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PubMed1997

The frequency of late-onset 21-hydroxylase and 11 beta-hydroxylase deficiency in women with polycystic ovary syndrome.

OBJECTIVE: To determine the frequency of late-onset adrenal hyperplasia (LOCAH) due to 21-hydroxylase (21-OH) and 11 beta-hydroxylase (11 beta-OH) deficiency in women with clinical and biochemical features of polycystic ovary syndrome (PCOS). DESIGN: Eighty-three consecutively selected women with PCOS and eighteen normal women were included in the study. METHODS: Ultrasound, clinical and hormonal parameters were used to define PCOS. Basal FSH, LH, testosterone, free testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEA-S), sex hormone-binding globulin (SHBG) and cortisol levels were measured. Serum 17-hydroxyprogesterone (17-OHP) and 11-deoxycortisol (11-DOC) levels were also measured before, 30 and 60 min after a single bolus injection of 0.25 mg ACTH (1-24) at 0900 h during the mid-follicular phase of the cycle. ACTH-stimulated 17-OHP levels > 30 nmol/l were considered as the criteria of 21-OH deficiency. The diagnosis 11 beta-OH deficiency was made if the adrenal 11-DOC response to ACTH stimulation exceeded threefold the 95th percentile of controls. RESULTS: Basal serum testosterone, free testosterone, androstenedione, DHEA-S, cortisol and 11-DOC levels were significantly higher in PCOS than in control subjects. ACTH-stimulated 17-OHP (P < 0.05) and 11-DOC (P < 0.0005) levels were found to be significantly higher in patients with PCOS than in controls. Seven (8.4%) patients had an 11-DOC response to ACTH higher than threefold the 95th percentile of controls, while no patients showed evidence of 21-OH deficiency. CONCLUSIONS: We have found that 8.4% of the women with clinical and biochemical features of PCOS could be presumed to have 11 beta-OH deficiency. No patients among the women with PCOS showed evidence of 21-OH deficiency. 11 beta-OH deficiency is unexpectedly more common than 21-OH deficiency in women with PCOS.

Adrenal Hyperplasia, Congenital↗

PubMed1999

Comparison of finasteride versus flutamide in the treatment of hirsutism.

OBJECTIVE: To compare the effectiveness of finasteride and flutamide in the treatment of hirsutism in patients with polycystic ovary syndrome (PCOS) and with idiopathic hirsutism. DESIGN: Randomized study. PATIENTS: One hundred and ten hirsute patients were selected: 64 women with PCOS and 46 with idiopathic hirsutism. METHODS: Patients were assigned randomly to receive 5mg finasteride once daily or 250mg of flutamide twice daily, for 12 consecutive months. Hirsutism was evaluated at 12 months of therapy, with the Ferriman-Gallwey score and with measurement of the terminal hair diameters (microm) taken from four different body areas. Blood samples were taken for assessment of endocrine and hematochemical parameters. Side effects were monitored during the treatment. RESULTS: Both finasteride and flutamide induced a significant decrease in the hirsutism scores and hair diameters at the end of 12 months. Finasteride reduced the Ferriman-Gallwey score by 31.4% in the PCOS cases and by 34.2% in the idiopathic hirsutism cases, and hair diameter by 27.0-34.1% in PCOS and by 29.6-37.9% in idiopathic hirsutism. Flutamide reduced the Ferriman-Gallwey score by 56.7% in PCOS and by 50.9% in idiopathic hirsutism, and hair diameter by 50. 3-60.0% in PCOS and by 47.7-56.5% in idiopathic hirsutism. Flutamide did not induce hormone variations, while finasteride increased testosterone levels by 40% in PCOS and by 60% in idiopathic hirsutism and decreased 3alpha-androstanediol glucuronide (3alpha-diolG) by 66.7% in PCOS and by 69.5% in idiopathic hirsutism. No important side effects or changes in the hematochemical parameters were observed with finasteride, while two patients (3.6%) in the flutamide group expressed abnormal transaminase levels after 6 months of treatment. Dry skin also appeared significantly more with flutamide (67.3%) than with finasteride (23.6%). CONCLUSIONS: Both drugs are effective in the treatment of hirsutism but flutamide is more effective than finasteride.

Adolescent↗

PubMed2006

The CC genotype of the GNAS T393C polymorphism is associated with obesity and insulin resistance in women with polycystic ovary syndrome.

