients were evaluated for the presence of PCOS according to conventional diagnostic criteria. The diagnostic performance of using serum AMH levels alone and in various combinations with the clinical features of PCOM, OA, and HA were investigated. For the diagnosis of PCOS, the combination of OA and/or HA with AMH showed 83% sensitivity and 100% specificity according to the Rotterdam criteria; 83% sensitivity and 89% specificity according to the National Institutes of Health (NIH) criteria; and 82% sensitivity and 93.5% specificity according to the Androgen Excess Society (AES) criteria. The serum AMH level is a useful diagnostic marker for PCOS and is correlated with conventional diagnostic criteria. The combination of AMH level with OA and/or HA markedly increased the clinical scope for PCOS diagnosis and can be introduced as a possible objective criterion for the diagnosis of this disease.

Pelvic ultrasound findings in prepubertal girls with precocious adrenarche born appropriate for gestational age

Precocious adrenarche (PA) refers to the clinical onset of excess androgen in girls before the age of 8. It is associated with an increased risk of functional ovarian hyperandrogenism after puberty. PA may be associated with polycystic ovary syndrome (PCOS). We compared pelvic ultrasound (US) findings of girls with PA born appropriate for gestational age (AGA) to healthy body mass index (BMI)-matched peers to determine whether US findings in AGA-born PA girls are associated with PCOS antecedents. We conducted a cross-sectional study on 56 AGA-born girls with PA (6·9 ± 0·6 years) and 33 BMI-matched prepubertal AGA-born peers (7·1 ± 1·0 years). Hormonal data, homeostasis model assessment of insulin resistance (HOMA-IR), insulin sensitivity index (ISIcomp ) and pelvic US findings were compared. Associations of pelvic US findings with clinical and metabolic data were investigated. Precocious adrenarche girls had greater height and bone age-adjusted uterine length (UL; P = 0·01) and UL standard deviation score (SDS) (P = 0·02) than BMI-matched peers. Mean ovarian volume (MOV), MOV SDS, uterine volume, uterine cross-sectional area and ovarian morphology were similar between the groups (P > 0·05). MOV and MOV SDS correlated with ISIcomp (r = -0·683, P < 0·001; r = -0·760, P < 0·001; respectively). Correlations of pelvic US findings with other biochemical data did not reach significance (P > 0·05). Multivariate regression analysis revealed that in girls with PA, ISIcomp had the most significant effect on MOV SDS (R(2) = 0·731, β = -4·784, P = 0·001). Appropriate for gestational age-born PA girls have greater UL measurements than AGA-born BMI-matched peers. In AGA-born girls with PA, decreasing insulin sensitivity is strongly and independently associated with an increase in MOV. Longitudinal follow-up of our cohort after menarche will allow us to establish how many AGA-born girls with PA will ultimately develop PCOS.

The gonadal effects of diabetes

The functional reproductive alterations seen in women with type 1 diabetes (T1D) have changed as therapy has improved. Historically, patients with T1D and insufficient metabolic control exhibited a high prevalence of amenorrhea, hypogonadism, and infertility. Recent publications have shown that in spite of intensive insulin therapy, some delay in the age of thelarche, pubarche and menarche is still observed in girls with T1D. In addition, ovarian hyperandrogenism may be observed during late adolescence and an increased prevalence of hirsutism and polycystic ovarian syndrome (PCOS) has been described in adult women with T1D. These endocrine abnormalities may be related to non-physiologic insulin replacement therapy and to hyperglycemia. Insulin is well known for its effects on carbohydrate metabolism, but this hormone also plays an important role in regulating ovarian function. Granulosa, theca and stromal ovarian cells may be affected by insulin deficiency or excess, which may be present in women with type 1 diabetes mellitus (T1D)[1]. Diabetes disrupts hypothalamic-pituitary-ovarian function, as documented by animal model studies which have helped to decipher the underlying basis of these conditions and have highlighted the variable contributions of defective leptin, insulin and kisspeptin signalling to the mechanisms of perturbed reproduction in T1D[2]. Effects of diabetes on gonadal function vary according to the age of the patient. Young girls during adrenarche exhibit an elevation of DHEAS, androstenedione, inhibin B and anti-mullerian hormone[3], an endocrine profile that is similar to the one observed in young girls in risk of developing polycystic ovarian syndrome later in life. During puberty a delay in pubertal development has been described which is followed by menstrual irregularities and hyperandrogenism during adolescence [1,4,5]. Despite these abnormalities in ovarian function, ovulatory functions is preserved in adolescents with type 1 diabetes[6]. Later in life, adult women with type 1 diabetes exhibit PCOS, polycystic ovaries at the ultrasonographic exam, menstrual irregularities and early decline in ovarian reserve[7-9]. Clearly, despite improvements in insulin therapy, T1D patients still suffer several significant clinical problems, such as pubertal delay, menstrual disturbances and hyperandrogenism which may ultimately lead to the development of PCOS in adulthood. (Fondecyt 1100123 y 1050452)

