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PubMed1993

Growth hormone response to L-dopa and pyridostigmine in women with polycystic ovarian syndrome.

OBJECTIVE: To evaluate the GH secretion and clarify the factors influencing the GH secretion in women with polycystic ovarian syndrome (PCOS). DESIGN: Comparison of the GH response to L-dopa with or without pyridostigmine (inhibitor of acetylcholinesterase) pretreatment and insulin response to oral glucose tolerance test in patients with PCOS and matched controls. SETTING: Outpatients and healthy volunteers studied at a clinical research unit of a university hospital. PATIENTS, PARTICIPANTS: Ten women with PCOS and 9 controls with regular cycles were recruited. INTERVENTIONS: After an overnight fast, each subject underwent a GH stimulation test with L-dopa with or without pyridostigmine pretreatment. Plasma insulin and glucose levels were measured after a 75-g glucose load. MAIN OUTCOME MEASURES: Plasma GH, insulin-like growth factor I (IGF-I), insulin, and nonesterified fatty acids. RESULTS: Growth hormone responses and GH area under the response curve (AUC) to L-dopa were significantly lower in PCOS than those in controls. Pyridostigmine enhanced the GH response to L-dopa significantly in PCOS. Insulin responses and insulin AUC to oral glucose load were significantly higher in PCOS than those in controls. Plasma IGF-I levels of PCOS were significantly higher than controls. Insulin AUC had a positive correlation with plasma IGF-I levels but an inverse correlation with GH AUC in PCOS and controls. CONCLUSION: Our result indicated that decreased GH secretion of PCOS may be associated with a high somatostatin activity and a high plasma IGF-I level.

Adolescent↗

PubMed1995

Alterations in the sensitivity of serum insulin-like growth factor 1 and insulin-like growth factor binding protein-3 to octreotide in polycystic ovary syndrome.

OBJECTIVE: To determine if the somatostatin analog, octreotide, affects insulin and related peptides and, hence, androgen levels differently between polycystic ovary syndrome (PCOS) patients and controls. DESIGN: Prospective controlled trial. SETTING: Reproductive endocrinology clinic of our medical center. PATIENTS: Eleven women with PCOS and six matched ovulatory controls. INTERVENTIONS: Octreotide (100 micrograms) was administered subcutaneously in the midfollicular phase. Serum was obtained before and at 60, 120, 180, and 240 minutes after octreotide. MAIN OUTCOME MEASURES: Fasting insulin, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), T, androstenedione (A), and LH. RESULTS: In PCOS, baseline levels of T, A, LH, and fasting insulin were significantly higher than in controls. Pretreatment IGF-1 and IGFBP-3 levels were similar in PCOS and controls. Octreotide reduced fasting insulin levels significantly but to a similar degree in control and PCOS patients (77% and 90%, respectively). Both groups also experienced a significant decrease in LH levels after octreotide administration, but no significant changes were demonstrated in serum T or A. However, serum IGF-1 suppression in PCOS was greater (63% versus 8% in controls). Serum IGFBP-3 levels increased after octreotide administration in both groups with a larger increase (40%) occurring in the PCOS patients. CONCLUSIONS: These data suggest that women with PCOS may be more sensitive to the effects of octreotide in decreasing IGF-1 and increasing IGFBP-3. Although no significant changes could be demonstrated in ovarian androgens after a single dose, octreotide effectively reduced serum LH and insulin and, as such, may prove useful in treating some patients with PCOS.

Adolescent↗

PubMed1996

The chronic administration of cabergoline normalizes androgen secretion and improves menstrual cyclicity in women with polycystic ovary syndrome.