OBJECTIVE: Variants in the Gs protein alpha subunit gene (GNAS1) are known to be involved in the pathogenesis of several endocrine and metabolic disorders. To understand genetic determinants of androgen excess, insulin resistance, and obesity in polycystic ovary syndrome (PCOS), we investigated the effect of the common GNAS1 T393C polymorphism on the phenotype of German PCOS women. DESIGN: Two hundred and seventy-eight PCOS women and 820 Caucasian controls were genotyped for the common T393C polymorphism in GNAS1. To this end, genomic DNA was amplified by PCR with specific oligonucleotides and genotypes were determined using the restriction enzyme FokI. In addition, we evaluated whether the T393C polymorphism had an influence on the response to 6 months metformin treatment in a subgroup of 105 PCOS women. METHODS: Anthropometric variables, metabolic parameters including indices of insulin resistance measured by oral glucose tolerance testing, and endocrine biochemical as well as clinical parameters were measured in all PCOS subjects. RESULTS: GNAS1 genotype distributions were not significantly different between PCOS women and controls. In PCOS women, no significant differences in endocrine clinical and biochemical variables were found between the genotypes. However, the C-allele carrier group had significantly higher mean body weight, body mass index, leptin levels, and higher indices of insulin resistance compared with women with GNAS1 TT-genotype. Metformin treatment significantly improved hyperandrogenism, menstrual cyclicity, body weight, and insulin resistance independent of GNAS1 genotype. The major determinant of weight loss was body weight before treatment. CONCLUSION: The T393C polymorphism is not associated with PCOS in Caucasian women, but may represent a genetic marker for increased susceptibility for obesity in this cohort.

Androgens↗

PubMed2005

Resistin levels of serum and follicular fluid in non-obese patients with polycystic ovary syndrome during IVF cycles.

OBJECTIVES: To measure serum and follicular resistin, steroids hormone levels in women with PCOS (polycystic ovary syndrome) (BMI (body mass index)<25 kg/m(2)), to assess possible correlations of resistin to hormonal and metabolic parameters and to analyze the clinical outcomes of in vitro fertilization-embryo transfer (IVF-ET) in women with PCOS and tubal infertility. STUDY DESIGN: We analyzed the clinical outcomes of IVF-ET in women with PCOS (BMI<25 kg/m(2)) and tubal infertility during the years 2002 to 2004 and compared the serum and follicular fluid resistin levels, estradiol (E(2)), progesterone (P), testosterone (T) levels in 20 PCOS and 20 healthy, age-matched women without PCOS during IVF-stimulated cycles. The correlations between the resistin levels and the outcomes of IVF-ET were evaluated. RESULTS: No significant differences in resistin levels of either serum or follicular fluid between PCOS and control group were found. However, resistin levels in serum were higher than that in follicular fluid in both groups. Multiple regression analysis showed that resistin levels in serum did not correlate with BMI, estradiol, LH (luteinizing hormone) and insulin level in fasting blood. No significant correlations were found between follicular fluid reisistin levels and fertilization rate, implantation rate, clinical pregnancy rate or early miscarriage rate in both PCOS and control groups. CONCLUSION: Our results show that resistin does not have correlation with the hormonal and metabolic parameters as well as the outcomes of IVF. These data suggest that resistin is unlikely to be a local determinant factor in steroidogenesis and growth and maturation of oocytes during IVF-ET in lean women with PCOS.

Adult↗

PubMed2025

Genomic relationship between polycystic ovary syndrome and bipolar disorder.

Women with bipolar disorder (BIP) have a higher risk of developing polycystic ovary syndrome (PCOS). Shared genetic architecture may underlie this comorbidity. Valproate, a mood-stabilizer commonly used to treat BIP, increases the risk of PCOS. Still, the mechanism underlying PCOS in BIP remains unknown. Here, we aimed to identify genetic variants shared between BIP and PCOS, as well as their interaction with valproate. We used the results of large-scale genome-wide association studies of BIP (41,510 cases and 354,340 controls), and PCOS (3,609 cases and 229,788 controls). Using conditional false discovery rate, we discovered genetic variants jointly associated with BIP and PCOS. Gene mapping of identified variants was performed using the Open Targets platforms. We analyzed the tissue-specific expression, interaction with valproate, and involvement in biological pathways of the mapped genes. We identified two loci shared between BIP and PCOS. Among the 10 genes mapped to the locus on chromosome 8:11455262, GATA4, NEIL2, and FDFT1 showed expression profiles suggesting their role in the observed comorbidity. Mapped to the locus on chromosome 12:2499849, CACNA1C, FKBP4, DCP1B, and ITFG2 are expressed in both the ovaries and the brain. CACNA1C expression is affected by valproate, and CACNA1C plays a role in biological pathways involving other valproate-affected genes. We identified shared genetic underpinnings of BIP and PCOS, and implicated genes which may explain the biological mechanisms of the comorbidity between these disorders and a potential mechanism for the role of valproate.