What the Genetics of Lipodystrophy Can Teach Us About Insulin Resistance and Diabetes

Genetic lipodystrophic syndromes are rare diseases characterized by generalized or partial fat atrophy (lipoatrophy) associated with severe metabolic complications such as insulin resistance (IR), diabetes, dyslipidemia, nonalcoholic fatty liver disease, and ovarian hyperandrogenism. During the last 15years, mutations in several genes have been shown to be responsible for monogenic forms of lipodystrophic syndromes, of autosomal dominant or recessive transmission. Although the molecular basis of lipodystrophies is heterogeneous, most mutated genes lead to impaired adipogenesis, adipocyte lipid storage, and/or formation or maintenance of the adipocyte lipid droplet (LD), showing that primary alterations of adipose tissue (AT) can result in severe systemic metabolic and endocrine consequences. The reduced expandability of AT alters its ability to buffer excess caloric intake, leading to ectopic lipid storage that impairs insulin signaling and other cellular functions ("lipotoxicity"). Genetic studies have also pointed out the close relationships between ageing, inflammatory processes, lipodystrophy, and IR.

Testosterone (T) secreting tumor or insulin resistance? metformin (M) as a diagnostic (Dx) and therapeutic (Rx) trial

Virilization in a pre or post menopausal woman is a Dx & Rx challenge when imaging fails to reveal the source of markedly elevated T levels. Literature on ovarian hyperthecosis reveals most patients have insulin resistance (IR). We present two women with presumed ovarian hyperandrogenism using M as a Dx maneuver to differentiate elevated T from a tumor vs. from IR and resultant ovarian T over-production.

Alternatively spliced variants of androgen receptor in granulosa cells: an epigenetic cause of ovarian hyperandrogenism of polycystic ovary syndrome

Alternatively spliced variants of androgen receptor in granulosa cells: an epigenetic cause of ovarian hyperandrogenism of polycystic ovary syndrome

Serum Fetuin-A levels, insulin resistance and oxidative stress in women with polycystic ovary syndrome

This study was designed to determine serum Fetuin-A levels and establish whether serum Fetuin-A level is related with insulin resistance, oxidative stress, ovarian hyperandrogenism and dyslipidemia in women with polycystic ovary syndrome (PCOS). Twenty-two patients with PCOS and twenty-one healthy control women were evaluated in this controlled clinical study. Serum Fetuin-A, lipid fractions, glucose, insulin, malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), superoxide dismutase (SOD) and other hormone (gonadotropins, androgens) levels were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-R). The women with PCOS had significantly higher serum fasting glucose, insulin, luteinizing hormone (LH), MDA, Fetuin-A levels, and LH/follicle-stimulating hormone (FSH) ratio, free androgen index (FAI), HOMA-IR than healthy women. However, sex hormone-binding globulin (SHBG) and GSH levels were significantly lower in patients with PCOS compared with controls. Fetuin-A was positively correlated with insulin, HOMA-IR and FAI. Multiple regression analysis revealed that FAI was strong predictor of serum Fetuin-A level. Serum Fetuin-A level was related with insulin resistance and ovarian hyperandrogenism in women with PCOS. These results suggest that Fetuin-A may have a role in triggering the processes leading to insulin resistance and androgen excess in PCOS.

Partial lipodystrophy with severe insulin resistance and adult progeria Werner syndrome

