Increased circulating levels of immunoreactive beta-endorphin in polycystic ovary syndrome is not caused by increased pituitary secretion.

OBJECTIVE: Our purpose was to investigate the source and role of elevated levels of immunoreactive beta-endorphin in polycystic ovary syndrome. We wished to determine whether immunoreactive beta-endorphin secretion in patients with polycystic ovary syndrome is influenced by body weight and whether the pituitary release of immunoreactive beta-endorphin with corticotropin-releasing hormone is related to luteinizing hormone levels or adrenal androgen secretion. STUDY DESIGN: Eighteen patients with polycystic ovary syndrome and 10 ovulatory controls were studied. Each subject received 1 microgram/kg intravenous corticotropin-releasing hormone and an oral glucose tolerance test on alternate days. Levels of plasma immunoreactive beta-endorphin, corticotropin, luteinizing hormone, cortisol, adrenal androgens, and insulin were measured. RESULTS: Although immunoreactive beta-endorphin levels were elevated in patients with polycystic ovary syndrome (p < 0.01), incremental responses after corticotropin-releasing hormone were similar to controls and were not influenced by body weight. Serum luteinizing hormone levels were not affected by corticotropin-releasing hormone and did not correlate with immunoreactive beta-endorphin levels. Adrenal androgen responses after corticotropin-releasing hormone were increased in patients with polycystic ovary syndrome (p < 0.01) but were not correlated with immunoreactive beta-endorphin secretion. After oral glucose was given, elevated fasting insulin levels increased significantly in patients with polycystic ovary syndrome (p < 0.01), as did immunoreactive beta-endorphin levels (p < 0.05). The increases in insulin and immunoreactive beta-endorphin levels were correlated (p < 0.05). CONCLUSIONS: Pituitary secretion of immunoreactive beta-endorphin is normal in patients with polycystic ovary syndrome, and pancreatic secretion appears to be increased. Corticotropin-releasing hormone does not influence luteinizing hormone levels, and adrenal androgen sensitivity is not influenced by immunoreactive beta-endorphin secretion.     

The control of bioactive luteinizing hormone secretion in women with polycystic ovary syndrome

Serum bioactive luteinizing hormone (LH) is elevated in virtually all patients with polycystic ovary syndrome, whereas serum immunoreactive LH may not be increased. The resultant increase in the bioactive: immunoreactive LH ratio in polycystic ovary syndrome leads to the suggestion that a more biologically active form of LH may be secreted in patients with polycystic ovary syndrome. This study was designed to investigate the control of bioactive LH in polycystic ovary syndrome. Compared to matched control subjects, seven patients with polycystic ovary syndrome had higher levels of serum immunoreactive LH (24 +/- 3 mlU/ml), immunoreactive LH: follicle-stimulating hormone (FSH) ratios (4.6 +/- 0.6), bioactive LH (98 +/- 27 mlU/ml), and bioactive: immunoreactive LH ratios (4.6 +/- 0.5). Serum testosterone (64 +/- 10 ng/ml), unbound testosterone (16 +/- 3 mg/dl), and unbound estradiol (49 +/- 5 pg/ml) were also higher. In response to 150 micrograms of intravenous gonadotropin-releasing hormone, increments of both bioactive LH and immunoreactive LH were higher than those in control subjects, but the bioactive: immunoreactive LH ratio was unaltered. Although urinary homovanillic acid was lower in polycystic ovary syndrome, it did not correlate with the bioactive: immunoreactive LH ratio. Similarly, the bioactive: immunoreactive LH ratio was not altered by 1 week of L-dopa (500 mg) or after another week of L-dopa (400 mg) with carbidopa (100 mg) 1 month later. Although baseline unbound estradiol correlated with the delta maximum response of bioactive LH after gonadotropin-releasing hormone (r = 0.65, p less than 0.05), unbound estradiol did not correlate with the bioactive: immunoreactive LH ratio. However, there was a significant positive correlation between the baseline bioactive: immunoreactive LH and the increased delta maximum responses of both immunoreactive LH (r = 0.55) and bioactive LH (r = 0.58), p less than 0.05. These data suggest that, although gonadotropin-releasing hormone stimulation, dopamine, and estrogen may not selectively increase the pituitary secretion of bioactive LH, the sensitivity of the pituitary gland itself and the hyperdynamic state of gonadotropin secretion in polycystic ovary syndrome may result in the increased secretion of bioactive LH.     