bipolar disorder↗

PubMed1999

Insulin resistance, polycystic ovary syndrome and metformin.

Polycystic ovary syndrome (PCOS) is the most common disorder of ovarian function in premenopausal women. PCOS is characterised by chronic anovulation and androgen excess with clinical manifestation of irregular menstrual cycles, hirsutism and/or acne. Insulin resistance with resultant hyperinsulinaemia, irrespective of excess weight or frank obesity, has been reported in patients with PCOS, and, as insulin has a direct effect on ovarian androgen production in vitro, insulin resistance may play a crucial role in the physiopathology of PCOS. Although the molecular mechanism(s) of insulin resistance in PCOS is unclear, excessive insulin-independent serine phosphorylation of the beta subunit of the insulin receptor, as reported in some patients with PCOS, has been put forward as a new mechanism for insulin resistance. Insulin-sensitising agents have recently been investigated for their role in the short term treatment of insulin resistance in PCOS. Controlled studies have shown that metformin administration, by promoting bodyweight loss, can decrease fasting and stimulated plasma insulin levels. However, other studies have shown metformin 500 mg 3 times daily to decrease insulin secretion and to reduce ovarian production of 17alpha-hydroxyprogesterone with recovery of spontaneous or clomifene-induced ovulation, independently of weight loss. These findings suggest a new indication for metformin and present insulin-sensitising agents as a novel approach in the treatment of ovarian hyperandrogenism and abnormal ovulation in PCOS. They also suggest that long term administration of metformin might be helpful in treating insulin resistance, thus reducing risks of type 2 (non-insulin-dependent) diabetes and cardiovascular disease in these patients.

Cardiovascular Diseases↗

PubMed1999

Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome.

OBJECTIVE: NIDDM occurs commonly among women with polycystic ovary syndrome (PCOS). The prevalence and natural history of its precursor, impaired glucose tolerance (IGT), is less well known. The objective of this study was to characterize the prevalence and incidence of glucose intolerance in a large cohort of women with well-characterized PCOS. RESEARCH DESIGN AND METHODS: A total of 122 women with clinical and hormonal evidence of PCOS were recruited from the Medicine, Endocrinology, Gynecology, and Pediatrics Clinics at the University of Chicago. All women had a standard oral glucose tolerance test (OGTT) with measurement of glucose and insulin levels. A subset of 25 women were subsequently restudied with the aim of characterizing the natural history of glucose tolerance in PCOS. RESULTS: Glucose tolerance was abnormal in 55 (45%) of the 122 women: 43 (35%) had IGT and 12 (10%) had NIDDM at the time of initial study. The women with NIDDM differed from those with normal glucose tolerance in that they had a 2.6-fold higher prevalence of first-degree relatives with NIDDM (83 vs. 31%, P < 0.01 by chi 2) and were significantly more obese (BMI 41.0 +/- 2.4 vs. 33.4 +/- 1.1 kg/m2, P < 0.01). For the entire cohort of 122 women, there was a significant correlation between fasting and 2-h glucose concentrations (r = 0.76, P < 0.0001); among the subset with IGT, the fasting glucose concentration was poorly predictive of the 2-h level (r = 0.25, NS). After a mean follow-up of 2.4 +/- 0.3 years (range 0.5-6.3), 25 women had a second OGTT. The glucose concentration at 2 h during the second glucose tolerance test was significantly higher than the 2-h concentration during the first study (161 +/- 9 vs. 139 +/- 6 mg/dl, P < 0.02). CONCLUSIONS: The prevalence of IGT and NIDDM in women with PCOS is substantially higher than expected when compared with age- and weight-matched populations of women without PCOS. The conversion from IGT to NIDDM is accelerated in PCOS. The fasting glucose concentration does not reliably predict the glucose concentration at 2 h after an oral glucose challenge, particularly among those with IGT, the subgroup at highest risk for subsequent development of NIDDM. We conclude that women with PCOS should periodically have an OGTT and must be closely monitored for deterioration in glucose tolerance.

