Obesity, serum steroid levels, and pulsatile gonadotropin secretion in polycystic ovarian disease

Serum binding capacity of sex-hormone binding globulin (SHBG-BC), steroid concentrations, and secretion patterns of LH and FSH were compared between groups of seven nonobese and seven obese patients with polycystic ovarian disease (PCOD). Obese patients with PCOD differed from those with normal weight in having very low SHBG-BC and elevated serum levels of free and albumin bound testosterone. Compared to healthy women in the follicular phase, both nonobese and obese patients with PCOD showed equally elevated serum levels of androstenedione, estrone, and albumin-bound and free estradiol. Pattern of gonadotropin secretion was studied from blood samples taken at 15 min intervals for 6 h. In 6 patients of both groups low pulses of FSH were found coincidently with pulses of LH. Serum level of LH showed a clear pulsatile pattern in all patients with PCOD, varying from 4.5 to 7.5 pulses per 6 h. The mean pulse rate in the groups of nonobese and obese patients with PCOD was similar, 5.9 pulses per 6 h. In the obese patients the mean LH levels were, however, less elevated and the pulse amplitudes were smaller than those in the nonobese patients. We suggest that this difference is due to high levels of biologically active testosterone in obese patients with PCOD.     

The use of gonadotrophin-releasing hormone antagonists in polycystic ovarian disease

Polycystic ovarian disease (PCOD) is characterized by anovulation, eventually high luteinizing hormone (LH) levels, with increased LH pulse frequency, and hyperandrogenism. As the aetiology of the disease is still unknown, gonadotrophin-releasing hormone (GnRH) antagonists, competitive inhibitors of GnRH for its receptor, are interesting tools in order to study and treat the role of increased LH levels and pulse frequency in this disease. Their administration provokes a rapid decrease in bioactive and immunoactive LH followed by a slower decrease in follicle-stimulating hormone (FSH). In patients with PCOD, the suppression of gonadotrophin secretion eradicates the symptoms of the disease as long as the treatment lasts. Several authors have suggested that increased plasma LH levels have deleterious effects on the fertility of women with PCOD. Indeed, fewer spontaneous pregnancies with more miscarriages are observed when plasma LH levels are high. Assisted reproduction techniques such as in vitro fertilization (IVF) have provided other clues to the role of the LH secretory pattern in women with PCOD. The number of oocytes retrieved, the fertilization rate and the cleavage rate are lower in PCOD patients undergoing IVF and this is inversely correlated with FSH:LH ratio. These abnormalities are corrected when endogenous secretion of LH is suppressed. On the other hand, implantation and pregnancy rates after IVF are similar to those observed in control women. New GnRH antagonists are devoid of side effects and suppress LH secretion within a few hours without a flare-up effect. This action lasts for 10-100 hours. When GnRH antagonists are associated with i.v. pulsatile GnRH, this combination both suppresses the effect of endogenous GnRH and because of the competition for GnRH receptors restores a normal frequency of LH secretion. We have studied two women with PCOD, administering first 10 mg s.c. every 72 hours for 7 days of the GnRH antagonist Nal-Glu, then adding on top i.v. pulsatile GnRH: 10 micrograms/pulse every 90 minutes for 15 days. We thus succeeded in normalizing LH secretion pattern and observed a significant decline in testosterone levels. We failed to induce appropriate ovarian response and ovulation. In conclusion, the combination of GnRH antagonist and GnRH pulsatile treatment can re-establish normal LH secretory pattern in patients with PCOD. The failure to induce ovulation with this regimen suggests the existence of an inherent ovarian defect in women with PCOD.     