OBJECTIVE: To investigate whether the administration of the long-lasting dopaminergic drug, cabergoline, improves endocrine and clinical features of women with polycystic ovary syndrome (PCOS). PATIENTS: Twenty-nine women participated in the study: 14 women with clinical and endocrinologic features of PCOS and 15 age- and weight-matched normal cycling women. Each subject was assigned randomly to receive either a tablet of cabergoline at the dose of 0.5 mg/wk or placebo for 4 months. Sixteen subjects (PCOS: n = 8; controls: n = 8) received cabergoline, whereas 13 (PCOS: n = 6; controls: n = 7) received placebo. INTERVENTIONS: Both before and during the 4th month of treatment, blood samples were collected every 10 minutes from 9:00 A.M. to 3:00 P.M., 3 to 7 days after spontaneous or medroxy-progesterone acetate (MPA; 5 mg daily for 5 days)-induced menses. Follicle-stimulating hormone and androgen levels were measured in the basal samples, whereas LH levels were measured in all samples. MAIN OUTCOME MEASURES: Menstrual cyclicity, LH pulsatility, and circulating levels of FSH, PRL, E2, total T, free T, androstenedione, 17 alpha-hydroxyprogesterone, DHEAS, and sex hormone-binding globulin. RESULTS: Both in controls and in PCOS-affected women, cabergoline administration blunted plasma PRL levels without affecting LH pulsatility. Androgen levels were reduced in controls and normalized in PCOS. Cabergoline, but not placebo, induced menses reappearance in amenorrheic and a normalization of menstrual cyclicity in oligoamenorrheic women with PCOS. CONCLUSIONS: The administration of cabergoline is capable to normalize androgen levels and to improve menstrual cyclicity in PCOS-affected women. Cabergoline may represent an useful treatment for menstrual irregularities of PCOS patients.

Adult↗

PubMed1999

Effect of opioid blockade on insulin and growth hormone (GH) secretion in patients with polycystic ovary syndrome: the heterogeneity of impaired GH secretion is related to both obesity and hyperinsulinism.

OBJECTIVE: To investigate the involvement of opioid tone, obesity, and hyperinsulinemia in GH secretion in women with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: Catholic University of Sacred Heart School of Medicine in Rome, Italy. PATIENT(S): Twenty-two patients with PCOS and 14 healthy, normally ovulating volunteers, matched for age and body mass index. INTERVENTION(S): Patients underwent a GH-releasing hormone (GHRH) test and an oral glucose tolerance test before and after 4-5 weeks of treatment with 50 mg/d of naltrexone. MAIN OUTCOME MEASURE(S): Serum concentrations of GH, insulin, glucose, steroids, and gonadotropins, as well as the GH area under the curve (AUC-GH) and the insulin area under the curve (AUC-I), were measured before and after naltrexone treatment. RESULT(S): In patients with PCOS, the administration of naltrexone increased the GH response to the GHRH test without interfering with the insulin response to the oral glucose tolerance test. However, the GH response to the GHRH test was improved significantly only in lean patients with PCOS, whereas obese patients with PCOS did not show any improvement in GH secretion. In obese control subjects, the treatment reduced plasma basal insulin concentrations and increased the AUC-GH, whereas in lean control subjects, the treatment reduced the GHRH-induced response. In normoinsulinemic patients with PCOS, the GH response to the GHRH test increased significantly after treatment, whereas the AUC-I was not affected. In hyperinsulinemic patients with PCOS, treatment with naltrexone significantly reduced the AUC-I, whereas the AUC-GH increased only in lean hyperinsulinemic patients with PCOS. CONCLUSION(S): Naltrexone treatment improves GHRH-induced GH secretion in patients with PCOS. However, this GH response is heterogeneously represented in relation to both obesity and hyperinsulinism.

Adult↗

PubMed1997

Linkage and association of insulin gene VNTR regulatory polymorphism with polycystic ovary syndrome.

BACKGROUND: Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting up to 10% of women of reproductive age. Women with anovulatory PCOS have hyperinsulinaemia, insulin resistance, and dyslipidaemia, and the syndrome is associated with greatly increased risks of non-insulin-dependent diabetes mellitus and cardiovascular disease and it often clusters in families. The VNTR (variable number of tandem repeats) locus upstream of the insulin gene (INS) regulates insulin expression. We have studied INS VNTR as a candidate genetic locus for susceptibility to PCOS. METHODS: We evaluated linkage of PCOS to the INS VNTR locus on chromosome 11p15.5 in 17 families with several cases, and looked for an association between VNTR and PCOS in two additional clinic populations. VNTR genotypes were designated I/I, I/III, and III/III and linkage disequilibrium mapping was used to test the primary role of the VNTR. FINDINGS: In a group of PCOS/male pattern baldness families, we obtained positive evidence for linkage to 11p15.5 (p = 0.002). The INS VNTR III/III genotype was associated with an increased risk of PCOS in two independent case-control studies (odds ratios 8.20 [p = 0.005] and 5.70 [p = 0.043]). Multilocus linkage disequilibrium mapping suggests that VNTR itself is the predisposing locus. INTERPRETATION: Mapping of susceptibility to PCOS to the INS VNTR implies that PCOS is due, in part, to an inherited alteration in insulin production. The data suggest a mechanistic link between type 2 diabetes and PCOS, which is a risk factor for diabetes later in life.

