SEARCH · PubMed Health

Results for “PCOS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

PubMed1999

The treatment of insulin resistance does not improve adrenal cytochrome P450c17alpha enzyme dysregulation in polycystic ovary syndrome.

OBJECTIVE: To determine whether metformin. when given to non-diabetic women with polycystic ovary syndrome (PCOS), results in a reduction of insulin resistance and hyperinsulinemia while body weight is maintained. Also we aimed to see whether the reduction in insulin levels attenuates the activity of adrenal P450c17alpha enzyme in patients with PCOS. DESIGN: We investigated the 17-hydroxyprogesterone (17-OHP) and androstenedione responses to ACTH, insulin responses to an oral glucose tolerance test (OGTT) and glucose disposal rate in an insulin tolerance test before and after metformin therapy (500 mg, orally, twice daily, for 12 weeks). METHODS: The presence of hyperinsulinemia in 15 women with PCOS was demonstrated by an OGTT and results were compared with those of 10 healthy women. Insulin sensitivity was measured by the rate of endogenous glucose disposal after i.v. bolus injection of insulin. 17-OHP and androstenedione responses to ACTH were measured in all the women with PCOS and the normal women. RESULTS: Women with PCOS were hyperinsulinemic (102.0+/-13.0 (S.E.M.) VS 46.2+/-4.4 pmol/l) and hyperandrogenemic (free testosterone 15.3+/-1.7 vs 7.9+/-0.6 nmol/l; androstenedione 11.8+/-0.8 vs 8.2+/-0.6 nmol/l) and more hirsute (modified Ferriman-Gallwey score, 17.7+/-1.6 vs 3.0+/-0.3) than healthy women. In addition, women with PCOS had higher 17-OHP and androstenedione responses to ACTH when compared with healthy women. Metformin therapy resulted in some improvement in insulin sensitivity and reduced the basal and post-glucose load insulin levels. But 17-OHP and androstenedione responses to ACTH were unaltered in response to metformin. CONCLUSIONS: PCOS is characterized by hyperactivity of the adrenal P450c17alpha enzyme and insulin resistance. It seems that there is no direct relationship between insulin resistance and adrenal P450c17alpha enzyme dysregulation.

17-alpha-Hydroxyprogesterone↗

PubMed2000

Ovarian-adrenal cross-talk in polycystic ovary syndrome: evidence from wedge resection.

OBJECTIVE: To determine whether the ovary influences adrenal androgen secretion in women with polycystic ovary syndrome (PCOS). DESIGN: Six PCOS-affected patients with clomiphene resistance and gonadotrophin hyperresponsivity, and six controls with regular ovulatory cycles, matched for age and body mass index. METHODS: Bilateral ovarian wedge resection was performed to induce ovulation surgically for these refractory women with PCOS. The adrenal androgen secretions were evaluated in PCOS patients before and again 6 months after this surgery, and in the controls, using an ACTH stimulation test (0.25mg synthetic ACTH(1-24)). RESULTS: Biochemically, basal levels and the maximum net increases (Delta) of 17-hydroxyprogesterone (17-OHP) and androstenedione, Delta17-OHP/Delta progesterone and Delta androstenedione/Delta17-OHP ratios in response to exogenous ACTH were significantly higher in PCOS patients before operation than those of controls. This purely ovarian surgery in women with PCOS was found to significantly reduce their basal androstenedione, testosterone and LH levels, insulin/glucose ratio, and post-corticotrophic Delta17-OHP, Delta androstenedione, Delta17-OHP/Delta progesterone and Delta androstenedione/Delta17-OHP, without obvious changes in FSH, oestradiol, sex hormone-binding globulin, Delta dehydroepiandrosterone, Delta dehydroepiandrosterone sulphate, Delta aldosterone and Delta cortisol values. CONCLUSIONS: Ovarian hyperandrogenicity from polycystic ovary may contribute to the enhanced adrenal P450c17alpha activity and subsequent Delta(4) androgen reserve revealed by the pharmacological corticotrophin stimulation in our special PCOS cases.