Endocrine dynamics during pulsatile GnRH administration in patients with hypothalamic amenorrhea and polycystic ovarian disease

The LH secretory patterns and ovarian endocrine responses have been determined during pulsatile gonadotropin-releasing hormone (GnRH) administration for induction of ovulation in patients with hypothalamic amenorrhea (HA). However, until now these endocrine dynamics during GnRH therapy have not been thoroughly investigated in patients with polycystic ovarian disease (PCOD). Seven patients with HA and 4 patients with PCOD have therefore been studied to determine changes in LH pulsatile activity and in serum sex steroid levels in response to chronic intermittent GnRH stimulation. GnRH was administered intravenously (5-10 micrograms/90 minutes) by means of a portable infusion pump. Blood samples were obtained at 15-minute intervals for 4 hours on the day before the start of GnRH stimulation (control day) and on treatment days 5, 10 and 15. LH was determined in all samples and FSH, serum androgens and estrogens were measured in baseline samples by RIA. While 8 (62%) ovulations and 5 conceptions were observed in 13 treatment cycles in patients with HA, no ovulations were achieved during 9 treatment cycles in patients with PCOD. On the control day significantly (p less than 0.05) higher basal LH and testosterone (T) levels and significantly (p less than 0.05) lower FSH levels were found in the PCOD patients. The LH pulsatile profiles of the PCOD patients showed significantly (p less than 0.05) higher pulse amplitudes and areas under the curve (integrated responses). Pulsatile GnRH administration induced a significant (p less than 0.05) increase in LH pulse amplitudes in both HA and PCOD patients, and also increased (p less than 0.05) the integrated responses in patients with HA. During the GnRH stimulation, the LH interpulse intervals of both HA and PCOD patients were found to be similar to the frequency in which exogenous GnRH was administered. FSH levels rose continuously (p less than 0.001) during stimulation in patients with HA, but remained unchanged in patients with PCOD. In HA patients, T, androstenedione (AD) and estrone (E1) did not change during the GnRH treatment, but estradiol (E2) rose so that the ratios of aromatized estrogens to non-aromatized androgens (E1/AD, E2/T) increased. In contrast, T and AD increased significantly (p less than 0.05 or less) and E2 remained unchanged during stimulations in PCOD patients, which resulted in decreasing ratios of estrogens to androgens. These observations confirm that pulsatile GnRH administration can successfully induce ovulation in patients with HA by restoring the ovarian physiology. The data also demonstrate that pulsatile GnRH administration can influence the LH secretory patterns in PCOD patients.(ABSTRACT TRUNCATED AT 400 WORDS)     

Pulsatile luteinizing hormone secretion in hypothalamic amenorrhea, anorexia nervosa, and polycystic ovarian disease during naltrexone treatment.

OBJECTIVE: To determine if chronic treatment with the long-acting oral opioid antagonist naltrexone can increase luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion in women with secondary amenorrhea. DESIGN: Prospective. SETTING: Large reproductive endocrinology unit of an academic hospital. PATIENTS: Three groups of women with oligomenorrhea or amenorrhea: (1) hypothalamic amenorrhea; (2) anorexia nervosa; and (3) polycystic ovarian disease (PCOD). INTERVENTION: Naltrexone 50 mg every day for 4 days. MAIN OUTCOME MEASURES: Luteinizing hormone pulse pattern, frequency and amplitude, mean LH and FSH levels, measured by serial blood sampling over a 6-hour period before and after naltrexone. RESULTS: Naltrexone caused a significant increase (P less than 0.05) of the LH pulse frequency in patients with hypothalamic amenorrhea and in PCOD but not in anorexia nervosa. The mean levels of LH and FSH and LH pulse amplitudes were not significantly changed by naltrexone. The naltrexone nonresponders were underweight either because of simple weight loss or anorexia nervosa and had low levels of estradiol and an LH pulse pattern similar to the luteal one. CONCLUSION: The luteal LH pulse pattern in weight loss-related amenorrhea is caused by a nonopioid, undernutrition-linked factor.     