Alleles↗

PubMed2005

[Effect of procyanidolic oligomers on corneal collagen fibrillogenesis].

PURPOSE: We showed in a previous study that procyanidolic oligomers (PCOs) from grape seeds effectively protect corneal stroma against degradation by bacterial collagenase. Here we report the study of the effect of PCOs on protein and collagen composition of cornea and on the biosynthesis of corneal collagens. METHODS: Bovine corneas were used in explant cultures. We quantitatively determined total proteins and collagen as well as the incorporation of 3H-proline in separated collagen types. Collagens type I, V, and VI were separated and quantitated. In order to understand some of the results obtained, we studied the interaction of PCO with collagen type I separately. RESULTS: In the absence of PCOs, collagen typing and 3H-proline incorporation yielded the expected results for a normal cornea, with the usual proportion of the three major types of collagens. In presence of PCOs at 1 mg/ml and after 24 h incubation, total proteins and collagens decreased, as did papain-extractable collagens. Proteins in the final residue solubilized in 1 M KOH-80% v/v aqueous ethanol increased. The proportion of the three principal collagens was also modified: type I became preponderant, and the proportions of the two others (type V and VI) decreased. The study of the interaction of collagen type I with PCOs showed that 30% of total PCOs do not interact with collagen, 20% interact reversibly, and 50% of PCOs are strongly and irreversibly fixed. This strongly fixed fraction could not be separated from collagen by either column chromatography or collagenase or KOH in aqueous ethanol. CONCLUSIONS: Bovine corneas in explant cultures in presence of PCOs undergo a modification of their protein and collagen content, with a concurrent modification of the proportion of collagens types I, V, and VI. Collagen type I predominates, and the two other types decrease. Study of the collagen type I-PCO interaction showed that roughly 50% of PCOs become irreversibly fixed to collagen, resisting collagenase or other methods of separation. This strong PCO-collagen type I interaction explains the decrease in solubility.

Animals↗

PubMed1996

Disturbances in insulin secretion and sensitivity in women with the polycystic ovary syndrome.

Insulin resistance, defined as a diminished effect of a given dose of insulin on glucose homeostasis, is a highly prevalent feature of women with PCOS. Insulin resistance in PCOS is closely associated with an increase in truncal-abdominal fat mass, elevated free fatty acid levels, increased androgens, particularly free testosterone through reduced SHBG levels, and anovulation. The causes for insulin resistance in PCOS are still unknown. One line of evidence suggests that an increase in truncal-abdominal fat mass and subsequently increased free fatty acid levels induce insulin resistance in women with PCOS. Increased effects of corticosteroids and a relative reduction in oestrogen and progesterone seem to be involved in the aberrant body fat distribution. Conversely, there are also results supporting primary, genetic target cell defects as a cause of insulin resistance in PCOS. An explanation for these seemingly contradictory results could be that the group of women with PCOS is heterogeneous with respect to the primary event in carbohydrate/insulin disturbances. Also insulin secretion in PCOS is characterized by heterogeneity. At one end of the spectrum is a large subgroup of mainly obese women with reduced insulin secretion, which appears to result from failure of the beta cells to compensate for insulin resistance in susceptible women, resulting in glucose intolerance and NIDDM. In the insulin-resistant patients with normal glucose tolerance, most of the hyperinsulinaemia is probably due to secondarily increased insulin secretion and decreased insulin degradation. However, a component of the increased first-phase insulin release is not due to measurable insulin resistance. Notably, this is also found in lean women with normal insulin sensitivity, and is not reversed after weight reduction, in contrast to the findings for insulin resistance. The implications of this enhanced insulin release are not fully clear, but it may tentatively be associated with carbohydrate craving and subsequently increased risks for development of obesity and insulin resistance. It may represent a primary disturbance of insulin secretion in PCOS or may be associated with the perturbed steroid balance in anovulation. The insulin-androgen connection in PCOS appears to be amplified by several different mechanisms, notably in both directions, the initiating event probably varying between individuals. Thus insulin increases the biological availability of potent steroids, primarily testosterone, through the suppression of SHBG synthesis. Insulin is also involved as a progonadotrophin in ovarian steroidogenesis, with the possible net result of interfering with ovulation and/or increasing ovarian androgen production in states of hyperinsulinaemia. Conversely, testosterone may indirectly contribute to insulin resistance through facilitating free fatty acid release from abdominal fat, but perhaps also through direct muscular effects at higher serum levels. It seems likely that this constitution, presumably genetic, would provide evolutionary advantages in times of limited nutrition, given the energy-saving effects of insulin resistance. Hypothetically, hyperinsulinaemia (primary) could provide a stimulus to ensure intake of nourishment, but unlimited food supplies could in some cases initiate a vicious 'anabolic' circle, in which several of the proposed amplifying mechanisms between insulin and androgens--in both directions--could take part.