Serum inhibin levels in polycystic ovary syndrome: effect of insulin resistance and insulin secretion

Insulin resistance is common in women with the polycystic ovary syndrome. We investigated the relationship between insulin resistance and the serum inhibin concentration in a group of 19 women with polycystic ovary syndrome and eight control subjects at different phases of the menstrual cycle. Insulin resistance was measured by the frequently sampled intravenous glucose tolerance test, and inhibin was measured by a specific radioimmunoassay. Insulin sensitivity (mean +/- SE) was significantly reduced in the polycystic ovary syndrome group compared with controls: reduced insulin sensitivity 46.7 +/- 5.0 min-1/(nmol/mL), normally insulin-sensitive 106.6 +/- 11.7 min-1/(nmol/mL) (P less than .01). The women with polycystic ovary syndrome had inhibin levels (126 +/- 15.2 microLEq/mL) comparable to those found during the early follicular phase of the control group (117 +/- 22.1 microLEq/mL), but significantly lower than late follicular phase (259 +/- 25.6 microLEq/mL) or luteal phase (448 +/- 91.8 microLEq/mL) levels in the control group. No association was found between the degree of insulin resistance and the inhibin concentration, which remained unaltered over a 3-hour period despite maximal stimulation of endogenous insulin secretion. The inhibin concentrations in polycystic ovary syndrome may reflect impaired follicular maturation. Inhibin secretion is not acutely affected by insulin secretion in normal or in hyperandrogenic women.     

Effects of unkei-to, an herbal medicine, on endocrine function and ovulation in women with high basal levels of luteinizing hormone secretion

OBJECTIVE: To treat anovulatory women with high plasma LH levels with unkei-to. STUDY DESIGN: A total of 100 patients with polycystic ovary syndrome (n = 38) or non-polycystic ovary syndrome (n = 62) were allocated randomly into two groups. Endocrine levels (FSH, LH and estradiol), follicle growth and response to unkei-to were compared for 52 subjects in the unkei-to group and 48 subjects in the control group. RESULTS: Unkei-to induced significant decreases in plasma LH in polycystic ovary syndrome and non-polycystic ovary syndrome with high LH levels. Plasma estradiol levels increased significantly (43.5%) in eight weeks of treatment with unkei-to. Significant development of the dominant follicle was also observed in patients treated with unkei-to. When women suffering from ovulatory failure or irregular menstruation and having high plasma LH concentration were treated with unkei-to for eight weeks, a reduction in the serum LH level of at least 1 SD from baseline was noted in 45.5% of polycystic ovary syndrome patients and in 80.0% of non-polycystic ovary syndrome patients. The mean rate of reduction of serum LH was 22.2 +/- 35.7% in polycystic ovary syndrome patients and 49.7 +/- 15.3% in non-polycystic ovary syndrome patients. This reduction was significant in the non-polycystic ovary syndrome patients (P = .030). The rate of menstrual cycle improvement, including successful ovulation, was 50.0% in the polycystic ovary syndrome group and 60.0% in the non-polycystic ovary syndrome group, with no significant difference between the two groups.     

Ovarian follicular fluid beta-endorphin levels in normal and polycystic ovaries

The possibility of local ovarian production of beta-endorphin prompted us to measure beta-endorphin levels in 19 follicular fluid samples obtained from normal ovaries and compare them with beta-endorphin plasma levels in 19 women with normal ovulation. beta-Endorphin was extracted through Sepharose-treated chromatography columns and assayed with a specific anti-beta-endorphin antibody. Follicular fluid beta-endorphin levels (21.3 +/- 10.8 pg/ml) were significantly higher (p less than 0.01) than the plasma levels (15.5 +/- 3.35 pg/ml). There was no significant correlation between plasma and follicular fluid beta-endorphin concentrations. Follicles greater than 1 cm in size contained more beta-endorphin than follicles less than 1 cm in size (22.7 +/- 3.5 versus 18.7 +/- 4.4 pg/ml, p less than 0.05). Five follicular fluid samples were obtained from polycystic ovaries. The mean beta-endorphin content (45.1 +/- 7.7 pg/ml) in these follicles was significantly higher than that of normal ovaries (p = 0.001). It is concluded that the ovaries produce beta-endorphin and that polycystic ovaries produce more beta-endorphin than normal ovaries.     

