PubMed Health⌕ Search

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 1,189 records · Page 66Linked to original sources

Serum PSA levels are not affected by the menstrual cycle or the menopause, but are increased in subjects with polycystic ovary syndrome.

BACKGROUND/AIMS: Prostatic specific antigen (PSA) is the most specific prostatic tumor marker in man. Recently, PSA has been detected in a variety of tissues and fluids in women, and its determination suggested as a marker of hyperandrogenism. However, precise information about the physiology of PSA in females is not available. The goal of this study was to assess serum concentrations of PSA in healthy pre-menopausal women (healthy pre-menopausal group), menopausal women (menopause group) and patients with polycystic ovary syndrome (PCOS group). METHODS: PSA, androgens, LH, FSH, 17-beta-estradiol (E2), progesterone (Pg) were assessed in 40 post-menopausal women, 35 fertile controls and 35 women with PCOS. RESULTS: No significant difference in PSA concentrations could be demonstrated in different phases of the menstrual cycle in healthy pre-menopausal group and between pre- and post-menopausal groups. No correlations could be demonstrated between serum PSA levels and the following parameters: age, body mass index (BMI), LH, FSH, E2, testosterone (T), DHEAS, and SHBG, both in pre- and post-menopausal women. Significantly higher PSA levels (median=14 pg/ml) were found in the PCOS group compared to both pre-menopausal (median=5 pg/ml) and menopausal (median= 5 pg/ml) groups (p< 0.05). CONCLUSIONS: only minor fluctuations of serum PSA concentrations are observed in healthy pre- and post-menopausal women, while serum level is higher in PCOS, and therefore PSA can be considered a suitable marker of female hyperandrogenism.

Adult↗

CYP17 gene analysis in hyperandrogenised women with and without exaggerated 17-hydroxyprogesterone response to ovarian stimulation.

Nine patients with polycystic ovary syndrome (PCOS) and exaggerated serum level of 17-hydroxyprogesterone (17-OHP) response to gonadotropin (GnRH) agonist stimulation, and seven patients with PCOS, but normal 17-OHP response have been analysed for possible linkage of PCOS with genetic defects on the 17 alpha-hydroxylase/17,20-lyase gene (CYP17). A portion of the regulatory and the entire coding domain for this enzyme have been analysed by PCR-SSCP analysis. Samples have been also screened for the previously reported -34 bp polymorphism, which creates a new SP1-type promoter site, but was excluded as the primary genetic defect. We have varied gel concentrations, reduced running temperatures, added glycerol to polyacrylamide gels and performed electrophoresis on longer gels in order to improve the resolving power of SSCP. Screening of the CYP17 gene revealed no mutations associated with the disease in the examined group of patients. Also, the -34 bp polymorphism proved to be equally distributed among patient and control samples, which in our case were non-related. The results indicate that, when germline mutations in question, CYP17 may be excluded as a candidate gene for these subtypes of PCOS.

17-alpha-Hydroxyprogesterone↗

Gonadotropin evaluation in the diagnosis of polycystic ovary syndrome using either a monoclonal or a polyclonal antibody radioimmunoassay.

The LH/FSH ratio values between gonadotropins dosed with a monoclonal antibody assay (IRMA) in the micropolycystic ovary syndrome (PCOS), are discussed and compared to those obtained with the classic assays using polyclonal antibodies. Because of the higher selectivity of this IRMA assay it is noteworthy that the cut-off value between normal and PCOS patients is now equal to or above one. The evaluation of the LH/FSH ratio between the peak values of the two gonadotropins after a GnRH 100 micrograms iv bolus, may be useful in the diagnosis of PCOS in those patients who present an LH/FSH less than 1 in basal conditions even in the presence of clinical and ecographic aspects of PCOS.

Adolescent↗

Polysystic ovary syndrome--loss of the apoptotic mechanism in the ovarian follicles?