Adult↗

PubMed2000

Impaired insulin action on granulosa-lutein cells in women with polycystic ovary syndrome and insulin resistance.

We studied the in vitro response to insulin of granulosa-lutein cells derived from patients with polycystic ovary syndrome (PCOS) and clinically defined insulin resistance. Insulin sensitivity was assessed by continuous infusion of glucose with model assessment test (CIGMA). Insulin resistant (PCOS-IR; n = 8), noninsulin resistant (PCOS-NIR; n = 9) patients with PCOS, and women with tubal factor infertility (TF; n = 8) underwent controlled ovarian stimulation with long-term gonadotropin-releasing hormone (GnRH) agonist, recombinant follicle stimulating hormone (FSH), and in vitro fertilization. Primary cultures of granulosa-lutein cells were incubated with insulin (10, 100, 500 ng/ml) and/or luteinizing hormone (LH) (10, 100 ng/ml) in the presence of low density lipoprotein (100 micrograms/ml). The progesterone and lactate accumulation were measured in the culture medium. LH potently stimulated the progesterone secretion in all groups. Insulin alone had no effect on progesterone release in any of the groups, but stimulated lactate formation in the PCOS-NIR and TF groups. Insulin augmented the effect of LH on progesterone secretion selectively in the PCOS-NIR group. The expression of the insulin receptor was determined by Western blotting in separate cultures of granulosa-lutein cells, and showed receptor down-regulation in the PCOS-IR patients. We infer that the in vitro effect of insulin on progesterone and lactate release by granulosa-lutein cells is impaired in insulin resistant PCOS patients.

Androstenedione↗

PubMed1996

The relationship between insulin sensitivity and insulin-like growth factor-binding protein-1.

Insulin has been shown to regulate insulin-like growth factor-binding protein-1 (IGFBP-1) in vivo and in vitro. Insulin resistance is a feature of the polycystic ovary syndrome (PCOS). We have studied the relationship between insulin sensitivity (S1) and the circulating concentration of IGFBP-1 in a group of young women and in some who had PCOS. A case-control study has been carried out comparing reproductively normal women with women with PCOS (defined as women with oligo- or amenorrhea associated with androgen excess). Fifteen women with clinical PCOS and ten age- and weight-matched controls were studied. S1 was measured by the frequently sampled intravenous glucose tolerance test (FSIGT) using the minimal model technique. IGFBP-1, insulin-like growth factor-I (IGF-I) and growth hormone levels were measured before and during the FSIGT. Circulating testosterone, dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) levels were measured while the subjects were fasting. S1 and IGFBP-1 levels were significantly lower in the PCOS group than in controls (S1/10(-5) min-1/pM] mean +/- SE 3.8 +/- 0.8 vs. 8.5 +/- 1.3, p < 0.03; IGFBP-1 [ng/ml] mean +/- SE 26.6 +/- 4.2 vs. 56.0 +/- 5.9, p < 0.005). In women with PCOS, IGFBP-1 concentrations related negatively to the body mass index (BMI) (r = -0.77, p < 0.003) and positively to S1 (r = 0.76, p < 0.003). S1 remained a significant predictor of IGFBP-1 concentrations when controlled for BMI (combined r2 = 0.35, p < 0.05). No relationship was found between androgen levels and IGFBP-1. Insulin sensitivity contributed to the difference in IGFBP-1 levels found in women with PCOS. Whether the reduced concentrations of IGFBP-1 play a role in the pathophysiology of PCOS is uncertain, but it may act to alter delivery of IGF to peripheral tissues in insulin-resistant individuals.

Androstenedione↗

PubMed1999

Are women with polycystic ovary syndrome at an increased risk of pregnancy-induced hypertension and/or preeclampsia?