Fetal intermediate lobe is stimulated by parturition

The fetal pituitary gland secretes beta-endorphin in blood in response to delivery. However, other forms of endorphin have recently been observed in the fetal pituitary, such as N-acetyl-beta-endorphin, which is devoid of opiate activity, and a desacetylated form of alpha-melanocyte-stimulating hormone. Both endorphins originate in the pituitary intermediate lobe. The sensitivity of this lobe to labor stress was assessed by the evaluation of beta-endorphin, N-acetyl-beta-endorphin, melanocyte-stimulating hormone, and desacetylated alpha-melanocyte-stimulating hormone in maternal plasma and cord blood in 11 cases of vaginal delivery and 10 cases of elective cesarean section without labor. Plasma peptide levels were determined by specific radioimmunoassays after extraction on Sep-Pak C-18 cartridges and high-performance liquid chromatography fractionation. Cord blood samples of infants delivered vaginally showed higher beta-endorphin (8.5 +/- 1.6 pmol/L, mean +/- SE) and desacetylated alpha-melanocyte-stimulating hormone (13.6 +/- 3.2 pmol/L) levels than those delivered by elective cesarean section (3.7 +/- 0.8 and 4.2 +/- 1.1 pmol/L, for beta-endorphin and desacetylated alpha-melanocyte-stimulating hormone, respectively). N-acetyl-beta-endorphin and alpha-melanocyte-stimulating hormone levels do not differ in relation to the mode of delivery. In maternal circulation beta-endorphin levels were higher in those delivered vaginally (5.2 pm 1) than in women who had cesarean sections (2.5 +/- 0.5 pmol/L), whereas no changes were found for the other peptides. In vaginal deliveries, the level of desacetylated alpha-melanocyte-stimulating hormone was higher in cord blood (13.6 +/- 3.2 pmol/L) than in maternal plasma (6.5 +/- 3 pmol/L); there were no significant differences with regard to the other peptides. Fetal and maternal levels of all the peptides were similar in cases of cesarean section. We conclude that parturition activates proopiomelanocortin peptide release from both the anterior and the intermediate pituitary lobe and that the fetus secretes the appropriate beta-endorphin molecule, that is, the peptide able to bind opiate receptors. Concomitant secretion of desacetylated alpha-melanocyte-stimulating hormone may occur with adrenal androgen activation at birth.     

Elevated plasma levels of beta-endorphin in a group of women with polycystic ovarian disease

The relationship of endogenous opiates in patients with polycystic ovarian disease (PCOD) and their influence on body weight was studied. The study group consisted of 19 women with PCOD. They were amenorrheic, hirsute, and hyperandrogenic, and their average weight was 124% of the ideal body weight. They had luteinizing hormone/follicle-stimulating hormone ratios greater than or equal to 2. The control group consisted of ten women with regular ovulatory menses. Plasma beta-endorphin (beta-EP) was measured by using a very specific radioimmunoassay. beta-Lipotropin (beta-LPH) was entirely removed from the sample by preincubation of the plasma with rabbit anti-beta-LPH/Sepharose complex (Pharmacia, New Brunswick, NJ). The mean +/- standard deviation of the plasma beta-EP in the control group was 70.18 +/- 18.06 pg/ml, and the mean +/- standard deviation of beta-EP in the study group was 185.6 +/- 93.4 pg/ml, which was significantly higher than the control levels (P less than 0.001). A significant correlation was also found between plasma beta-EP level and the patient's weight in the PCOD group (r = 0.462, P = 0.025). The data from this study suggest that the elevated levels of endogenous opiates may be involved in the pathophysiology of PCOD and be related to inappropriate secretion of gonadotropins influencing body weight.     

Suppression of testosterone-estradiol binding globulin by medroxyprogesterone acetate in polycystic ovary syndrome