Adrenal Glands↗

PubMed2004

The prevalence of 4G5G polymorphism of plasminogen activator inhibitor-1 (PAI-1) gene in polycystic ovarian syndrome and its association with plasma PAI-1 levels.

OBJECTIVE: To investigate the prevalence of 4G5G polymorphism of plasminogen activator inhibitor-1 (PAI-1) gene in polycystic ovary syndrome (PCOS) and its functional significance. DESIGN: Case-control study. METHODS: We studied 98 patients and 64 controls. Body mass index (BMI) and waist-to-hip (WHR) ratio were determined. Blood samples were obtained for DNA analysis. PAI-1 plasma levels, serum total testosterone, fasting insulin and fasting glucose were measured and the glucose-to-insulin ratio was estimated in all subjects. RESULTS: There was a statistically significant difference in the distribution of PAI-1 gene variations among the groups. The PCOS group had significantly higher 4G/4G and 4G/5G combinations than the control group, whereas there were significantly less 5G/5G. Among the PCOS women, 39.8% had the genotype 4G/4G, 39.8% 4G/5G and 20.4% 5G/5G. From the control group, 20.3% had genotype 4G/4G, 28.1% 4G/5G and 51.6% 5G/5G. In the 4G/4G genotype subgroup 75% were PCOS and 25% were controls, in the 4G/5G were 68.42% and 31.58% and in the 5G/5G were 31.58% and 62.26% respectively. The population of PCOS women had significantly higher PAI-1 levels, WHR, total testosterone, and fasting glucose than the population of controls. CONCLUSIONS: 1) The genotypic subtypes 4G/4G and 4G/5G, in PCOS, were present with a statistically higher frequency compared with controls. 2) PCOS women have higher levels of PAI-1 compared with the control group. 3) The presence of the 4G allele in PAI-1 promoter region of the gene further increases the PAI-1 levels.

Adult↗

PubMed2005

Clinical and psychological correlates of quality-of-life in polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCOS) has been shown to cause a reduction in quality of life. This study examines the extent of different PCOS symptoms on quality-of-life, psychosocial well-being and sexual satisfaction. METHODS: Complete metabolic, hormonal, clinical and psychosocial data were obtained from a total of 120 women with PCOS. Patients were compared with 50 healthy women to establish reductions in quality-of-life and emotional well-being. In addition, the correlation between psychosocial variables and the major clinical PCOS features obesity (body mass index (BMI)), excessive body hair (hirsutism score), acne, hyperandrogenism (serum testosterone levels), disturbed insulin regulation (area under the insulin response curve and homeostasis model assessment of insulin resistance), menstrual cycle disturbances and infertility were analyzed. RESULTS: PCOS patients showed significant reductions in quality-of-life, increased psychological disturbances, and decreased sexual satisfaction when compared with healthy controls. BMI and hirsutism scores, but not the presence of acne, were associated with physical aspects of quality-of-life and sexual satisfaction. No clear effect of androgens or insulin resistance on psychosocial variables was detected. Similarly, the type of menstrual cycle disturbances or infertility had no impact on psychological well-being. CONCLUSION: In PCOS, changes in appearance, particularly obesity and hirsutism, reduce physical dimensions of quality-of-life and decrease sexual satisfaction. The role of biochemical, endocrine and metabolic parameters as well as menstrual irregularities and infertility appeared to be less important. Clinicians should pay attention to the psychosocial dimensions of PCOS on an individual basis, regardless of symptom severity or treatment response.

Acne Vulgaris↗

PubMed2005

Subcutaneous adipocytes from obese hyperinsulinemic women with polycystic ovary syndrome exhibit normal insulin sensitivity but reduced maximal insulin responsiveness.