Impact of high basal FSH/LH ratio in women with normal FSH levels on in vitro fertilization outcomes

Abstract

Basal luteinizing hormone (LH) levels have also been suggested to impact on ovarian responsiveness as well as basal follicular stimulating hormone (FSH) levels. The aim of this study was to compare the in vitro fertilization (IVF) outcomes according to cycle day 3 FSH/LH ratio and to assess the proper stimulation protocol between gonadotropin-releasing hormone (GnRH) agonist and GnRH antagonist protocols. The retrospective cohort study recruited a total of 1211 women having the laboratory values of FSH (<10?IU/L) and LH within 3 months before IVF. Patients were treated with GnRH agonist long or GnRH antagonist protocols and stimulated with recombinant FSH (rFSH). The number of total retrieved oocytes and mature oocytes, implantation rate, clinical pregnancy rate and ongoing pregnancy rate were analyzed between groups: Group I: FSH/LH?<?2 and Group II: FSH/LH?≥?2. The Group II had the small number of retrieved oocytes and mature oocytes compared to the Group I (p?=?0.000). Clinical and ongoing pregnancy rate were lower in Group II (p?=?0.006, 0.006, respectively). In comparison of each protocol within groups, Group II showed significantly low pregnancy rate when GnRH antagonist was administered. In women with normal FSH level, high day 3 FSH/LH ratio can present subclinically low ovarian reserve and be predictive of lower pregnancy outcomes in fresh IVF cycles, and the choice of GnRH agonist can be related to favorable IVF outcomes.     

Abolishment of the positive feedback mechanism: a criterion for temporary medical hypophysectomy by LH-RH agonist

The hypothalamic pituitary axis was studied in patients with an abnormal pattern of gonadotropin release during chronic treatment with LH-RH agonist. Two patients had PCOD and the third demonstrated the early luteinization phenomenon. Following a well-defined gonadotropin rise with initiation of LH-RH treatment, no further response was noted. Stabilization of the LH:FSH ratio in PCOD patients was noted after 4 weeks of treatment. Administration of both native LH-RH (100 micrograms) and intravenous pulsatile LH-RH did not evoke any rise in LH. In addition to the above LH-RH challenges, the positive feedback was examined by administration of estradiol benzoate (EB). The study demonstrated that, although the pituitary did not respond to any LH-RH challenge, it may still respond by a rise in LH following EB administration. Both functions of the hypothalamic pituitary axis should be examined in order to determine the state of medical hypophysectomy.     

Pituitary response during pulsatile luteinizing hormone-releasing hormone ovulation--induction in patients with clomiphene citrate-resistant polycystic ovary-like disease

The pituitary response to pulsatile luteinizing hormone-releasing hormone (LRH) was studied in 6 women with clomiphene-resistant polycystic ovary-like disease (PCOD). PCOD was defined as oligomenorrhea, elevated luteinizing hormone (LH), normal follicle-stimulating hormone (FSH), and, in general, elevated androgens. LRH was administered in a pulsatile way, chronically, with a pulse dose of 20 micrograms and a pulse interval of 60, 90 and 120 minutes. Blood was drawn every 10 minutes for 6 hours, at the start of therapy (pulse study 1) and 9-15 days after the start of therapy (pulse study 2). Five patients ovulated within 10 days of therapy, which meant that pulse study 2 was performed during the luteal phase. One patient remained anovulatory. The follicular and luteal response during LRH therapy was comparable to that of normal cycles, although the pituitary response was enhanced in PCOD at the start of therapy, which might be related to the state in which the ovary finds itself with respect to follicular development. Desensitization for LH to LRH occurred only incidentally during pulse study 1. Desensitization for FSH to LRH already developed during pulse study 1 and continued to existed during therapy. The 60, 90 and 120 minute LRH pulse interval regimes resulted in LH nadir intervals with wide ranges, although the medians were 60, 90 and 120 minutes respectively.     