Serum androgen binding capacity is decreased in hirsute women and normal women receiving medroxyprogesterone acetate. A sensitive radioimmunoassay was used to measure the main androgen binding protein, testosterone-estradiol-binding globulin, in 13 patients with hirsutism and the polycystic ovary syndrome. Testosterone-estradiol-binding globulin concentrations were determined before, during, and after treatment with medroxyprogesterone acetate. Testosterone-estradiol-binding globulin was lower in untreated polycystic ovary syndrome patients than in normal controls (21.9 +/- 3.7 versus 64 +/- 4 nmol/L, P less than .01). Administration of medroxyprogesterone acetate (400 mg intramuscularly every 15 days for nine months) to polycystic ovary syndrome patients caused a decrease of serum testosterone and further lowering of testosterone-estradiol-binding globulin (7.6 +/- 1.9 nmol/L, P less than .01). In two patients the concentration of testosterone-estradiol-binding globulin reached values as low as 0.9 and 0.8 nmol/L, approximately 1/60 and 1/70 of the normal level. Testosterone-estradiol-binding globulin returned to basal levels (15.1 +/- 1.3 nmol/L) between one and two years after discontinuation of medroxyprogesterone acetate. Corticosteroid binding globulin levels were normal in polycystic ovary syndrome and did not change with medroxyprogesterone acetate. It was concluded that: medroxyprogesterone acetate causes marked lowering of plasma testosterone-estradiol-binding globulin; the effect is not mediated by sex hormone levels; and the decrease in testosterone-estradiol-binding globulin offsets, at least partially, the beneficial action of medroxyprogesterone acetate.     

Compartmental ovarian steroidogenesis in polycystic ovary syndrome

Compartmental ovarian steroidogenesis in vitro was investigated in polycystic ovary syndrome. Basal estrogen secretion by granulosa cells ranged from 60 to 284 pg/micrograms cell protein for 24 hours and progesterone secretion from 24 to 1646 pg/micrograms cell protein for 24 hours. In three of four specimens, the addition of either 10(-5)M testosterone or androstenedione significantly increased estrogen production, demonstrating the presence of aromatase activity. Treatment with human follicle-stimulating hormone (100 ng/mL) or human chorionic gonadotropin (100 ng/mL) significantly increased the progesterone production in three of four specimens. The thecal compartment of every patient secreted significantly more testosterone and androstenedione than the capsule and stroma and more estrogen in tissue from two of the four women. The androgen/estrogen ratio was significantly greater for the theca (16.9) than the capsule (1.1) or stroma (1.7). These data demonstrate that in polycystic ovary syndrome a portion of the follicles possess the qualitative characteristics of developing follicles, granulosa cell aromatase activity and gonadotropin responsiveness, and that the theca is likely the principal site of ovarian androgen synthesis. These findings suggest that the small follicles characteristic of polycystic ovary syndrome consist of a mixed population of developing and atretic follicles and that the peripheral androgen excess is attributable to the large mass of the thecal compartment from both follicle populations.     

Clinical, endocrine and ultrasonographic features of polycystic ovary syndrome in Thai women

AIM: To study the prevalence, reproductive hormone profiles and ovarian sonographic appearance of Thai women with polycystic ovary syndrome (PCOS). METHODS: One thousand and ninety-five women were screened for oligomenorrhea/amenorrhea, and the clinical symptoms of hyperandrogenism. Ovarian morphology and volume were assessed by ultrasonography in diagnosed cases. Blood was taken for the measurement of the follicle stimulating hormone, luteinizing hormone, prolactin, testosterone, androstenedione, dehydroepiandrosterone and 17-hydroxyprogesterone. RESULTS: The prevalence of PCOS was 5.7%. The mean age of women with PCOS was less than that of non-PCOS cases (27.4 +/- 6.5 and 31.1 +/- 6.4 years, respectively; P < 0.0001). Abnormal uterine bleeding and infertility were the leading presenting symptoms. The mean ovarian volume in women with PCO appearance was 9.22 +/- 4.36 mL compared to 6.53 +/- 3.31 mL in those without this appearance (P = 0.04). Hyperandrogenemia was confirmed in 23 of the 62 cases (37.1%). CONCLUSIONS: The prevalence and clinical presentations of Thai women with PCOS were similar to those in other reports. However, hirsutism, elevated testosterone level and acanthosis nigricans were uncommon in our population. Serum androstenedione was a more sensitive indicator of hyperandrogenemia than total testosterone. Further research is needed to clarify whether there is an ethnic difference in endocrine profiles and risks of metabolic syndrome.     