Polycystic ovary syndrome (PCOS) is the most prevalent female endocrinopathy and the largest single cause of anovulatory infertility. The PCOS is characterized by multiple small antral follicles arrested in their development but nonatretic and viable. The hyperexpression of some growth factors (e.g. EGF/TGF alpha) in PCOS, considered to be survival or antiapoptotic factors, led to the hypothesis of their involvement in the blocking of apoptosis and atresia leading to an accumulation of multiple small antral follicles. Diminished FSH stimulation and accumulation of androgens could explain the arrest of progress to the preovulatory stage. Further investigation of the pathogenesis of PCOS is needed on the modulation of tumour suppressor and apoptosis genes such as p53, BAX or the APO/FAS system and the over expression of survival genes such as BCL2.

Apoptosis↗

Insights into hypothalamic-pituitary dysfunction in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is characterized by menstrual dysfunction and hyperandrogenism in the absence of other known causes. While the pathogenesis of PCOS remains elusive and is likely to involve abnormalities in several systems, there has long been an association of abnormal gonadotropin secretion with this disorder. In recent studies we have determined that 94% of women meeting the broad criteria for PCOS have an increased LH/FSH ratio. Several lines of evidence suggest that the mechanisms underlying the increased LH/FSH ratio in PCOS include an increased frequency of GnRH secretion. Decreased sensitivity to progesterone negative feedback on the GnRH pulse generator may play a role in this neuroendocrine defect. Additional factors which may contribute to the low to normal FSH levels in the face of increased LH include chronic mild estrogen increases and possibly inhibin. In addition to these effects on the differential control of FSH, there is increased pituitary sensitivity of LH secretion to GnRH. Both estrogen and androgens have been proposed as candidates mediating these effects. Superimposed on these underlying abnormalities in gonadotropin secretion is a marked inhibitory effect of obesity on LH secretion which may be mediated at either a pituitary or hypothalamic level.

Female↗

Serum prostate specific antigen levels in women with polycystic ovary syndrome and the effect of flutamide+desogestrel/ethinyl estradiol combination.

BACKGROUND: Prostate-specific antigen (PSA) is expressed in many female tissues and its concentrations were higher in hirsute subjects. We aimed to determine serum PSA level in hirsute women and evaluate the effect of flutamide+desogestrel/ethynil estradiol combination. SUBJECTS AND STUDY DESIGN: Thirty patients with polycystic ovary syndrome (PCOS) and 30 healthy controls were studied. Hirsutism was defined by modified Ferriman-Gallwey score (FGS). Free androgen index (FAI) was used for hyperandrogenism. Patients received flutamide (500 mg/d) and oral contraceptive (desogestrel+ethinyl estradiol) for 9 months. RESULTS: Mean FGS (p<0.0001), insulin (p<0.01), FAI (0.0001), androstenedione (p<0.0001), LH (p<0.05), and free testosterone (p<0.003) levels of patients with PCOS were higher than the control group. Mean serum total and free PSA level of PCOS patients were higher than the control group (p<0.0001 and p<0.0001). We found a positive correlation between total PSA levels and FGS (r=0.568, p<0.001), FAI and FGS (r=0.456 and p<0.01). There was also a positive correlation between FAI and total PSA (r=0.503 and p<0.005). At the end of treatment, FGS, androstenedione, free and total testosterone, FAI, serum PSA and LH levels decreased significantly [serum total PSA was 0.0208 +/- 0.0178 ng/ml at baseline and 0.0061 +/- 0.0044 ng/ml after treatment (p<0.0001)]. CONCLUSIONS: 1. Serum prostate specific antigen level is higher in patients with PCOS; 2. There is a positive correlation among FGS, FAI and PSA levels; 3. Serum PSA levels decrease with antiandrogen treatment; 4. Serum PSA measurement might be a marker for hirsutism.

Adolescent↗

Polycystic ovary syndrome: etiology and pathogenesis.