Temporal coupling of luteinizing hormone and follicle stimulating hormone secretion in polycystic ovary syndrome

The aim of this study was to assess the luteinizing hormone (LH) and follicle stimulating hormone (FSH) pulsatile secretion and their temporal relation (concordance) in subjects with polycystic ovary syndrome (PCOS). Fifteen subjects were included in the study (age 17–30 years ,body mass index (BMI) 19.38–33.46 kg/m²). For the LH and FSH determinations ,blood sampling started at 23.00 and lasted for 6 h with an intersample interval of 10 min. Pulse analysis was carried out using the PulsDetekt program. LH/FSH pulse concordance was calculated using the specific concordance index. Gonadotropin co-pulsatility was found in six subjects who were significantly younger than the others (median 18.5 vs. 22.5 years ,p = 0.036). BMI ,hirsutism grade ,insulin sensitivity ,estradiol ,progesterone, testosterone ,prolactin ,cortisol and results obtained from the pulsatility analysis did not significantly differ between the groups. A serum cortisol concentration was correlated with the increased LH/FSH lag time (ρ = 0.851 ,p = 0.036) all subjects were included. In conclusion ,two distinct LH/FSH secretory patterns were found in PCOS patients ,manifested by the presence or absence of the concordance of gonadotropin secretion. In the group where LH/FSH co-pulsatility was present ,correlation was found between the serum cortisol and the LH/FSH lag. We also confirmed the finding of previous studies that LH and FSH secretion are regulated by two different mechanisms.     

Gonadotropin pulsatility in Cushing's syndrome compared with polycystic ovary syndrome

Many of the presenting features in women with Cushing's syndrome (CS) are similar to those observed for patients with polycystic ovary syndrome (PCOS). The aim of this study was to compare gonadotropin pulsatility characteristics in CS and PCOS. We evaluated 32 females divided into three groups. The first group comprised 12 females with clinically and biochemically proven CS, subsequently confirmed by histology (seven with Cushing's syndrome, five with adrenal adenoma). The second group comprised ten females with clinical, endocrine and ultrasonographic parameters for PCOS, while the third group comprised ten healthy females with regular menstrual cycles to serve as controls. Blood samples were taken at 15-min intervals for 6?h in the follicular phase, for determination of luteinizing hormone (LH) and follicle-stimulation hormone (FSH). Pulse analysis was carried out using the PulsDetekt program, and statistical analysis was done using the Kruskal–Wallis test. The following data, presented as median (minimum–maximum), were found for the three groups respectively. Number of LH pulses: 0 (0–5), 7 (3–8) and 3 (2–7); LH pulse amplitude: 2.29 (1.98–3.49), 2.27 (1.15–5.90) and 2.03 (1.02–4.46) mU/l; LH pulse mass: 17.81 (14.82–26.20), 29.85 (8.59–185.82) and 27.57 (7.63–66.69) mU/l?×?min. Number of FSH pulses: 3 (0–3), 2 (0–5) and 3 (1–5); FSH pulse amplitude: 1.62 (1.29–1.94), 1.49 (1.19–4.40) and 2.02 (1.37–2.52) mU/l; FSH pulse mass: 12.17 (9.64–41.69), 11.18 (8.92–33.02) and 15.16 (10.31–18.93) mU/l?×?min. Only the number of pulses was compared because other parameters of pulsatile secretion cannot be estimated when no pulses are detected. The difference in number of LH pulses between groups was statistically significant (p?<?0.05); however, there was no difference in the number of detected FSH pulses between groups (p?>?0.05). Attenuation of pulsatile LH secretion indicating gonadotropin deficiency in the majority of women with CS is mostly due to alterations in serum cortisol levels. Our data also suggest that different mechanisms alter LH pulsatile secretion in CS and PCOS.     