Adipose Tissue↗

PubMed2004

Is plasminogen activator inhibitor-1 a cardiovascular risk factor in young women with polycystic ovary syndrome?

This study aimed to evaluate plasminogen activator inhibitor-1 (PAI-1) activity in PCOS. Thirty women with PCOS - 15 normal-weight and 15 obese - and 30 healthy women matched as a group for age and body mass index (BMI) were recruited. The homeostasis model assessment (HOMA) score was significantly elevated in obese compared with normal-weight women, in both PCOS women and controls. HOMA score was significantly higher in both PCOS groups relative to controls. After further adjustment for BMI, PAI-1 activity (IU/ml +/- SD) was significantly higher in the PCOS groups compared with controls. A significant positive correlation was found between HOMA score and BMI in PCOS and control groups. Serum PAI-1 activity was significantly related to BMI and HOMA score. When considering two BMI subgroups, there was no significant difference in the relationship between serum PAI-1 activity and HOMA score in both the control and PCOS groups. No other significant relationship was found between serum PAI-1 activity and any other hormonal or metabolic parameter. In conclusion, women with PCOS have significantly elevated PAI-1 activity independent of obesity, and it is speculated that elevated PAI-1 activity may be a factor in the increased cardiovascular morbidity seen in PCOS.

Adolescent↗

PubMed2002

Obesity and the polycystic ovary syndrome.

The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype. Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and/or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.

Androgens↗

PubMed1998

Evidence for a genetic basis for hyperandrogenemia in polycystic ovary syndrome.

Our preliminary family studies have suggested that some female first-degree relatives of women with polycystic ovary syndrome (PCOS) have hyperandrogenemia per se. It was our hypothesis that this may be a genetic trait and thus could represent a phenotype suitable for linkage analysis. To investigate this hypothesis, we examined 115 sisters of 80 probands with PCOS from unrelated families. PCOS was diagnosed by the combination of elevated serum androgen levels and </=6 menses per year with the exclusion of secondary causes. The sisters were compared with 70 healthy age- and weight-comparable control women with regular menses, no clinical evidence of hyperandrogenemia, and normal glucose tolerance. Twenty-two percent of the sisters fulfilled diagnostic criteria for PCOS. In addition, 24% of the sisters had hyperandrogenemia and regular menstrual cycles. Circulating testosterone (T) and nonsex hormone-binding globulin-bound testosterone (uT) levels in both of these groups of sisters were significantly increased compared with unaffected sisters and control women (P < 0.0001 for both T and uT). Probands, sisters with PCOS, and hyperandrogenemic sisters had elevated serum luteinizing hormone levels compared with control women. We conclude that there is familial aggregation of hyperandrogenemia (with or without oligomenorrhea) in PCOS kindreds. In affected sisters, only one-half have oligomenorrhea and hyperandrogenemia characteristic of PCOS, whereas the remaining one-half have hyperandrogenemia per se. This familial aggregation of hyperandrogenemia in PCOS kindreds suggests that it is a genetic trait. We propose that hyperandrogenemia be used to assign affected status in linkage studies designed to identify PCOS genes.

Adolescent↗

PubMed2004

Prevalence of gestational diabetes mellitus and pregnancy outcomes in Asian women with polycystic ovary syndrome.