OBJECTIVE: To provide a review of the pathogenesis of polycystic ovary syndrome. DESIGN: Literature survey. RESULT(S): Three major pathophysiologic hypotheses have been proposed to explain the clinical findings of polycystic ovary syndrome (PCOS) related to three major laboratory findings: the LH hypothesis, the insulin hypothesis and the ovarian hypothesis. Although the presence of many small follicles with a high androgen to estrogen ratio was first thought to represent a high rate of follicular atresia in polycystic ovaries, recent studies have demonstrated that the granulosa cells are viable and able to respond to FSH stimulation with normal increases in estradiol production. Thus, a new hypothesis has arisen that FSH activity is somehow blocked at the ovarian level. CONCLUSION(S): PCOS is a syndrome involving defects in primary cellular control mechanisms that result in the expression of chronic anovulation and hyperandrogenism. In this syndrome, the relation between the various parameters is of particular interest. These relations constitute the cornerstone of the pathogenesis of PCOS. The fact that the pathogenesis of PCOS has not yet been clarified, despite the plethora of relative information, may be the result of a general way of thinking in the interpretation of several scientific data, and especially those that refer to biochemical phenomena. The use of the various models of the theory of chaos, that permits a concrete approach for the interpretation of data, may constitute an optional procedure for the future understanding of the association of different parameters and their disturbances in the pathogenesis of the polycystic ovary syndrome.

Female↗

Odd variation of 75 g oral glucose tolerance test results in a Japanese patient with polycystic ovary syndrome: a case report.

We report a young woman of normal body weight who was diagnosed with polycystic ovary syndrome (PCOS) and had an odd variation of 75 g oral glucose tolerance test (OGTT). This woman underwent the 75 g OGTT to evaluate the association between PCOS and insulin secretion capacity. Although the blood sugar levels were within normal range before the OGTT load test, we noted an odd variation of insulin response in which a condition of hyperinsulinemia after the load test was followed suddenly by hypoglycemia. Hyperandrogenism in the PCOS patient and insulin resistance indicated by 75 g OGTT suggest that insulin may influence the ovary and that there could be an association between this disease and insulin resistance. The insulinogenic index in this case showed higher than normal values, demonstrating that there was a positive correlation between hyperinsulinemia and insulin resistance. This patient experienced ovulation followed by pregnancy after treatment with an herbal medicine called Shakuyaku-Kanzo-To. We believed that identifying the subset of PCOS woman who is insulin resistant may be useful, as this resistance could be import in terms of follow-up and future exploration.

Adult↗

Metformin improves ovulation and pregnancy rates in patients with polycystic ovary syndrome.

We evaluated the fertility promoting effect of metformin in infertile patients with polycystic ovary syndrome. Twenty-nine infertile patients with polycystic ovary syndrome (PCOS) are included in our prospectively designed study and 15 normal menstruating women served as controls for reproductive hormones and ovarian volumes. All PCOS patients received a total of 78 cycles of clomiphene citrate (CC) in the beginning, then patients who could not get pregnant were switched to metformin plus clomiphene citrate. PCOS patients served as their own controls for the ovulation and pregnancy rates. At the end of the CC cycles 4.2% of patients got pregnant and 65.2% of the remaining group got pregnant with metformin plus CC cycles (p=0.0001). We have not observed any serious side effects of metformin. The high pregnancy rate of our study population is consistent with the hypothesis that insulin resistance plays an important role in the pathogenesis of anovulation in patients with PCOS.

Adult↗

Prenatal Androgenization Modifies H3K9me3 Binding in the Promoter of the Androgen Receptor Gene in the Arcuate Nucleus of the Adult Female Mouse.