BACKGROUND: Polycystic ovary syndrome (PCOS) has a high prevalence in women and is often associated with insulin resistance and hence with aspects of the so-called metabolic syndrome. METHODS: Ten women diagnosed with PCOS were consecutively included (aged 21-39 years, average 30.2 +/- 1.9 years; body mass index 28.4-42.5 kg/m2, average 37.5 +/- 1.7 kg/m2 (mean +/- s.e.)). Adipocytes were isolated from the subcutaneous fat and, after overnight incubation to recover from insulin resistance due to the surgical cell isolation procedures, they were analyzed for insulin sensitivity. RESULTS: The patients with PCOS exhibited marked clinical hyperinsulinemia with 3.6-fold higher blood levels of C-peptide than a healthy lean control group (1.7 +/- 0.2 and 0.5 +/- 0.02 nmol/l respectively, P < 0.0001). The patients with PCOS also exhibited 2.4-fold higher concentrations of serum triacylglycerol (2.1 +/- 0.3 and 0.9 +/- 0.06 mmol/l respectively, P < 0.0001), but only slightly elevated blood pressure (118 +/- 12/76 +/- 6 and 113 +/- 7/72 +/- 6 mmHg respectively, P = 0.055/0.046). However, insulin sensitivity for stimulation of glucose transport in the isolated adipocytes was indistinguishable from a non-PCOS, non-diabetic control group, while the maximal insulin effect on glucose uptake was significantly lower (2.2 +/- 0.2- and 3.8 +/- 0.8-fold respectively, P = 0.02). CONCLUSIONS: Subcutaneous adipocytes from patients with PCOS do not display reduced insulin sensitivity. The findings show that the insulin resistance of PCOS is qualitatively different from that of type 2 diabetes.

Abdominal Fat↗

PubMed2006

Decreased soluble leptin receptor levels in women with polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and a high incidence of obesity. Leptin, the product of the ob gene, is involved in the regulation of energy balance and obesity and circulates in both free and bound forms. The soluble leptin receptor (sOB-R) is the most important leptin-binding protein, thus influencing the biologically active free leptin level. DESIGN: We assessed the correlation of metabolic and endocrine parameters with leptin and sOB-R levels in 122 PCOS women (aged 27 +/- 5.7 years) and 81 healthy controls (aged 25 +/- 4.0 years). METHODS: Leptin and sOB-R levels were measured using ELISA kits. In addition, anthropometric variables, body fat and endocrine parameters were evaluated and a glucose tolerance test performed to assess indices of insulin resistance and glucose metabolism. RESULTS: In PCOS patients, no correlation was found between leptin or sOB-R and parameters of hyper-androgenism. However, as expected, body mass index (BMI), body fat, waist circumference and indices of insulin resistance were significantly correlated with leptin in PCOS subjects and controls. In a subgroup analysis of lean, overweight and obese PCOS patients, significant differences were found in leptin (29.7 +/- 20.7 vs 45.4 +/- 25.0 vs 67.7 +/- 28.8 ng/ml, P < 0.0001) and sOB-R (8.0 +/- 3.4 vs 6.4 +/- 2.5 vs 5.7 +/- 2.3 ng/ml, P < 0.05). Compared with BMI-matched controls, lean PCOS patients had lower sOB-R levels (8.0 +/- 3.4 vs 12.7 +/- 4.7 ng/ml, P < 0.0001) and higher free leptin indices (4.5 +/- 3.9 vs 2.8 +/- 2.2, P = 0.0285). CONCLUSION: Taking into account that low sOB-R levels supposedly compensate diminished leptin action, PCOS per se might cause leptin resistance.

Adult↗

PubMed2006

Enhanced mitogenic signaling in skeletal muscle of women with polycystic ovary syndrome.

Insulin resistance in polycystic ovary syndrome (PCOS) results from a postbinding defect in signaling. Insulin receptor and insulin receptor substrate (IRS)-1 serine hyperphosphorylation by an unidentified kinase(s) contributes to this defect. We investigated whether insulin resistance is selective, affecting metabolic but not mitogenic pathways, in skeletal muscle as it is in cultured skin fibroblasts in PCOS. Extracellular signal-regulated kinase (ERK)1/2 activation was increased in skeletal muscle tissue and in cultured myotubes basally and in response to insulin in women with PCOS compared with control women. Mitogen-activated/extracellular signal-regulated kinase kinase (MEK)1/2 was also activated in PCOS, whereas p38 mitogen-activated protein kinase phosphorylation and signaling from the insulin receptor to Grb2 was similar in both groups. The activity of p21Ras was decreased and Raf-1 abundance increased in PCOS, suggesting that altered mitogenic signaling began at this level. MEK1/2 inhibition reduced IRS-1 Ser312 phosphorylation and increased IRS-1 association with the p85 subunit of phosphatidylinositol 3-kinase in both groups. We conclude that in PCOS skeletal muscle, 1) mitogenic signaling is enhanced in vivo and in culture, 2) ERK1/2 activation inhibits association of IRS-1 with p85 via IRS-1 Ser312 phosphorylation, and 3) ERK1/2 activation may play a role in normal feedback of insulin signaling and contribute to resistance to insulin's metabolic actions in PCOS.