The aim of this study was to determine the prevalence of gestational diabetes mellitus (GDM) and the pregnancy outcomes in Asian women with polycystic ovary syndrome (PCOS). The retrospective cohort study was performed to compare pregnancy outcomes of 47 pregnancies in 41 PCOS women with 264 pregnancies in 222 women with normal menstruation. Logistic regression was used to assess the risk of PCOS on GDM, hypertensive disorder in pregnancy (HDP) and premature delivery. The mean age of both groups was 31 years. The mean body mass index (BMI) and proportion of BMI of > 25 kg/m2 were significantly higher in the PCOS than in the control group. There was no difference in the prevalence of GDM between the PCOS women and the high-risk group of the controls. The prevalence of HDP and premature delivery was significantly greater in PCOS women (21.3 and 13.3%) than in the controls (6.4 and 5.4%), respectively. PCOS was demonstrated as a risk factor for GDM and HDP with borderline statistical significance, but not for premature birth. The Cesarean section rate was higher in the PCOS than in the control group. In conclusion, the prevalence of GDM in Asian women with PCOS is high and comparable to those of a high-risk group.

Adult↗

PubMed2004

The impact of insulin resistance on the outcome of laparoscopic ovarian electrocautery in infertile women with the polycystic ovary syndrome.

In this study we assessed how insulin resistance affects pregnancy rates in infertile women with the polycystic ovary syndrome (PCOS) treated with laparoscopic ovarian electrocautery. Sixty-four PCOS women were included in the study in a consecutive fashion. Following the CIGMA (continuous infusion of glucose with model assessment) test, 28 women were classified as insulin resistant and 36 women as non-insulin resistant. After the ovarian electrocautery patients were observed for 12-18 months. If pregnancy did not ensue, they were referred for one or more cycles of in vitro fertilization (IVF). Following ovarian electrocautery the non-insulin-resistant women more frequently achieved a regular menstrual cycle and ovulation than the insulin-resistant PCOS women. Consequently 18 (50%) of the non-insulin-resistant PCOS women achieved a pregnancy versus only five (18%) of women in the insulin-resistant PCOS group. Following treatment with both ovarian electrocautery and IVF, 27 (75%) of the non-insulin resistant PCOS women achieved a successful pregnancy, while 13 (46%) of the insulin-resistant PCOS group achieved this. In conclusion, insulin resistance may be an important marker of a poor outcome of treatment in PCOS infertility. Further studies are needed to evaluate the possible effect of treatment alternatives to alleviate the unfavorable influences of insulin resistance and hyperinsulinemia on ovulation induction in PCOS women.

Adult↗

PubMed2005

Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-gamma gene in first-degree relatives of subjects with polycystic ovary syndrome.

AIM: This study was designed to examine the relationship between the Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-gamma (PPAR-gamma) gene and insulin resistance (IR) in first-degree relatives of subjects with polycystic ovary syndrome (PCOS). MATERIALS AND METHODS: One hundred and twenty family members of 55 patients with PCOS and 80 unrelated healthy control subjects without a family history of diabetes or PCOS were studied. IR was assessed by homeostatic model assessment (HOMA-IR) and area under the curve (AUC) for insulin during an oral glucose tolerance test in subjects with normal glucose tolerance and controls. Genetic analysis of the PPAR-gamma gene Pro12Ala polymorphism was performed by restriction fragment length polymorphism. RESULTS: Fasting insulin, HOMA-IR and AUC insulin were significantly higher in first-degree relatives of PCOS subjects than in controls. A significantly different allele distribution of the Pro12Ala polymorphism of PPAR-gamma was observed between the two groups, with the frequency of the variant Ala isoform being significantly reduced in the first-degree relatives of PCOS subjects (10.8%, 13 subjects) compared with the control group (22.5%, 18 subjects). All Pro12Ala polymorphisms of the PPAR-gamma gene were heterozygous. Compared with first-degree relatives of PCOS subjects with the Pro12Pro polymorphism of PPAR-gamma, first-degree relatives of PCOS subjects with the Pro12Ala polymorphism had low fasting insulin, HOMA-IR and AUC insulin levels. The combined prevalence rate for impaired glucose tolerance, impaired fasting glucose and diabetes was 40% (16 subjects) in mothers and 52% (20 subjects) in fathers of PCOS women. CONCLUSION: Our findings suggest that Pro12Ala PPAR-gamma gene polymorphism may be protective against IR and might prevent the development of diabetes mellitus in the first-degree relatives of subjects with PCOS.

Adolescent↗

PubMed2006

Vascular endothelial growth factor and basic fibroblast growth factor in polycystic ovary syndrome during controlled ovarian hyperstimulation.