Clinical features and circulating gonadotropin, insulin, and androgen interactions in women with polycystic ovarian disease

OBJECTIVE: To investigate the interactions of hyperinsulinemia and inappropriate gonadotropin secretion in women with polycystic ovarian disease (PCOD). DESIGN: Comparative study of endocrinologic parameters in subjects with PCOD. SETTING: Open patient clinic of reproductive endocrinology at University Central Hospital of Turku, Finland. PATIENTS: Fourteen nonobese and 10 obese patients with PCOD. Seven healthy women for reference data collection. Normal thyroid function, serum prolactin concentration, normal diurnal cortisol variation, euglycemia in all subjects. MAIN OUTCOME MEASURES: Serum concentrations of insulin, testosterone, androstenedione, dehydroepiandrosterone sulfate, sex hormone-binding globulin, immunoreactive luteinizing hormone (LH), bioactive LH, and follicle-stimulating hormone (FSH). RESULTS: The concentration of insulin was higher and that of bioactive LH was lower in obese than in nonobese PCOD women in whom the levels were also above the upper reference value. There was a negative correlation between insulin and bioactive LH levels (r = -0.57). Bioactive LH correlated inversely with the body mass index (BMI) (r = -0.50). After eliminating the effect of the BMI, the correlation between bioactive LH and insulin was no longer significant (r = -0.37). The bioactive LH and immunoreactive LH/FSH ratio correlated significantly (r = 0.68). CONCLUSIONS: These data demonstrate that hyperandrogenic women can be divided into two subgroups: those with insulin resistance, normal or minimally elevated LH, and markedly elevated insulin levels; and those with elevated LH levels, no insulin resistance, and normal insulin concentrations. Obesity is associated with the former, and high bioactive LH levels with the latter subgroup.     

Serum androgen and gonadotropin levels decline after progestogen-induced withdrawal bleeding in oligomenorrheic women with or without polycystic ovaries.

OBJECTIVE: To examine the effect of short-term progestogen treatment on androgen, gonadotropin, and sex hormone-binding globulin (SHBG) levels in oligomenorrheic women. DESIGN: Comparative study of changes in hormonal parameters in patients with or without ultrasonographically diagnosed polycystic ovarian disease (PCOD). SETTING: Open patient clinic of reproductive endocrinology at University Central Hospital of Turku, Finland. PATIENTS: Seventy-five oligomenorrheic women with (n = 51) or without (n = 24) PCOD. MAIN OUTCOME MEASURES: Serum concentrations of testosterone (T), androstenedione (A), dehydroepiandrosterone sulfate, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and SHBG. RESULTS: The levels of T, A, LH, and the LH:FSH ratios decreased significantly after oral treatment with medroxyprogesterone acetate (10 mg/d for 10 days) in non-PCOD women and in women with PCOD decreasing the frequencies of pathological laboratory findings, in particular elevated levels of LH:FSH ratio and A in PCOD women and of LH:FSH ratio in non-PCOD women. The levels of T, A, and LH as well as the LH:FSH ratio were significantly higher in women with PCOD. Obesity was associated with high free androgen indices, low LH:FSH ratios, and low concentrations of LH, A, and SHBG. CONCLUSIONS: The serum samples for hormonal analyses used as an aid in diagnosing PCOD should be obtained without pretreatment with progestogen because it masks the biochemical findings of PCOD.     

Gonadotropin pulsatility in Cushing's syndrome compared with polycystic ovary syndrome.