Animal models have shown that prenatal exposure to excess androgens is associated with the development of polycystic ovary syndrome (PCOS) features. We have identified that prenatally androgenized (PNA) mice modelling PCOS show suppressed androgen receptor mRNA (Ar) expression in the arcuate nucleus (ARC) across development. This could contribute to PCOS-related impaired gonadal steroid hormone feedback to GnRH neurons. However, the mechanism of Ar mRNA suppression following PNA is not determined. We performed a chromatin immunoprecipitation (ChIP) assay coupled with quantitative PCR (qPCR) to investigate histone and transcription factor binding within the Ar gene promoter or enhancer regions in the ARC of female mice at postnatal day (P)60 or gestational day (GD)18.5. In comparison to adult vehicle control (VEH) mice, our ChIP-qPCR revealed that H3K9me3, a repressive histone mark, was increased in adult PNA mice at the promoter regions of the Ar gene. H3K27ac, an active histone mark, and SP1, a transcription factor that acts as a positive regulator of gene expression, were unchanged in the same regions. Increased H3K9me3 seen at the promoter region in adult PNA mice, however, was not observed in the GD18.5 mice ARC following PNA. These results suggest that the deposition of H3K9me3 on the Ar promoter is unlikely to be established by PNA at the time of excess androgen exposure, and instead is likely to be established later in postnatal development or in adulthood. These data provide greater understanding of the developmental mechanisms and timeline underpinning PNA-mediated female dysfunction and PCOS-like reproductive physiology.

Animals↗

Pituitary response to bolus and continuous intravenous infusion of luteinizing hormone-releasing factor in normal women and women with polycystic ovarian syndrome.

Plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were measured in response to luteinizing hormone-releasing factor (LRF), given as a 100 microgram intravenous bolus and/or as a 4 hour infusion of 0.2 microgram per minute to 27 normal menstruating women and 15 women with the polycystic ovarian syndrome (PCOS). In PCOS, LH response to bolus LRF was significantly greater than those of normal women at days 1 to 4 and 8 to 10 of the cycle, whereas FSH responses were similar in all women studied. Continuous LRF infusion resulted in a biphasic LH release pattern. In normal women, the early phase was low until days 12 to 14 of the normal cycle, whereas the second phase rose progressively from the early follicular to the periovulatory period. In PCOS, the early phase was relatively large and qualitatively resembled the normal periovulatory pattern. The increased pituitary LH response to LRF in PCOS is associated with a relatively large early releasable LH pool and a low FSH response.

Adolescent↗

Effect of para-chloromercuribenzenesulfonic acid and temperature on cell water osmotic permeability of proximal straight tubules.

The apparent Arrhenius energy of activation (Ea) of the water osmotic permeability (Pcos) of the basolateral plasma cell membrane of isolated rabbit proximal straight tubules has been measured under control conditions and after addition of 2.5 mM of the sulfhydryl reagent, para-chloromercuribenzenesulfonic acid (pCMBS), of mersalyl and of dithiothreitol. Ea (kcal/mol) was 3.2 +/- 1.4 (controls) and 9.2 +/- 2.2 (pCMBS), while Pcos decreased with pCMBS to 0.26 +/- 0.17 of its control value. Mersalyl also decreased Pcos both in vitro and in vivo (using therapeutical doses). These actions of pCMBS and mersalyl were quickly reverted with 5 mM dithiothreitol and prevented by 0.1 M thiourea. Ea for free viscous flow is 4.2 and greater than 10 for non-pore-containing lipid membranes. By analogy with these membranes and with red blood cells, where similar effects of pCMBS on Pos are observed, it is concluded that cell membranes of the proximal tubule are pierced by aqueous pores which are reversibly shut by pCMBS. Part of the action of mercurial diuretics can be explained by their action on Pcos.

Animals↗

Effects of the somatostatin analogue, octreotide, in polycystic ovary syndrome.