BackgroundLaminopathies, due to mutations in LMNA, encoding A type-lamins, can lead to premature ageing and/or lipodystrophic syndromes, showing that these diseases could have close physiopathological relationships. We show here that lipodystrophy and extreme insulin resistance can also reveal the adult progeria Werner syndrome linked to mutations in WRN, encoding a RecQ DNA helicase.MethodsWe analysed the clinical and biological features of two women, aged 32 and 36, referred for partial lipodystrophic syndrome which led to the molecular diagnosis of Werner syndrome. Cultured skin fibroblasts from one patient were studied.ResultsTwo normal-weighted women presented with a partial lipodystrophic syndrome with hypertriglyceridemia and liver steatosis. One of them had also diabetes. Both patients showed a peculiar, striking lipodystrophic phenotype with subcutaneous lipoatrophy of the four limbs contrasting with truncal and abdominal fat accumulation. Their oral glucose tolerance tests showed extremely high levels of insulinemia, revealing major insulin resistance. Low serum levels of sex-hormone binding globulin and adiponectin suggested a post-receptor insulin signalling defect. Other clinical features included bilateral cataracts, greying hair and distal skin atrophy. We observed biallelic WRN null mutations in both women (p.Q748X homozygous, and compound heterozygous p.Q1257X/p.M1329fs). Their fertility was decreased, with preserved menstrual cycles and normal follicle-stimulating hormone levels ruling out premature ovarian failure. However undetectable anti-müllerian hormone and inhibin B indicated diminished follicular ovarian reserve. Insulin-resistance linked ovarian hyperandrogenism could also contribute to decreased fertility, and the two patients became pregnant after initiation of insulin-sensitizers (metformin). Both pregnancies were complicated by severe cervical incompetence, leading to the preterm birth of a healthy newborn in one case, but to a second trimester-abortion in the other. WRN-mutated fibroblasts showed oxidative stress, increased lamin B1 expression, nuclear dysmorphies and premature senescence.ConclusionsWe show here for the first time that partial lipodystrophy with severe insulin resistance can reveal WRN-linked premature aging syndrome. Increased expression of lamin B1 with altered lamina architecture observed in WRN-mutated fibroblasts could contribute to premature cellular senescence. Primary alterations in DNA replication and/or repair should be considered as possible causes of lipodystrophic syndromes.

In PCOS patients the addition of low-dose spironolactone induces a more marked reduction of clinical and biochemical hyperandrogenism than metformin alone

Background & aimsPolycystic ovary syndrome (PCOS) is characterized by ovarian dysfunction and hyperandrogenism and by insulin resistance and related metabolic alterations. Both metformin and anti-androgens, such as spironolactone, are used to ameliorate the different aspects of this disorder. We investigated whether therapy with metformin plus low-dose spironolactone is more effective than metformin alone in PCOS patients. Methods and resultsFifty-six PCOS patients were randomized in two groups: group A (28 patients) was treated with metformin (1700 mg/die) and group B (28 patients) was treated with metformin (1700 mg/die) plus low-dose spironolactone (25 mg/die). Anthropometric, hormonal and metabolic parameters were evaluated at baseline and after six months of treatment. After therapy regular menses were restored in approximately 82% of group A patients (P < 0.001) and in 68% of group B patients (P < 0.001). Circulating testosterone, Δ-4-androstenedione and Hirsutism Score (HS) significantly decreased in both groups. However, dehydro-epiandrosterone sulphate significantly decreased only in group B, and HS underwent a stronger reduction in group B (P < 0.001). At baseline, 39/56 (69.6%) patients met the diagnostic criteria for metabolic syndrome, but only one patient met these criteria after treatment. ConclusionsThis study confirms the beneficial effects of metformin in PCOS patients. It also indicates that the addition of low-dose spironolactone induces a more marked reduction of clinical and biochemical hyperandrogenism as compared to metformin alone. Clinicaltrial.gov numberNCT01526616.

Treatment of acne in women ovarian hyperandrogenism and insulin resistance

Objective. To determine the efficacy of Glucophage, a biguanide manufactured by MERCK SANTE s.a.s) (France), in the treatment of women with acne, ovarian hyperandrogenism and insulin resistance. Materials and methods. The study involved 65 women aged 20—40, who were administered Glucophage (a biguanide) for a year. The dynamical analysis of acne components and mean values of the acne dermatology index was performed, the therapeutic effect was assessed, and the subjects underwent gynecological and anthropometric examinations as well as laboratory tests: blood hormone level; urine steroid profile; metabolic status; cholesterol, triglycerides and blood biochemistry test as well as ultrasonic examination of small pelvis organs and sebometry. Results. The treatment reduced the acne dermatology index by 89.12%; the therapeutic effect was achieved in 84.62% of the patients; the treatment also produced a positive effect on anthropometric characteristics and resulted in the normalization of the hormonal status, urine steroid profile indices as well as lipid and carbohydrate metabolism, and moderate suppression of the skin fat secretion. Conclusion. The treatment of women suffering from acne, ovarian hyperandrogenism and insulin resistance with Glucophage normalized carbohydrate metabolism, hormonal status and urine steroid profile, which resulted in a positive therapeutic effect on acne.