Opioid peptides in pseudocyesis

Five women with pseudocyesis were evaluated during a two-year period. A random, nontimed blood sample was obtained from each woman at the time of initial encounter that revealed a hormone pattern most consistent with polycystic ovarian disease; mean (+/- SE) concentration of luteinizing hormone (LH) was 14.2 +/- 2.1 mIU/mL, follicle-stimulating hormone (FSH) was 3.3 +/- 0.7 mIU/mL, prolactin (PRL) was 23.5 +/- 1.3 ng/mL, estrone was 74.7 +/- 15.0 pg/mL, and estradiol was 54.7 +/- 13.0 pg/mL. In four of these patients, serum progesterone concentration was elevated over expected follicular phase values. The opiate antagonist, naloxone, was administered to four women before disclosure of their diagnosis. Naloxone treatment failed to induce LH or PRL release. Because naloxone did not cause a change in hormone concentration, naloxone-sensitive opioid mechanisms are apparently not involved in this disorder. After resolution of pseudocyesis, naloxone-induced LH release was appropriate for the phase of the cycle in which the narcotic blocking agent was administered.     

促性腺激素释放激素激动剂在多囊卵巢综合征促排卵高危周期中的 …

OBJECTIVE: To evaluate the efficacy and safety of gonadotropin-releasing hormone agonist (GnRH-a) instead of hCG for triggering ovulation in high risk gonadotropin stimulating cycles of infertile polycystic ovary syndrome (PCOS) patients. METHODS: GnRH-a was given for triggering follicular final maturation and ovulation in 18 gonadotropin stimulating cycles of 14 PCOS patients with mean serum estradiol (E2) level of 8,379 +/- 2,958 pmol/L. Their outcomes and complications were analysed. RESULTS: Ovulation achieved in 15 (83.3%) treated cycles, 4 (22.2%) became pregnant. Only 1 developed moderate ovarian hyperstimulation syndrome (OHSS) and another 1 had multiple pregnancy. CONCLUSIONS: The use of GnRH-a instead of hCG in high risk gonadotropin stimulating cycles is able to successfully induce ovulation and pregnancy and decrease the incidence of severe OHSS and multiple gestation.     

Role of dehydroepiandrosterone sulfate as a prehormone for ovarian steroidogenesis

The endocrine effects of induction of ovulation with menotropins were studied in 43 patients: 11 with hypothalamic amenorrhea and 32 with the polycystic ovary syndrome. Patients with polycystic ovary syndrome had higher base-line values of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), 17 beta-estradiol, dehydroepiandrosterone sulfate, testosterone, and a higher testosterone-free index than those with hypothalamic amenorrhea. During treatment with menotropins, patients with polycystic ovary syndrome had higher values of serum LH, prolactin, dehydroepiandrosterone sulfate, testosterone, percent free testosterone, testosterone-free index, and body weight than those with hypothalamic amenorrhea; serum FSH, dose of menotropins per kilogram body weight, and total follicular volume were higher in patients with hypothalamic amenorrhea than in those with polycystic ovary syndrome. Multiple linear regression after log transformation demonstrated that the testosterone-free index was predicted statistically by total ovarian volume and dehydroepiandrosterone sulfate and that serum 17 beta-estradiol was predicted statistically by total ovarian volume and testosterone-free index. Adding dexamethasone to menotropins in six patients with polycystic ovary syndrome produced significant decreases in 17 beta-estradiol, dehydroepiandrosterone sulfate, testosterone, and testosterone-free index. Higher concentrations of endogenous serum LH and dehydroepiandrosterone sulfate in patients with polycystic ovary syndrome in comparison with those with hypothalamic amenorrhea were associated with higher concentrations of serum testosterone, a lower total follicular volume, and an effective response to menotropins at a lower serum FSH and a lower dose of menotropins per kilogram body weight. These data suggest that serum dehydroepiandrosterone sulfate may be a precursor for ovarian steroidogenesis.     

The effects of somatostatin in the polycystic ovary syndrome.

Eighteen obese women (body mass index 30 +/- 6.1 kg/m2) with hyperinsulinaemia and with the polycystic ovary syndrome took octreotide at the dose of 100 mug s.c. The effect of the drug was assessed on plasma levels of gonadotropins luteinising hormone (LH), follicle stimulating hormone (FSH), of insulin, insulin-like growth factor-1 (IGF-1), androstenedione, testosterone, dehydroepiandrosterone sulphate (DHEAS), sex hormone binding globulin (SHBG) and insulin-like growth factor-binding protein-3 (IGFBP-3). Octreotide significantly reduced LH (31.8%), insulin (52%), IGF-1 (14%), androstenedione (22.6%) and testosterone (20%) and increased IGFBP-3 (25%).     