BACKGROUND: Polycystic ovary syndrome (PCOS) is a common endocrine disorder that causes anovulation and consequent subfertility. It is well established that increased ovarian mass, supported by new blood vessel proliferation in stroma and theca, is a key feature of PCOS. Recent studies suggest a role for angiogenetic factors in this phenomenon. AIM: To evaluate of levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in serum and follicular fluid of PCOS patients during a controlled ovarian hyperstimulation. METHODS: In 52 patients undergoing in vitro fertilization treatments, 26 PCOS patients and 26 controls, serum VEGF and bFGF levels were assessed before starting administration of follicle-stimulating hormone (FSH) (day 0), on the day of administration of human chorionic gonadotropin (hCG) and on the day of oocyte retrieval. Follicular fluid levels of the two growth factors were detected on the day of oocyte retrieval. RESULTS: PCOS patients showed higher serum VEGF levels than controls before starting FSH administration, on the day of hCG administration and on the day of oocyte retrieval. Serum VEGF levels showed a rise after hCG administration only in the PCOS patients. In addition, serum bFGF levels were higher in PCOS patients than in controls on the day of hCG administration and the day of oocyte retrieval. Furthermore, on the day of hCG administration, serum bFGF levels were directly correlated to the amount of FSH previously administered (p < 0.0001). In follicular fluid, higher VEGF and bFGF levels were found in PCOS patients than in controls. Furthermore, follicular-fluid bFGF concentrations were inversely correlated with the percentage of mature oocytes collected (p < 0.05). CONCLUSIONS: The present study revealed elevated levels of VEGF and bFGF in serum and follicular fluid in PCOS patients compared with controls. bFGF seems to be an FSH-dependent growth factor and its levels in follicular fluid are inversely correlated with the percentage of mature oocytes collected.

Case-Control Studies↗

PubMed1997

The chromosomal normality of unfertilized oocytes from patients with polycystic ovarian syndrome.

The present study was designed to compare the cycle characteristics of in-vitro fertilization (IVF) and the chromosomal normality of oocytes in patients with polycystic ovarian syndrome (PCOS) with those of patients with tubal factor infertility. In all, 28 cycles of 24 PCOS patients and 55 cycles of 31 patients with tubal factor infertility (control) were investigated. Although a significantly greater number of oocytes were retrieved from PCOS patients (mean +/- SD: 15.6 +/- 6.4 versus 9.0 +/- 4.0, PCOS versus control group, P < 0.05), the percentage of fertilized oocytes was significantly lower in the PCOS group compared with controls (40.1 versus 73.8%, P < 0.01). The pregnancy rate per embryo transfer did not differ between the two groups. Cytogenetic analysis was performed on 74 oocytes from PCOS patients and 73 oocytes from control patients. In the PCOS group, 10 of the 74 oocytes (13.5%) demonstrated aneuploidy, four (5.4%) oocytes were diploid and six (8.1%) oocytes were metaphase II with a prematurely condensed sperm chromosome (PCC). In the tubal infertility group, nine of the 73 (12.3%) oocytes showed aneuploidy, four (5.5%) oocytes were diploid and five (6.8%) oocytes were found to have PCC. There was no significant difference in the aneuploidy, diploidy and PCC rates between the two groups. These results suggest that the reduced fertilization observed in PCOS is not attributable to chromosomal aberrations or immaturity of oocytes recruited from patients with PCOS.

Adult↗

PubMed1997

17-Hydroxyprogesterone responses to gonadotrophin-releasing hormone agonist buserelin and adrenocorticotrophin in polycystic ovary syndrome: investigation of adrenal and ovarian cytochrome P450c17alpha dysregulation.

Abnormal regulation of cytochrome P450c17alpha causes the exaggerated secretion of ovarian androgens in polycystic ovary syndrome (PCOS). This enzyme is active in both the ovaries and adrenal glands. We examined whether there is an abnormal regulation of cytochrome P450c17alpha in the adrenal gland by investigating the relationship of 17-hydroxyprogesterone (17-OH progesterone) hyperresponsiveness to the gonadotrophin releasing hormone (GnRH) agonist, buserelin, testing with 17-OH progesterone response to adrenocorticotrophic hormone (ACTH) in PCOS. In all, 68 women with PCOS and 24 normal women were included in the study. Ultrasound, clinical and hormonal parameters were used to define PCOS. 17-OH progesterone response to ACTH was measured in all the women. In 52 of the 68 women with PCOS, 17-OH progesterone response to buserelin was measured. The mean basal 17-OH progesterone concentrations were similar in both PCOS and control groups. PCOS women had significantly higher net increment in 17-OH progesterone after ACTH administration (P<0.02). No significant correlations were found between the peak 17-OH progesterone values, the net increments in 17-OH progesterone and the area under the 17-OH progesterone-response curves after ACTH stimulation and buserelin test. Although 17-OH progesterone response to ACTH was significantly higher in the patients with PCOS than in the control subjects, the lack of relationship between 17-OH progesterone response to GnRH agonist buserelin and 17-OH progesterone response to ACTH stimulation suggests that the dysregulation of the cytochrome P450c17alpha enzyme may not play a role in adrenal androgen excess seen in PCOS.