Many of the presenting features in women with Cushing's syndrome (CS) are similar to those observed for patients with polycystic ovary syndrome (PCOS). The aim of this study was to compare gonadotropin pulsatility characteristics in CS and PCOS. We evaluated 32 females divided into three groups. The first group comprised 12 females with clinically and biochemically proven CS, subsequently confirmed by histology (seven with Cushing's syndrome, five with adrenal adenoma). The second group comprised ten females with clinical, endocrine and ultrasonographic parameters for PCOS, while the third group comprised ten healthy females with regular menstrual cycles to serve as controls. Blood samples were taken at 15-min intervals for 6 h in the follicular phase, for determination of luteinizing hormone (LH) and follicle-stimulation hormone (FSH). Pulse analysis was carried out using the PulsDetekt program, and statistical analysis was done using the Kruskal-Wallis test. The following data, presented as median (minimum-maximum), were found for the three groups respectively. Number of LH pulses: 0 (0-5), 7 (3-8) and 3 (2-7); LH pulse amplitude: 2.29 (1.98-3.49), 2.27 (1.15-5.90) and 2.03 (1.02-4.46) mU/l; LH pulse mass: 17.81 (14.82-26.20), 29.85 (8.59-185.82) and 27.57 (7.63-66.69) mU/l x min. Number of FSH pulses: 3 (0-3), 2 (0-5) and 3 (1-5); FSH pulse amplitude: 1.62 (1.29-1.94), 1.49 (1.19-4.40) and 2.02 (1.37-2.52) mU/l; FSH pulse mass: 12.17 (9.64-41.69), 11.18 (8.92-33.02) and 15.16 (10.31-18.93) mU/l x min. Only the number of pulses was compared because other parameters of pulsatile secretion cannot be estimated when no pulses are detected. The difference in number of LH pulses between groups was statistically significant (p < 0.05); however, there was no difference in the number of detected FSH pulses between groups (p > 0.05). Attenuation of pulsatile LH secretion indicating gonadotropin deficiency in the majority of women with CS is mostly due to alterations in serum cortisol levels. Our data also suggest that different mechanisms alter LH pulsatile secretion in CS and PCOS.     

Pulsatile luteinizing hormone-releasing hormone treatment of male hypogonadotropic hypogonadism

Luteinizing hormone-releasing hormone (LH-RH) secretion from the hypothalamus follows a rhythmic pattern, inducing pulsatile luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion from the pituitary gland. Consideration of this physiologic principle led to the introduction of pulsatile LH-RH therapy via infusion pump for the treatment of different forms of hypogonadotropic hypogonadism. We report on 10 male patients, 16 to 28 years of age, suffering from idiopathic hypogonadotropic hypogonadism (IHH) including Kallman's syndrome (n = 2) and delayed puberty (n = 2). All presented with complete eunuchoidism and had undergone no treatment for their conditions during the previous 2 years. LH-RH was administered in subcutaneous pulses of 4 to 16 micrograms, with a portable infusion pump (ZYKLOMAT, Ferring Corp., Kiel, FRG); treatment periods ranged from 6 to 24 months. With therapy, the subjects improved secretion of LH, FSH and testosterone. Testicular volumes and penis size increased; all patients developed normal secondary sexual characteristics. Spermatogenesis was induced in all patients. The time to onset of spermatogenesis ranged from 3 to 15 months. No major side effects were observed, and no patient dropped out of the study. The results indicate that pulsatile LH-RH therapy is an highly effective treatment for IHH and delayed puberty.     

Evaluation of prolonged use of statins on the clinical and biochemical abnormalities and ovulation dysfunction in single young women with polycystic ovary syndrome

Objective: The aim of the current work was to investigate the effects of prolonged use of Statins on the clinical and biochemical abnormalities and ovulation dysfunction in young single women with polycystic ovary syndrome (PCOS).

Patients and methods: It was a randomized, double-blind, placebo-controlled study. Where 200 single young women with PCOS were randomized into either 100 (n?=?100) women using Simvastatin 20?mg daily considered as group A (study group), or 100 (n?=?100) women using placebo and considered as group B (control group), for six months treatment period. The main outcome measures were the changes in serum androgen levels (testosterone, androstendione and dehydro-epiandrostenion sulfate-DHEAS), LH, FSH, LH/FSH ratio and insulin resistance (IR), in addition to menstrual regularity, hirsutism, BMI and W/H ratio. Follow-up of spontaneous ovulation, confirmed with both trans-abdominal sonography (TAS) and luteal serum progesterone had been performed as well.