Lipid peroxidation in follicular fluid of women with polycystic ovary syndrome during assisted reproduction cycles

OBJECTIVE: To investigate the ovarian lipid peroxidation pattern in polycystic ovary syndrome (PCOS). STUDY DESIGN: Twenty-six women with PCOS who underwent in vitro fertilization and embryo transfer (IVF-ET) cycles between January 1999 and November 2000 at the hospital IVF unit were included in the study. Seventeen regularly cycling women with male factors (oligospermia or azoospermia) were enrolled as the control group. Malondialdehyde (MDA) levels in preovulatory follicular fluid were measured. RESULTS: There was a significant difference in follicular fluid MDA levels among the control (median, 2.23 nmol/mL; range, 0.98-4.93) and PCOS group (median, 3.53 nmol/mL; range, 1.51-4.81). Follicular fluid MDA and plasma progesterone levels correlated positively in the subjects (r = 0.55, p = 0.041) and PCOS group (r = 0.074, p = 0.0001). Plasma luteinizing hormone/follicle stimulating hormone (LH/FSH) levels correlated positively with follicular fluid MDA levels in the PCOS group (r = 0.72, p = 0.0001). CONCLUSION: The specific ovarian lipid peroxidation profile of PCOS patients is probably related to insufficient progesterone production and higher FSH/LH levels.     

Microsatellite polymorphism (tttta)(n) at -528 base pairs of gene CYP11alpha influences hyperandrogenemia in patients with polycystic ovary syndrome

OBJECTIVE: To investigate the functional significance of CYP11alpha microsatellite polymorphism (tttta)(n) (-528 base pairs) in patients with polycystic ovary syndrome. DESIGN: Follow-up study. SETTING: Academic research center.Patient(s): Eighty patients and 90 controls. INTERVENTION(s): Body mass indices and waist-to-hip ratios were determined. Blood samples were obtained for DNA analysis and hormone measurements. MAIN OUTCOME MEASURE(s): CYP11alpha marker (tttta)(n) genotyping and serum total testosterone levels. RESULT(s): All the women were assigned to one of two genotype groups: 216+ (for women who had at least one copy of high frequency allele 216 with four repeat units) or 216- (for women who did not have allele 216). Fifty-nine patients (73.75%) had genotype 216+; their mean (+/-SD) total testosterone level was 78.0 +/- 19.8 ng/dL. Twenty-one patients (26.25%) had genotype 216-; their mean (+/-SD) total testosterone level was 100.0 +/- 23.3 ng/dL. The difference in total testosterone levels was statistically significant. Seventy-eight controls (86.67%) had genotype 216+ and 12 controls (13.33%) had genotype 216-; the total testosterone levels of these two groups were similar (38.6 +/- 15.5 vs. 40.3 +/- 12.1 ng/dL). The difference in genotype distribution between the women with polycystic ovary syndrome and the controls (26.25% vs. 13.33% with genotype 216-) was statistically significant. CONCLUSION(s): CYP11alpha (tttta)(n) allelic variants were associated with both polycystic ovary syndrome and total testosterone levels in women with polycystic ovary syndrome, suggesting the existence of an epistasis phenomenon.     

Serum levels of inhibins are differentially altered in patients with polycystic ovary syndrome: effects of being overweight and relevance to hyperandrogenism

OBJECTIVE: To explore the abnormalities of serum inhibin isoform concentrations in a large group of patients with polycystic ovary syndrome (PCOS) and to evaluate the influence of body mass index (BMI), age, LH, and androgens on serum inhibin levels. DESIGN: Prospective study. SETTING: Reproductive endocrinology unit of an academic medical center. PATIENT(s): Forty-one women with PCOS were compared with 24 healthy women. INTERVENTION(s): Blood sampling was performed in the early follicular phase in patients and in control women. MAIN OUTCOME MEASURE(s): Serum levels of inhibin A, inhibin B, alpha-inhibin, pro-alphaC (alpha-inhibin precursor proteins), LH, FSH, E(2), T, and androstenedione (A) were assessed in all subjects. RESULT(s): Serum alpha-inhibin levels together with LH, T, and A levels were significantly increased in women with PCOS. Serum inhibin A levels were lower in patients with PCOS than controls (median +/- SD: 7.35 +/- 2.9 vs. 9.4 +/- 4.7 pg/mL), pro-alphaC levels were higher (264 +/- 136.7 vs. 127 +/- 81.5 pg/mL), and inhibin B levels did not differ between the groups (110.5 +/- 51.5 vs. 108 +/- 47.5 pg/mL). Simple regression analysis showed that inhibin A and B levels were negatively correlated with BMI in patients with PCOS (r = -0.43 and r27 kg/m(2)) displayed significantly lower inhibin A and inhibin B levels and a higher pro-alphaC-inhibin A ratio than nonobese patients with PCOS (BMI 相似文献   