OBJECTIVE: To study whether there is an increased risk of glucose intolerance and hypertensive complications during pregnancy in women with polycystic ovary syndrome (PCOS) and if there is an adverse pregnancy outcome. METHODS: In a retrospective case-control study, pregnancies and neonatal outcome were compared in 33 women with PCOS and 66 women without PCOS. The women were treated at Huddinge University Hospital; antenatal care was given at associated outpatient units. MAIN OUTCOME MEASURES: Blood glucose and blood pressure during the different trimesters. Pregnancy outcome in terms of gestational length, birth weight, and need for neonatal intensive care. RESULTS: No significant differences were found in blood glucose levels between the groups. There were also no differences in blood pressure during the first and second trimester. However, during the third trimester and labor, the PCOS group had a significantly higher blood pressure than the control group. Apart from a tendency toward reduced growth of twins in PCOS mothers, the babies were healthy, overall, with few problems in the neonatal period. CONCLUSIONS: No major differences with regard to perinatal outcome in pregnant women with and without PCOS were found. An increased risk of hypertensive disorders in the third trimester and during labor was demonstrated in the PCOS group. This suggests that in the antenatal care of women with PCOS, attention should focus on blood pressure in order to reduce the risks of morbidity associated with hypertension.

Adult↗

PubMed2006

[Outcome of in vitro fertilization-embryo transfer in treatment of polycystic ovarian syndrome].

OBJECTIVE: To evaluate the outcome of in vitro fertilization embryo transfer (IVF-ET) in treatment of polycystic ovarian syndrome (PCOS) with infertility. METHODS: A retrospective analysis was performed from 52 patients with PCOS (PCOS group) and 408 cases with tubal infertility (control group). Both groups underwent IVF-ET treatment from 2001 to 2004. The duration of stimulation, amps of gammaFSH, the level of serum E2, P on the day of HCG injection, the number of oocytes retrieved, the rates of fertilization, cleavage, implantation and pregnancy, the incidence of ovarian hyperstimulation syndrome (OHSS) and cancelled rate of ET were compared between the two groups. RESULT: The duration of stimulation and amps of gammaFSH were not significantly different between the two groups. The concentration of serum E2, P on the day of HCG injection, the numbers of oocytes retrieved and cleavaged embryos were significantly higher in PCOS group (P <0.01, <0.05). Fertilization rate was significantly lower in PCOS group (P <0.01). The implantation, pregnancy and miscarriage rates per ET were not statistically significant. The OHSS rates and cancelled rates of ET were higher in PCOS group (P <0.01). CONCLUSION: Women with PCOS have a lower fertilization rate compared with those with tubal-factor fertility during IVF-ET. However, more oocytes are recovered and the preimplanted embryo has a normal chance of implantation leading to similar pregnancy rates. The OHSS rates and cancelled rates of ET are higher in PCOS because of a greater number of oocytes developed and a higher level of E2.

Adult↗

PubMed2000

[Study on the relationship between a polymorphism of tumor necrosis factor-alpha gene and the pathogenesis of polycystic ovary syndrome].

OBJECTIVE: To investigate the relationship between -308 bp polymorphism in tumor necrosis factor-alpha (TNF-alpha) gene promoter region and the pathogenesis of polycystic ovary syndrome (PCOS). METHODS: One hundred eighteen Chinese women with PCOS (44 were obese, and 74 nonobese) and 54 controls were genotyped according to the fragment length [87 bp and(or) 107 bp] of TNF-alpha gene promoter by the technique of polymerase chain reaction-restriction fragment length polymorphism. The distribution of TNF1 genotype (87/87) and TNF2 genotype (87/107 + 107/107) in the two groups and their relations to parameters of glucose metabolism associated with PCOS were compared. RESULTS: There was no significant difference in the distribution of TNF1 and TNF2 genotypes between PCOS group and the controls (P > 0.05). In obese PCOS group, only significant lower insulin sensitivity index was found in TNF-1 genotype as compared with TNF2 genotype (P < 0.05). In nonobese PCOS group, there was no significant difference in all parameters of glucose metabolism between TNF1 and TNF2 genotype. All parameters of glucose metabolism in obese patients with TNF1 genotype were significantly different from those in nonobese with TNF1 genotype. However, significant differences were found only in some parameters when comparison was made between obese and nonobese within the TNF2 genotype group. CONCLUSION: There is no association between TNF-alpha gene -308 bp polymorphism and the pathogenesis of polycystic ovary syndrome, but PCOS patients with TNF2 genotype may associate with improvement to certain degree on abnormal glucose tolerance usually existed in obese PCOS women.

Adult↗

PubMed2002

Common treatment of polycystic ovarian syndrome and major depressive disorder: case report and review.