Result(s): After 6 months’ treatment, in group A serum testosterone showed decreased level by 28%, with significant decrease of LH (40%) and a decline of the LH/FSH ratio (43%). There was also a clear decrease of total cholesterol (26%), low-density lipoprotein (LDL; 39%) and triglycerides (23%). IR did not show a significant difference in the two groups. High-density lipoprotein (HDL) increased by 17%. Improved menstrual regularity and decreased hirsutism, acne, ovarian volume, BMI had been clearly noticed in the study group. Spontaneous ovulation had been confirmed songoraphically (TAS), and biochemically (progesterone >10?ng) in 10 women (10%) in the study group compared to none in the control group.

Conclusions: Long-term Statins' treatment was associated with clear improvement of all PCOS clinical and biochemical abnormalities, in addition to ovarian dysfunction as well.     

Differences in serum LH and FSH levels using depot or daily GnRH agonists in controlled ovarian stimulation: influence on ovarian response and outcome of ART

Purpose: To study effects of endogenous LH levels on ovarian response and outcome in ART cycles a controlled study was performed with two patient groups differing in the intensity of pituitary downregulation. Methods: Group I (n = 27) received 3.75 mg of the GnRH agonist triptorelin acetate depot, group II (n = 54) was given 0.1 mg triptorelin acetate daily, followed by ovarian stimulation with recombinant FSH. Results: After downregulation serum LH and FSH levels were significantly lower in group I. Patients of group I needed significantly higher FSH doses to achieve comparable levels of serum estradiol and preovulatory follicles. The number of retrieved oocytes and transferable embryos was lower in group I. Conclusion: Patients with profound endogenous LH suppression by depot GnRH agonists show higher FSH stimulation dose requirements and lower oocyte number and fertilization rate, indicating a need for minimal LH activity in folliculogenesis and oocyte development.     

Ovarian size and response to laparoscopic ovarian electro-cauterization in polycystic ovarian disease.

OBJECTIVES: To evaluate endocrine and ovulatory changes in polycystic ovarian disease (PCOD) in relation to patients' ovarian size. METHODS: Three hundred and seventy-one women with clomiphene citrate-resistant PCOD underwent laparoscopic ovarian cauterization [type I or typical with ovarian volume >8 cm(3) or cross-sectional area >10 cm(2) (n=211), type II with normal size ovary (n=160)]. Serum levels of LH, FSH, DHEAS, PRL, and T before and 10 days after ovarian cautery, spontaneous and induced ovulation and pregnancy rates were compared. RESULTS: Both groups responded to therapy in a similar manner, with a marked decrease in LH, FSH, DHEAS and T levels, with ovulation rates in type I 90.99%, type II 88.75% and pregnancy rates, 73.45% and 71.25%, respectively, with no statistical differences. CONCLUSIONS: Hormonal changes, ovulation and pregnancy rates were similar in the two types of PCOD, therefore it can be concluded that ovarian size is not a prognostic factor for response of PCOD patients to laparoscopic ovarian electro-cauterization.     

Ovulation induction with pulsatile luteinizing hormone-releasing hormone in women with clomiphene citrate-resistant polycystic ovary-like disease: endocrine results

The pituitary and gonadal response to pulsatile luteinizing hormone-releasing hormone (LH-RH) administration during the first and consecutive second treatment unit (TU) was studied in nine women with clomiphene citrate-resistant polycystic ovary-like disease (PCOD). The control group consisted of eight eumenorrheic women. Luteinizing hormone levels, LH amplitudes, and total urinary excretion/24 hours did not differ between ovulatory and anovulatory TUs, but were significantly higher compared with the control group. Follicle-stimulating hormone (FSH) in PCOD did not differ from normal cycles. Androgen values in the anovulatory TUs were significantly higher compared with the ovulatory TUs (P = 0.001). We conclude that LH-RH therapy may result in ovulation; however, it does not redress the intrinsic abnormality in PCOD and FSH, and androgen levels do not seem to be critical in ovulation induction.     