In view of the association of hyperinsulinemia with elevated luteinizing hormone (LH) levels and hyperandrogenism in polycystic ovary syndrome (PCOS), the effect of octreotide was investigated in women with PCOS. Twelve amenorrheic women were treated with 100 micrograms octreotide twice a day for 7 days; 13 infertile women unresponsive to clomiphene citrate were treated either with octreotide (100 micrograms twice a day from day 1 of the menstrual cycle until corpus luteum formation) in addition to human menopausal gonadotropins (HMG) or with HMG alone. Octreotide significantly reduced the 4-hour integrated LH concentrations. LH pulse amplitude and nadir concentrations, and LH, testosterone, androstenedione, and estradiol responses to a gonadotropin-releasing hormone (GnRH) analogue in amenorrheic PCOS women. Octreotide treatment also resulted in a more "appropriate" hormonal milieu at the time of human chorionic gonadotropin (HCG) injection in the infertile women, with LH and testosterone levels being reduced while follicle-stimulating hormone (FSH) levels increased. Orderly follicular growth occurred, with one or two mature follicles being present at the time of HCG injection in cycles in which octreotide was given together with HMG. There were no cases of hyperstimulation, even in women who had previously hyperstimulated after HMG alone. Octreotide thus inhibits LH and androgen secretion and may improve ovulatory performance in infertile women with PCOS.

Adolescent↗

Ovulation induction in polycystic ovary syndrome: a review of conservative and new treatment modalities.

Polycystic ovary syndrome (PCOS) is a complex disorder with heterogeneous clinical and endocrine features. Chronic anovulation and infertility are common and affect about 75% of the patients. Ovulation induction in PCOS patients is a challenge for the physicians who treat these patients. Several different treatment modalities have been proposed to induce ovulation in PCOS, each of which deals with a different clinical or endocrine disorder which is present in these patients. This review presents traditional and new methods for ovulation induction in PCOS patients, the theoretical background, the pros and cons for each treatment and success rate.

Clomiphene↗

Inhibitory effect of sandostatin on secretion of luteinising hormone and ovarian steroids in polycystic ovary syndrome.

Hyperinsulinism accompanies the raised luteinising hormone (LH) concentrations in women with the polycystic ovary syndrome (PCOS). Somatostatin inhibits insulin and LH secretion in healthy adults, so the effect of treatment with a long-acting somatostatin analogue ('Sandostatin') on gonadotropin and androgen secretion in PCOS was investigated. LH pulsatility, androgen concentrations, and hormonal responses to an oral glucose load and to administration of a GnRH agonist (buserelin) were measured before and after 7 days' treatment with sandostatin 100 micrograms subcutaneously twice a day in 10 amenorrhoeic women with classic features of PCOS. Sandostatin significantly reduced integrated LH concentrations and LH pulse amplitudes, oestradiol, testosterone, and androstenedione concentrations, and LH responses to buserelin; it also suppressed insulin and C-peptide responses to an oral glucose load. Thus sandostatin inhibits pituitary and ovarian hormonal responses in part by a direct influence on pituitary activity, and the possibility of an indirect effect mediated by changes in insulin concentrations requires investigation. These findings have implications for the treatment of infertility in women with PCOS.

Adolescent↗

Insulin-like growth factor binding protein-2, 28 kDa and 24 kDa insulin-like growth factor binding protein levels are decreased in fluid of dominant follicles, obtained from normal and polycystic ovaries.

In order to investigate potential changes in insulin-like growth factor binding proteins (IGFBPs) during human follicle maturation, we examined the IGFBP profiles in follicular fluid from follicles in different stages of maturation. Samples were obtained from ovaries of women with regular menstrual cycles and of subjects with cycle abnormalities and polycystic ovaries (diagnosed as polycystic ovary syndrome (PCOS)) and analyzed by Western ligand blotting. IGFBPs of 43 kDa, 37 kDa, 31 kDa, a doublet around 28 kDa and a minor band of 24 kDa were detected in follicle fluid of normal non-dominant (size < 10 mm) and atretic (androstenedione/estradiol ratio > 4) follicles of both regularly menstruating women and PCOS patients. The 43 and 37 kDa IGFBPs could be identified as IGFBP-3 and the 31 kDa IGFBP as IGFBP-2, whereas the 28 kDa IGFBP could not be identified as IGFBP-1, all by immunoblotting techniques. A dramatic decrease in IGFBP-2, the 28 kDa and 24 kDa IGFBPs was observed in follicular fluid of dominant follicles (size > 10 mm) of both regular menstruating individuals and one PCOS patient as compared with follicular fluid of normal non-dominant or atretic follicles. These observations indicate that the PCOS follicle may not be different from normal with respect to IGFBP profiles. Furthermore, these results suggest that at least one of these IGFBPs might be involved in human folliculogenesis.