Polycystic ovarian syndrome during puberty and adolescence

PCOS has reasonably well defined clinical, biochemical and radiological features in adult women, but in the adolescent population, some of these features may overlap with normal puberty leading to difficulties in making a diagnosis. In addition, the rising prevalence of obesity in the paediatric population may compound insulin resistance in girls predisposed to ovarian hyperandrogenism leading to younger age of presentation and more severe phenotype. It is important to distinguish between normal puberty and true ovarian hyperandrogenism, as well as excluding other causes of androgen excess such as adrenal tumours or non classical congenital adrenal hyperplasia. The long term co-morbidities associated with ovarian hyperandrogenism presenting during adolescence are not well defined but there is likely to be increased cardiovascular risk. There are little data on intervention in the adolescent population and studies in adult women often focus on ovulation and fertility which are less of a concern to adolescents. Current options include insulin sensitisation with metformin, anti androgens, or the oral contraceptive pill, with each girl being treated on an individual basis. There is a requirement for establishment of normative data in adolescence, in conjunction with physiological phenotyping in order to elucidate potential mechanisms thus informing potential intervention.

Nonhuman primate models of polycystic ovary syndrome

With close genomic and phenotypic similarity to humans, nonhuman primate models provide comprehensive epigenetic mimics of polycystic ovary syndrome (PCOS), suggesting early life targeting for prevention. Fetal exposure to testosterone (T), of all nonhuman primate emulations, provides the closest PCOS-like phenotypes, with early-to-mid gestation T-exposed female rhesus monkeys exhibiting adult reproductive, endocrinological and metabolic dysfunctional traits that are co-pathologies of PCOS. Late gestational T exposure, while inducing adult ovarian hyperandrogenism and menstrual abnormalities, has less dysfunctional metabolic accompaniment. Fetal exposures to dihydrotestosterone (DHT) or diethylstilbestrol (DES) suggest androgenic and estrogenic aspects of fetal programming. Neonatal exposure to T produces no PCOS-like outcome, while continuous T treatment of juvenile females causes precocious weight gain and early menarche (high T), or high LH and weight gain (moderate T). Acute T exposure of adult females generates polyfollicular ovaries, while chronic T exposure induces subtle menstrual irregularities without metabolic dysfunction.

Serum calcitonin gene-related peptide levels in women with polycystic ovary syndrome

Calcitonin gene-related peptide (CGRP) is an amino acid neuropeptide with widespread expression. It has potent effects on lipid and energy metabolism. It induces insulin resistance. This study was planned to determine CGRP levels in women with polycystic ovary syndrome (PCOS). Forty-seven women with PCOS and 34 healthy controls were evaluated in this controlled clinical study. Serum lipid sub-fractions, postprandial and fasting glucose, insulin and other hormones (gonadotropins, androgens) and CGRP levels were measured. Homeostasis model assessment (HOMA-IR) was used to estimate insulin resistance. Waist measurements, postprandial and fasting glucose and fasting insulin levels and free androgen index and HOMA-IR were significantly higher in subjects with PCOS. However, the women with PCOS had considerably lower high-density lipoprotein cholesterol levels than healthy subjects. Serum CGRP levels were higher in study subjects than in controls, although it was statistically insignificant. Serum CGRP level was not related with insulin resistance, ovarian hyperandrogenism and dyslipidemia in abdominally obese women with PCOS. These outcomes propose that CGRP may not play a pivotal role in the pathogenesis of PCOS.

Opposing effects of dehydroepiandrosterone sulfate and free testosterone on metabolic phenotype in women with polycystic ovary syndrome

To study the association of adrenal and ovarian androgen levels with metabolic parameters in a large cohort of women with polycystic ovary syndrome (PCOS). Cross-sectional study. Outpatient clinic of an academic hospital. Six hundred twenty-two women with PCOS. None. Analysis of the association of endocrine dehydroepiandrosterone sulfate (DHEAS) and free testosterone (FT) parameters with metabolic measurements. In multivariate adjusted logistic regression analyses, the odds ratio (OR) for insulin resistance was statistically significantly higher (4.42, range: 2.26-8.67) for women with PCOS who had elevated FT levels compared with the women with normal DHEAS and FT levels (reference group). We found no statistically significant differences when women with PCOS with elevated DHEAS or a combined elevation of DHEAS and FT levels were compared with the reference group. Women with PCOS and a high DHEAS/FT ratio had a more beneficial metabolic profile compared with the women with a low DHEAS/FT ratio. In multivariate adjusted binary logistic regression analyses, we found a statistically significantly lower risk for insulin resistance in the women with PCOS in the highest DHEAS/FT-ratio quartile compared with women with PCOS in the lowest quartile (OR 0.35, range: 0.14-0.89). Our results suggest that the distinction between adrenal and ovarian hyperandrogenism is important when evaluating metabolic risk in PCOS.