The effect of different hormone therapies on anti-müllerian hormone serum levels in anovulatory women of reproductive age

Objective.?To investigate the effect of oral contraceptives (OC), metformin and ovulation induction with gonadotropins on circulating anti-müllerian hormone (AMH).

Design.?Prospective clinical study.

Patients.?Thirty patients with PCOS (Group 1), 15 normogonadotropic anovulatory infertile women (WHO 2) (Group 2) and 15 normoovulatory control women (Group 3). Patients in Group 1 received OC (n?=?12), metformin (n?=?11) or no-treatment (n?=?7) for 6 months. Ovulation induction with FSH or hMG was used in Group 2.

Main outcome measures.?Total follicle number (TFN) and hormonal (fasting insulin and glucose, testosterone, SHBG, LH, androstenedione and AMH) measurements at baseline and during therapy.

Results.?Basal AMH and TFN were higher in Groups 1 and 2 than in controls. Only TFN was significantly related to AMH level in Groups 1 and 2. AMH level was significantly reduced during OC treatment, and there was a trend for AMH decrease during metformin therapy. No significant changes in AMH level were observed during ovulation induction. TFN was the only parameter showing a significant positive correlation with circulating AMH over the 6-month treatment period in patients in Group 2.

Conclusions.?AMH is an accurate marker of the antral follicle pool in WHO-2/PCOS women but the measurement of AMH is not likely to be helpful in the management of those patients.     

The effect of 6 weeks of testosterone treatment on pulsatile luteinizing hormone secretion in eugonadal female-to-male transsexuals

Polycystic ovary disease generally is associated with elevated androgen levels and elevated luteinizing hormone (LH) levels, whereas follicle-stimulating hormone (FSH) levels are (sub)normal. To assess the role of androgens on gonadotropin secretion, we investigated the effect of 6 weeks of testosterone (T) undecanoate, 120 to 160 mg/d orally, on the parameters of the pulsatile secretion of LH in a group of six eugonadal female-to-male transsexuals with normal menstrual cycles. The treatment suppressed menstrual activity in all patients. Serum T and estrone were significantly elevated after treatment with oral T undecanoate. The parameters of the pulsatile secretion of LH were not affected by androgen administration. Levels of FSH, estradiol, and progesterone also did not change significantly.     

Endocrine and clinical effects of myo-inositol administration in polycystic ovary syndrome. A randomized study

Abstract

Objective: To evaluate the effects the administration of myo-inositol (MYO) on hormonal parameters in a group of polycystic ovary syndrome (PCOS) patients.

Design: Controlled clinical study.

Setting: PCOS patients in a clinical research environment.

Patients: 50 overweight PCOS patients were enrolled after informed consent.

Interventions: All patients underwent hormonal evaluations and an oral glucose tolerance test (OGTT) before and after 12 weeks of therapy (Group A (n¼10): MYO 2?g plus folic acid 200?mg every day; Group B (n¼10): folic acid 200?mg every day). Ultrasound examinations and Ferriman–Gallwey score were also performed.

Main outcome measures: Plasma LH, FSH, PRL, E2, 17OHP, A, T, glucose, insulin, C peptide concentrations, BMI, HOMA index and glucose-to-insulin ratio.

Results: After 12 weeks of MYO administration plasma LH, PRL, T, insulin levels and LH/FSH resulted significantly reduced. Insulin sensitivity, expressed as glucose-to-insulin ratio and HOMA index resulted significantly improved after 12 weeks of treatment. Menstrual cyclicity was restored in all amenorrheic and oligomenorrheic subjects. No changes occurred in the patients treated with folic acid.

Conclusions: MYO administration improves reproductive axis functioning in PCOS patients reducing the hyperinsulinemic state that affects LH secretion.