Adult↗

PubMed2001

Prevalence of polycystic ovary syndrome among premenopausal women with type 2 diabetes.

OBJECTIVE: Women with polycystic ovary syndrome (PCOS) have an increased risk for developing type 2 diabetes. Few studies have assessed women with type 2 diabetes to determine the frequency of PCOS in this population. RESEARCH DESIGN AND METHODS: To determine the prevalence of PCOS among premenopausal women with type 2 diabetes, we conducted a retrospective cross-sectional prevalence study. We reviewed the medical records of all women seen in the Diabetes Clinic of the Medical College of Virginia Hospitals between January 1995 through February 2000. A diagnosis of PCOS was based on 1) oligomenorrhea, 2) hyperandrogenism (biochemical or clinical), and 3) exclusion of other related disorders. RESULTS: We reviewed the medical records of 618 women with diabetes and identified 47 women eligible for study. Of the 47 women, 30 consented to an evaluation. Of the 30 women evaluated, 8 were identified as having PCOS (6 women reported a previous PCOS diagnosis and 2 women were newly diagnosed), resulting in a prevalence of 26.7%. CONCLUSIONS: We concluded that PCOS occurs frequently among premenopausal women with type 2 diabetes.

Abortion, Spontaneous↗

PubMed2006

Altered D-chiro-inositol urinary clearance in women with polycystic ovary syndrome.

OBJECTIVE: Evidence suggests that some actions of insulin are effected by inositolphosphoglycan (IPG) mediators. We hypothesize that a deficiency in D-chiro-inositol (DCI) and/or a DCI-containing IPG (DCI-IPG) may contribute to insulin resistance in humans. RESEARCH DESIGN AND METHODS: To assess this possibility in polycystic ovary syndrome (PCOS), we determined insulin sensitivity (Si by frequently sampled intravenous glucose tolerance test), plasma and urinary DCI and myo-inositol (MYO) levels (by gas chromatography/mass spectrometry), and the release of insulin and DCI-IPG during the oral glucose tolerance test (area under the curve [AUC]) in 23 women with PCOS and 26 normal women. RESULTS: Women with PCOS were heavier than control subjects (P = 0.002 for BMI), but also had decreased Si (P < 0.001) and increased AUC(insulin) (P < 0.001) compared with normal women, even when corrected for BMI. The urinary clearance of DCI (uCl(DCI)) was increased almost sixfold in PCOS compared with normal women (P = 0.001), but not MYO clearance (P = 0.10). uCl(DCI) correlated inversely with Si when all women were analyzed together (n = 49, r = -0.50, P < 0.001) and was one of the three best independent parameters predicting Si. Finally, the ratio of AUC(DCI-IPG) to AUC(insulin) was decreased threefold in women with PCOS (P < 0.001). CONCLUSIONS: uCl(DCI) is inversely correlated with insulin sensitivity in women and is a strong independent predictor of insulin resistance in multivariate models. PCOS, which is characterized by insulin resistance, is associated with a selective increase in uCl(DCI) and impaired DCI-IPG release in response to insulin. These findings are consistent with a defect in tissue availability or utilization of DCI in PCOS that may contribute to the insulin resistance of the syndrome.

Adolescent↗

PubMed1996

Superovulation with urinary human follicle-stimulating hormone: correlations with body mass index and body fat distribution.