We present the case of a young woman with treatment-resistant major depression, who presented to the Mood Disorders Clinic with a Hamilton Psychiatric Rating Scale for Depression (HAM-D-21) score of 28, after a year-long treatment with Effexor-XR. The patient also had untreated Polycystic Ovarian Syndrome (PCOS). The resolution of her depressive symptoms resulted from the treatment for PCOS with metformin and spironolactone. The patient remained euthymic 5 months after discontinuation of the antidepressant while continuing therapy for PCOS. We briefly overview of the pertinent literature of the pathophysiology of PCOS and affective disorders, highlighting an overlap in phenotypical presentations between these two disorders. Dysregulation of the hypothalamo-pituitary axis and various end organ systems are implicated in both PCOS and affective disorders. As such, several clinical and biochemical markers are common to both disorders, namely insulin resistance, obesity, and hyperandrogenism. In addition, these metabolic abnormalities are interrelated, causing women with PCOS or affective disorders to get caught in a "vicious cycle" of hormonal dysregulation. The case report presented here illustrates how treatment of symptoms such as insulin resistance and hyperandrogenism can lead to remission of major depressive disorder and PCOS. We suggest that through treatment of underlying metabolic defects, both the mood of the patient and the metabolic condition of PCOS can be assisted.

Adult↗

PubMed2003

The effect of age on the ovarian response to gonadotropin and on pregnancy rate in polycystic ovary syndrome.

Recent studies have proposed that, in women affected by the polycystic ovary syndrome (PCOS), aging is able to regularize the menstrual cyclicity. To evaluate the ovarian response in PCOS patients according to their age, we studied 33 PCOS patients, 20 of whom with an age ranging from 28 to 34 years (younger PCOS) and 13 ranging from 35 to 45 years (older PCOS). All patients underwent an ovulation induction therapeutic protocol with low-dose recombinant follicle stimulating hormone, for a total of 80 cycles (44 cycles for the younger PCOS group and 36 cycles for the older PCOS group). No significant difference was found between the days of therapy (12.3 +/- 5.4 vs. 13.5 +/- 5.6 days), total amount of drugs (980.7 +/- 568.9 IU vs. 1063.9 +/- 469.5 IU) or ovulation rate (93% vs. 89%) in the two groups. The two groups showed a significant difference in the maximum estradiol level (2053.5 +/- 1497.2 vs. 1269.0 +/- 911.5 pmol/l, p < 0.01), the number of the recruited and preovulatory follicles (1.7 +/- 2.5 vs. 0.64 +/- 0.9, p < 0.05 and 1.7 +/- 1.1 vs. 1.2 +/- 0.5, p < 0.01, respectively) and the pregnancy rate (36% vs. 14%, p < 0.05). In conclusion, our data clearly showed that, also in PCOS, advanced age is a negative prognostic factor in the ovarian response to ovulation induction therapies.

Adult↗

PubMedDate not supplied

Evaluation of the pituitary-adrenal axis in hyperandrogenic women with polycystic ovary syndrome.

OBJECTIVES: Impaired adrenal function is common in patients with polycystic ovary syndrome (PCOS). Abnormal regulation of cytochrome P450 17 alpha is believed to cause the exaggerated 17-hydroxyprogesterone (17OHP) response to ACTH stimulation. The aim of the study was to evaluate cortisol and 17OHP response to low dose (1 microg) ACTH test and to compare it with the standard ACTH (250 microg) test in hyperandrogenic women with PCOS. DESIGN AND MEASUREMENTS: We studied 27 PCOS and 22 control women. All participants were examined for mutations of the CYP21 gene, Cortisol and 17OHP levels before, 30 and 60 minutes after the IV injection of 250 microg ACTH (SDT) and after 1 microg ACTH (LDT). Fasting serum levels of LH, FSH, testosterone, DHEAS were determined in all participants. RESULTS: Basal and ACTH stimulated Cortisol during the SDT (470+/-138 nmol/L and 761+/-143, respectively) were significantly higher in PCOS vs. controls (232+/-124 and 670+/-130, respectively) (p<0.03, p<0.02, respectively). Basal 17OHP (6.1+/-2.1 nmol/L) and the peak response to SDT (14.2+/-3.6 nmol/L) were significantly higher in PCOS vs. controls (4.2+/-2.1, 10.9+/-3.0, respectively) (p<0.003, p<0.004, respectively). Abnormally elevated 17OHP response to SDT was detected in 6/27 PCOS women (22%). No statistically significant difference between the PCOS and control groups were noted during the LDT in both cortisol and 17OHP levels. CONCLUSIONS: These data suggest that the exaggerated 17-hydroxyprogesterone (17OHP) response to ACTH stimulation in PCOS is revealed by stimulation at a pharmacological dose (250 microg) but not by a physiological dose (1 microg).