Adult↗

Sex hormone-binding globulin and female reproductive function.

Although sex steroids have long been known to influence serum concentrations of SHBG, it is now recognized that nutritional factors may be more important in the regulation of SHBG in women. Thus, SHBG concentrations are negatively correlated with body mass index (BMI) and, more particularly, to indices of central adiposity. Polycystic ovary syndrome (PCOS), the most common cause of anovulatory infertility, is associated with truncal obesity, hyperandrogenism and hyperinsulinaemia. There is evidence that insulin may be the humoral mediator of the weight-dependent changes in SHBG. Serum SHBG concentrations are inversely correlated with both fasting and glucose-stimulated insulin levels, and insulin has been shown to have a direct inhibitory effect on SHBG synthesis and secretion by hepatocytes in culture. However, the interrelationship of BMI, insulin and SHBG appears to be different in women with PCOS from that in normal subjects. The clinical importance of the weight-related suppression of SHBG is illustrated by the finding of a greater prevalence of hirsutism in obese women PCOS compared with their lean counterparts. Obese subjects with PCOS have similar total testosterone concentrations to lean PCO women but have lower SHBG and reciprocally higher free testosterone levels. Calorie restriction results in reduction of serum insulin followed by an increase in SHBG and a fall in free testosterone but an isocaloric, low-fat diet has no significant effect on SHBG concentrations. Weight reduction in obese, hyperandrogenaemic women with PCO is an important approach to the management of both anovulation and hirsutism.

Diet↗

The insulin resistant subphenotype of polycystic ovary syndrome: clinical parameters and pathogenesis.

OBJECTIVE: This study was undertaken to compare clinical and biochemical characteristics of the insulin resistant (IR) and non-IR subphenotypes of polycystic ovary syndrome (PCOS). STUDY DESIGN: Infertile PCOS women were classified as IR (n=32) or non-IR (n=46) on the basis of fasting glucose and insulin levels. The incidence of acanthosis nigricans (AN), hirsutism, and ovulation in response to clomiphene citrate (CC) was compared between the 2 groups, along with serum levels of gonadotropins, and sex steroids. Blood samples from 28 PCOS patients and 8 controls were analyzed by enzymatic immunoassay for autophosphorylated insulin receptor (APIR) and total insulin receptor (TIR) content. RESULTS: Insulin resistance was associated with obesity (odds ratio [OR]=3.5, P <.05), AN (OR=6.0, P <.05), hirsutism (OR=3.1, P <.05), and resistance to CC (OR=5.0, P <.05). Mean levels of LH, LH/FSH ratios, and testosterone were lower in women with IR (11.5 +/- 6.8 mIU/mL, 2.0 +/- 1.0, and 56.6 +/- 29.0 ng/dL, respectively) compared with women without IR (15.0 +/- 13.4 mIU/mL, 2.4 +/- 1.5, and 72.5 +/- 29.8 ng/dL, respectively) (P <.05). Mean APIR/TIR ratios in IR women were lower than in non-IR women (P <.05 at 100 nmol/L of insulin) and controls (P <.01 at 1, 10 and 100 nmol/L insulin). CONCLUSION: Patients with IR are more likely to be obese and have AN, hirsutism, resistance to CC, and lower LH, LH/FSH ratios, and testosterone levels. Furthermore, IR patients appear to have defective autophosphorylation of the insulin receptor, a key element in insulin action, and a possible mechanism for IR in PCOS.

Adult↗