Our objective was to investigate the relationship between body mass index (BMI), waist/hip ratio (WHR), follicle-stimulating hormone (FSH) dose, length of stimulation and clinical outcome in infertile women with and without polycystic ovary syndrome (PCOS) undergoing controlled ovarian hyperstimulation. Controlled ovarian hyperstimulation was induced in 60 women for a total of 111 cycles (48% in PCOS patients) with urinary human FSH (u-hFSH). A significant correlation between BMI, u-hFSH dose and duration of stimulation was found in PCOS and non-PCOS patients with WHR < 0.8. These correlations were not present in PCOS patients with WHR > 0.8. Pregnant patients received significantly less ampules of u-hFSH. From our data we suggest a controlled ovarian hyperstimulation protocol, for obese non-PCOS patients and obese PCOS patients with WHR < 0.8, starting with a double dose of u-FSH.

Adipose Tissue↗

PubMed2000

The importance of diagnosing the polycystic ovary syndrome.

The polycystic ovary syndrome (PCOS) is an extremely common disorder that occurs in 4% to 7% of women of reproductive age. Although PCOS is known to be associated with reproductive morbidity and increased risk for endometrial cancer, diagnosis is especially important because PCOS is now thought to increase metabolic and cardiovascular risks. These risks are strongly linked to insulin resistance and are compounded by the common occurrence of obesity, although insulin resistance and its associated risks are also present in nonobese women with PCOS. Women with PCOS are at increased risk for impaired glucose tolerance, type 2 diabetes mellitus, and hypertension. Cardiovascular disease is believed to be more prevalent in women with PCOS, and it has been estimated that such women also have a significantly increased risk for myocardial infarction. Many lipid abnormalities (most notably low high-density lipoprotein cholesterol levels and elevated triglyceride levels) and impaired fibrinolysis are seen in women with PCOS. Early diagnosis of the syndrome and close long-term follow-up and screening for diabetes and cardiovascular disease are warranted. An opportunity exists for preventive therapy, which should improve the reproductive, metabolic, and cardiovascular risks.

Anovulation↗

PubMed1999

Polycystic ovary syndrome.

Many adolescents present with hirsutism and irregular menses. The challenge for the clinician is to distinguish physiologic anovulatory cycles from true menstrual disorders such as PCOS, and to differentiate PCOS from other causes of hyperandrogenism in hirsute adolescents. Common clinical features seen in adolescents with PCOS include hirsutism, acne, menstrual irregularity, and obesity. Biochemical abnormalities include hyperandrogenism, acyclic estrogen production, LH hypersecretion, decreased levels of SHBG, and hyperinsulinemia. Management strategies for a patient with PCOS include treatment of features which may cause distress to the adolescent, such as hirsutism, acne, and irregular menses, and prevention of long-term sequelae. Oral contraceptive pills, antiandrogens, and cosmetic treatments are used to treat hirsutism, acne, and menstrual irregularity. Oral contraceptive pills or medroxyprogesterone acetate are given to prevent endometrial hyperplasia and carcinoma. Counseling about weight loss and nutrition are essential, as weight loss may improve signs of hyperandrogenism and menstrual irregularity and may prevent NIDDM and cardiovascular disease. Insulin-sensitizing agents show promise in terms of decreasing hyperandrogenism, restoring ovulatory cycles, treating infertility, and preventing long-term sequelae. Finally, it is important to recognize that adolescents with PCOS may experience psychological distress because of the clinical manifestations of hyperandrogenism or when confronted with the information that they have a chronic illness. Psychological support should be available for these young women. Future research is likely to further elucidate the pathophysiology of PCOS, identify candidate genes, and clarify which adolescents are at risk for long-term sequelae. Prospective studies are needed to identify which therapies could potentially reduce the risk of infertility, diabetes, cardiovascular disease, and endometrial carcinoma in young women with PCOS.

Adolescent↗

PubMed2000

[Polycystic ovary syndrome].