17-alpha-Hydroxyprogesterone↗

PubMed2003

Minireview: Up-date management of non responder to clomiphene citrate in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder in which chronic anovulation is a common feature despite the presence of multiple micro- structures in the ovaries. A growing body of evidence has suggested that serum hyperinsulinemia contributes to the excess ovarian androgen secretion observed in women with PCOS. The standard therapy for anovulatory women with PCOS is oral administration of clomiphene citrate (CC). However, a significant proportion of women with PCOS fail to ovulate with the use of standard dosage of CC and are called CC-resistant PCOS. The recent introduction of the insulin-sensitizing agents as adjuvants to clomiphene citrate and gonadotropins has changed the treatment strategy. This is a comprehensive review of the literature, with an emphasis on the role of hyperinsulinemia in the pathogenesis of PCOS and on randomized controlled trials of the medical and surgical treatment options for women with CC-resistant PCOS. Although both standard and novel treatments were addressed in the present review, special attention was paid to the evidence in support of the recent introduction of insulin-sensitizing agents in the management of anovulatory woman with CC-resistant PCOS.

Anovulation↗

PubMedDate not supplied

Insulin resistance, insulin sensitization and inflammation in polycystic ovarian syndrome.

It is estimated that 5-10% of women of reproductive age have polycystic ovarian syndrome (PCOS). While insulin resistance is not part of the diagnostic criteria for PCOS, its importance in the pathogenesis of PCOS cannot be denied. PCOS is associated with insulin resistance independent of total or fat-free body mass. Post-receptor defects in the action of insulin have been described in PCOS which are similar to those found in obesity and type 2 diabetes. Treatment with insulin sensitizers, metformin and thiazolidinediones, improve both metabolic and hormonal patterns and also improve ovulation in PCOS. Recent studies have shown that PCOS women have higher circulating levels of inflammatory mediators like C-reactive protein, tumour necrosis factor-alpha, tissue plasminogen activator and plasminogen activator inhibitor-1 (PAI-1). It is possible that the beneficial effect of insulin sensitizers in PCOS may be partly due to a decrease in inflammation.

Abortion, Spontaneous↗

PubMed2004

[Ovarian insulin resistance and insulin sensitizer effect on polycystic ovary syndrome].

OBJECTIVE: To explore the molecular defects of insulin signalling in polycystic ovary and in vitro effects of troglitazone, one of the insulin sensitizers-thiazolidinediones on polycystic ovary syndrome (PCOS). METHOD: The metabolic and mitogenic effects of insulin and insulin-like growth factor 1 (IGF-1) were examined in cultured human ovarian luteinizing granulosa cells from PCOS (n = 11) and normally ovulatory (as control, n = 33) women with vehicle or troglitazone (1 microg/ml). RESULTS: Basal rates were similar, but there were significant decreases in insulin-stimulated glucose incorporation into glycogen in PCOS cells, a metabolic action of insulin. However, IGF-1 response was found to be about twice greater in PCOS cells at all experimental concentrations with respect to thymidine incorporation compared to control cells, a mitogenic action. Troglitazone increased 2-3 fold the insulin-induced glycogen synthesis, but reduced the IGF-1 augmented responses of DNA synthesis in PCOS cells to within the range of control granulosa cells. As compared with control, PCOS granulosa cells had higher insulin receptor substrate 1 (IRS -1) expression, but lower IRS-2 expression. IRS-2 protein levels were increased and IRS-1 levels were reduced by troglitazone treatment, with a greater extent in the former. CONCLUSIONS: There is a selective defect in insulin actions in PCOS granulosa cells, suggesting ovarian insulin resistance and this metabolic phenotype is associated with an enhanced IGF-1 mitogenic potential. Troglitazone could divergently alter signal protein expressions and thus insulin actions, as an ovarian insulin sensitizer and mitogen/steroidogenic inhibitor in PCOS.

Adult↗