Doppler, ultrasonographic and endocrinological environment with regard to the number of small subcapsular follicles in polycystic ovary syndrome.

The aim of this study was to evaluate how, in patients with polycystic ovary syndrome, the number of small subcapsular follicles correlates with uterine and ovarian blood flow and with specific hormonal parameters. At an ultrasonographic evaluation, 30 patients with polycystic ovary syndrome showed 5-10 (group I; n = 14) or > 10 (group II; n = 16) small follicles. These patients underwent ultrasonographic (ovarian volume and stroma echodensity; number, diameter and distribution of follicles) and color Doppler (uterine and intraovarian vessels) analyses, and hormonal assay. In group II, significantly lower pulsatility index values than in group I were observed in the ovarian stromal arteries. The Ferriman-Gallwey score, plasma androstenedione level and luteinizing hormone/follicle stimulating hormone (LH/FSH) ratio results were significantly higher in group II than in group I. Androstenedione plasma levels correlated with the number of small follicles. Furthermore, the LH/FSH ratio correlated with both the number of small follicles and the stromal artery pulsatility index. The combined assessment of ovarian morphology by transvaginal ultrasound and color Doppler may provide insight into the pathological state of polycystic ovary syndrome.     

Diagnosis of Sheehan's syndrome using a sequential pituitary stimulation test.

Systematic pituitary evaluation was performed in four patients suspected of having Sheehan's syndrome. A sequential pituitary stimulation test, consisting of insulin-induced hypoglycemia followed by stimulation of gonadotropin-(GnRH) and thyroid-releasing hormone (TRH), a metyrapone test, and adrenocorticotropic hormone (ACTH) stimulation test, was performed. All four patients failed to develop a normal increase in serum growth hormone, cortisol, and prolactin (PRL) following insulin-induced hypoglycemia. All patients demonstrated a blunted PRL, follicle-stimulating hormone, and luteinizing hormone response to the combination of GnRH and TRH. Although thyroid stimulating hormone (TSH) response was impaired in all patients, two patients had normal T3 resin uptake and thyroxine, demonstrating minimal TSH reserve maintaining normal baseline free thyroxine index. Metyrapone administration was followed by no increase in 11-deoxycortisol or 17-ketogenic steroids, thereby adding no additional information to the hypoglycemia stimulation. ACTH infusion revealed normal adrenal cortisol response. In conclusion, in patients with suspected postpartum hypopituitarism, a complete pituitary function investigation can be done in a short time by using the described pituitary sequential stimulation test.     

Serum immunoreactive beta-endorphin in the human ovulatory cycle

Daily serum immunoreactive beta-endorphin (IR-beta-EP) levels, in conjunction with luteinizing hormone, follicle-stimulating hormone, 17 beta-oestradiol, progesterone, and prolactin, were measured during the ovulatory cycle in five healthy Chinese women. Standardization of raw data by conversion to the statistical "Z scores" and composite plot of the five cycles showed that serum IR-beta-EP levels fluctuated during the follicular, late luteal, and menstrual phases. A preovulatory rise occurred two to three days prior to the luteinizing hormone surge, followed by a postovulatory dip for two to three days. The concentrations of IR-beta-EP were (mean +/- S.E.M.): 85.5 +/- 10.5 pg/mL (n = 36) in the follicular phase; 92.4 +/- 36.5 pg/mL (n = 5) in the ovulatory phase; 72.3 +/- 16.6 pg/mL (n = 7) in the early luteal phase; 100.0 +/- 10.7 pg/mL (n = 38) in the late luteal phase. The values in the luteal phase were the highest of any in the ovulatory cycle. The findings suggest that the fluctuation of endogenous beta-EP is under the influence of, among other factors, ovarian sex steroids. The significance of beta-EP in the regulation of gonadotropin release during normal menstrual cycles is discussed.