The polycystic ovary syndrome (PCOS) is the most frequent endocrine disease in women of reproductive age. Hyperandrogenism, anovulation and metabolic syndrome are the cardinal features of PCOS. Hyperandrogenism results from a diffuse enzymatic hyperactivity at the theca-interstitial cell level. Anovulation is due to an impairment of the selection of a dominant follicle, while the number of smaller follicles is exaggerated. The molecular grounds of insulin resistance could be an increased Serine phosphorylation of the insulin receptor. The clinical classification of PCOS distinguishes three forms: the classic PCOS, where the three above mentioned features are present, the non classic PCOS and the asymptomatic PCOS, revealed by ultrasonography. Only the increased ovarian volume or surface (>11ml and> 5.5cm(2), respectively) must be viewed as a specific ultrasonic sign of PCOS. Cyproterone acetate remains the basic treatment of hyperandrogenism. The treatment of anovulation and infertility follows a consensual strategy. The insulin sensitizing treatment allows to decrease hyperandrogenism, to reverse the menstrual cycle irregularity and to obtain spontaneous or induced pregnancies.

Anovulation↗

PubMed2000

The gonadotropic axis in hyperandrogenic adolescents.

Polycystic ovary syndrome (PCOS) is a common reproductive disorder that is first clinically diagnosable approximately 3 years after menarche. Women with PCOS have exaggerated gonadotropin secretion, with an elevated LH/FSH ratio, as well as an increased frequency and amplitude of LH pulsations. Since the elevated pulse frequency is a marker of unusually rapid hypothalamic GnRH secretion, these results imply a defect at the level of the hypothalamus. Such an abnormality could theoretically be a primary defect that could cause PCOS, and if so, would be expected to be detectable at the onset of puberty. How these abnormalities of hypothalamic and pituitary function relate to other, seemingly disparate, organ defects has not yet been delineated. We studied 99 PCOS patients and 42 normal controls with 8 to 12 hours of q10 min frequent blood sampling. Women with PCOS had significantly elevated mean LH levels, LH pulse amplitude, LH pulse frequency, and LH/FSH ratios compared to normal women. However, these abnormalities were not randomly distributed. All gonadotropin secretion parameters tended to be normal in PCOS patients when measured during the luteal phase or first 7 days after an ovulatory menses. There was a strong inverse relationship of mean LH, LH/FSH ratio, and LH pulse amplitude, but not frequency, with BMI. We hypothesize that this effect of body size occurs at the pituitary level. Several investigators have performed similar investigations in adolescent girls with regular and irregular menstrual cycles. Taken together, this evidence suggests that the gonadotropin defects appear as a very early finding in the development of PCOS, but the presence of abnormalities in both gonadotropin secretion and androgen secretion does not allow one to conclude that the gonadotropin defects are causal. We conclude that gonadotropin defects, particularly excess of serum LH, is a predominant finding in hyperandrogenic women, whether they are young peripubertal adolescents, or older perimenopausal women. Whether there is a primary neuroendocrine abnormality driving excess gonadotropin secretion that causes the hyperandrogenic condition, or whether the excess gonadotropin secretion reflects abnormal feedback of another factor, still remains unknown.

Adolescent↗

PubMed2000

Molecular defects of insulin action in the polycystic ovary syndrome: possible tissue specificity.

Insulin resistance is a highly common occurrence in PCOS. To determine the cellular and molecular mechanisms of this insulin resistance we studied subcutaneous abdominal adipocytes isolated from age and weight matched normal cycling (NC) and PCOS subjects. Insulin resistance in PCOS adipocytes was manifested as a reduction in insulin sensitivities for stimulation of glucose transport and suppression of catecholamine-activated lipolysis with no impact on final hormone responsiveness. Insulin sensitivity in adipocytes could be normalized by the addition of an adenosine analog. A number of key steps in insulin signaling pathways receptor autophosphorylation, IRS-1 phosphorylation, PI3-kinase activation and Akt phosphorylation--were found to display normal sensitivity and responsiveness in PCOS adipocytes. Insulin action measured in cultured fibroblasts was similar in NC and PCOS cells. Insulin resistance in PCOS involves tissue and response-specific defects in insulin signal transduction that remain to be identified. Interventions that can increase insulin sensitivity, such as adenosine, may have therapeutic potential in treating the unique insulin resistance of PCOS.

Female↗

PubMed2000

Family history as a risk factor for the polycystic ovary syndrome.