17-alpha-Hydroxyprogesterone↗

PubMed1998

Inhibin A, inhibin B and activin A concentrations in follicular fluid from women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is characterized by arrested follicle development at the early antral stage. Alterations in inhibin production by developing follicles could be involved in PCOS by suppressing follicle stimulating hormone concentrations during the follicular phase of the menstrual cycle as well as by increasing thecal androgen production. Inhibin B appears to be more important than inhibin A during the follicular phase; however, there are no data regarding the follicular fluid concentrations of inhibin B in PCOS. The purpose of this study was to compare inhibin A, inhibin B and activin A concentrations in the follicular fluid from regularly cycling women and women with PCOS. Inhibin A, inhibin B and activin A were measured in the follicular fluid of 4-7 mm follicles from PCOS ovaries and size-matched follicles from normally cycling women by specific and sensitive two-site enzyme-linked immunosorbent assays. In both control and polycystic ovaries, inhibin B was approximately 10-fold higher than activin A and more than 100-fold higher than inhibin A. There was no difference in activin A concentrations between PCOS and control follicles. In control ovaries, the inhibin B and inhibin A concentrations in dominant follicles were significantly higher than in cohort follicles. While inhibin A concentrations were lower in PCOS follicles than in normal cohort follicles, there was no difference in inhibin B concentrations between PCOS follicles and normal cohort follicles. These data are consistent with the concept that inhibin B is the physiologically most important form of inhibin during the follicular phase of the menstrual cycle and indicate that PCOS is not associated with increased inhibin B concentrations in follicular fluid.

Activins↗

PubMed1998

Utero-ovarian arterial blood flow and hormonal profile in patients with polycystic ovary syndrome.

Utero-ovarian arterial blood flow and hormonal profile were evaluated in 20 patients with polycystic ovary syndrome (PCOS) and in 22 patients with normal menstrual cycle (NMC) undergoing in-vitro fertilization (IVF) treatment. In this controlled prospective clinical study the vascular impedance in the utero-ovarian arteries was measured in both groups on days 4, 13, 22 [introduction of gonadotrophin releasing hormone agonist (GnRHa) administration], 36 (after the 14 day GnRHa administration) and on the day of human chorionic gonadotrophin (HCG) administration. Simultaneously, serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), oestradiol, androstendione and sex hormone-binding globulin (SHBG) were determined. In the PCOS group significantly (P < 0.05) higher concentrations of FSH and LH were found on day 22, whereas the excess of androstendione production and lower SHBG values were registered throughout the studied cycles. Also, no effect of the 14 day GnRHa administration on the androstendione discharge was registered. In both groups the serum LH concentration decreased significantly (P < 0.05); however, the value remained significantly (P < 0.05) higher in the PCOS group. In the PCOS group no changes regarding the vascular impedance in the uterine artery were registered in the phase of the cycle preceding the GnRHa administration. The resistance index (RI) on day 22 of the cycle was 0.86 in the PCOS and 0.82 in the NMC group. In the NMC group the active ovary showed dramatic changes during the cycle, with vascular impedance almost constant throughout the cycle in the inactive ovary. In the PCOS group the vascular impedance to ovarian arterial blood flow in both ovaries was similar to that in inactive ovaries in the NMC group. After the 14 day GnRHa administration the utero-ovarian vascular impedance was high in both groups with changes registered only in the NMC group, as the PCOS patients exhibited maximal vascular impedance throughout the cycle. On the day of HCG administration strong negative correlation between the vascular impedance in the uterine artery and the serum oestradiol concentration in stimulated cycles was found in both groups, but not in anovulatory PCOS patients. As in PCOS patients the utero-ovarian vascular impedance was raised throughout the cycle we concluded that the 14 day GnRHa administration neither affected the utero-ovarian arterial blood flow nor suppressed the androstendione discharge.

Arteries↗