Antimüllerian hormone levels are independently related to ovarian hyperandrogenism and polycystic ovaries

To determine the relationship of antimüllerian hormone (AMH) levels to polycystic ovaries and ovarian androgenic function. Prospective case-control study. General clinical research center. Eumenorrheic asymptomatic volunteers without (V-NO; n = 19; reference population) or with (V-PCO; n = 28) a polycystic ovary and hyperandrogenemic anovulatory subjects grouped according to ovarian function into typical PCOS (PCOS-T; n = 37) and atypical PCOS (PCOS-A; n = 18). Pelvic ultrasonography, short dexamethasone androgen-suppression test (SDAST), and GnRH agonist (GnRHag) test. Baseline AMH levels were related to polycystic ovary status, testosterone response to SDAST, and 17-hydroxyprogesterone response to GnRHag test. AMH levels correlated with SDAST and GnRHag test outcomes. AMH was elevated (>6.2 ng/mL) in 32% of V-PCO versus 5% V-NO. The 21% of V-PCO who met Rotterdam PCOS criteria all had functional ovarian hyperandrogenism, but AMH levels were similar to nonhyperandrogenic V-PCO. AMH >10.7 ng/mL discriminated V-PCO from PCOS with 96% specificity and 41% sensitivity for PCOS-T, and insignificantly for PCOS-A. AMH levels are independently related to ovarian androgenic function and polycystic ovaries. Very high AMH levels are specific but insensitive for PCOS. In the absence of hyperandrogenism, moderate AMH elevation in women with normal-variant polycystic ovaries seems to indicate an enlarged oocyte pool.

PCOS and hyperandrogenism in type 1 diabetes

Women with both type 1 diabetes and polycystic ovarian syndrome (PCOS) represent a unique population, with long term implications on fertility and diabetic complications, which need to be addressed. The studies reviewed herein address the increased incidence of PCOS in women with type 1 diabetes. The leading theories suggest that the underlying pathophysiology is related to intensive insulin therapy and resulting ovarian hyperandrogenism. We have searched the literature to determine what studies have been done to address the role of insulin resistance and insulin sensitizers for reduction of hyperandrogenism in these patients. According to the available evidence, we conclude that metformin may have a role in reducing the androgenic picture in type 1 patients with PCOS and insulin resistance.

Does PCOS have developmental origins?

PRO--The similarity of reproductive and metabolic phenotype between prenatally androgenized sheep, or monkeys, and women with PCOS provides strong supportive evidence for developmental programming being important in the etiology of PCOS. CON--While one would not exclude altogether developmental determinants of PCOS, it is difficult to view PCOS as purely developmental or resulting only from intrauterine exposures or simply an adaptation gone astray.

Paratubal cysts, obesity, and hyperandrogenism

Objective The aim of this study was to determine if an association exists between adolescents with polycystic ovarian syndrome (PCOS) or hyperandrogenism (HA), obesity, and paratubal cysts (PTCs). Design An institutional review board–approved retrospective chart review was performed between the years of 1998 and 2008 at a single children's hospital. Inclusion criteria were met if pathology reports demonstrated diagnosis of PTC. Age of menarche, body mass index, surgical procedure, and findings were correlated with the presence of HA. Results The incidence of PTCs was 7.3% among 1524 females presenting with adnexal masses. One hundred three patients had a confirmed pathology diagnosis of PTC and underwent surgery for suspected torsion or persistent adnexal mass on imaging studies. Forty-five percent of surgical cases had ovarian or adnexal torsion. Mean age of PTC diagnosis for the entire cohort was 13.7 ± 2.82 years. Mean age of menarche was 11.7 ± 1.34 years among pubertal females. Four patients were premenarchal at the time of PTC diagnosis. Forty percent of pubertal females had a diagnosis of PCOS. Pubertal adolescents with features of HA had a higher body mass index (31.3 vs 26.2 kg/m 2, P = .003) and had a trend toward larger cysts (7.6 vs 6 cm, P = .235). Overall, a significant association existed between obesity and PTC ( P = .007), although no definite association could be made about HA or PCOS. Conclusion This study demonstrated an association between PTCs and obesity. In addition, HA appears to be associated with a trend toward large PTCs, although results were not significant.