We have prospectively studied, by interview, clinical examination and biochemical evaluation, the relatives of 195 consecutive PCOS patients in order to: 1) accurately determine the prevalence of PCOS, as defined by current endocrinological criteria, among first-degree relatives of affected patients, and 2) determine the overall accuracy of proband-only and family member (self report) interview for the detection of clinically evident PCOS within families. We noted that 35% of mothers and 40% of sisters of patients with PCOS will be affected by PCOS themselves. Overall, the interview using a standardized form, whether of the proband or the family relative directly, appears to be a reliable predictor of affected status in mothers. Alternatively, approximately 50% of sisters will be missed using the proband interview, although self-reporting appears to be a reasonably reliable predictor of affected status for these relatives. While we are unable to exclude an autosomal or X-linked dominant mode of inheritance, the heritability of PCOS is probably more complex, similar to that of diabetes mellitus type 2 and cardiovascular disease. In absence of molecular diagnostic markers, a positive family history appears to be the most informative risk factor for the development PCOS.

Alabama↗

PubMed2000

[Study on parents phenotypes in women with polycystic ovary syndrome].

OBJECTIVE: To explore the parents phenotypes in women with polycystic ovary syndrome (PCOS). METHODS: Clinical data were collected by questionnaires from 139 parents of women with PCOS and from 137 parents of controls with normal menses. It was compared for the distribution of mother's menses irregularity, father's premature balding and parents hypertension by chi-square tests among parents of the PCOS group and of the controls. A multiple Logistic regression model was applied for more detailed analyses. RESULTS: The prevalences of mother's menses irregularity, the incidence of father's premature balding and father's hypertension was significantly higher in PCOS group (38.1%, 19.4% and 30.9%, respectively) than in the controls (3.6%, 5.1% and 16.1%, respectively P < 0.01). The prevalence of mother's hypertension was higher in the PCOS group (23.0%) than in the controls (13.9%), but the difference was not significant (P = 0.06). When mother's menses irregularity, father's premature balding and father's hypertension were entered the Logistic regression model, all the odds ratio (OR) values were still much higher than 1 (P < 0.005). The partial regression coefficients of the three predictors changed little when they were entered the model in turn. The partial regression coefficients for father's age was very small when it entered the model as a possible confounding factor(P > 0.05). The differences between maximum -2log likelihoods used to evaluate the role responsible for the occurrence of PCOS in their daughters indicated that: mother's menses irregularity > father's premature balding > father's hypertension. CONCLUSION: In addition to mother's menses irregularity and father's premature balding, father's hypertension may also be an independent phenotype in families of women with PCOS.

Alopecia↗

PubMed2001

Menstrual irregularity in the first postmenarchal years: an early clinical sign of polycystic ovary syndrome in adolescence.

We determined the hormonal, metabolic and ultrasonographic pattern of adolescents with menstrual irregularity since menarche but without clinical signs of hyperandrogenism with the aim of evaluating whether this condition represents an early stage of polycystic ovary syndrome (PCOS). These adolescents were divided in two groups: 13 adolescents with irregular cycles (IC) within the first 3 postmenarchal years (IC < or = 3) and 15 adolescents having persistent irregular cycles for more than three postmenarchal years (IC > 3). These adolescents were compared with 15 adolescents with PCOS and 18 normal adolescents. The values of free testosterone, free androgen index, luteinizing hormone (LH) and LH/follicle-stimulating hormone (FSH) ratio were similar in IC < or = 3, IC > 3 and PCOS, and higher than in the normal group (p < 0.005). The total testosterone and androstenedione levels were higher and sex hormone-binding globulin (SHBG) lower in PCOS only when compared with the normal group (p < 0.05). The ovarian volume was similar in IC < or = 3, IC > 3 and PCOS, and higher than in the normal group (p < 0.005). A higher incidence of polycystic structure was found in IC < or = 3, IC > 3 and PCOS, whereas normal structure was more common in normal adolescents (p < 0.0005). There were no significant differences in glucose and insulin parameters between groups. These results indicate that menstrual irregularity within the first postmenarchal years can be an early clinical sign of PCOS.

Adolescent↗