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Objectives: The prevalence of ovulation disorder (OD) is 3-fold higher in obese than normal-weight women. Most ODs are associated with concomitant polycystic ovary syndrome (PCOS), but obesity by itself can cause OD, through mechanisms that remain poorly documented. The literature on obese non-PCOS women with OD is sparse. The aim of the present study was to analyze a population of obese non-PCOS women with OD to shed further light on the mechanism of ovulation disorder., Material and Methods: This retrospective observational study of infertile obese women without PCOS compared a control group without OD (n=45) to a study group with OD (n=30) (OD group). Clinical, hormonal, and ultrasound characteristics were collected between cycle days 2 and 5. Women older than 37 years and women with PCOM (polycystic ovarian morphology) or hormonal disorder were excluded., Results: Body mass index (BMI) was significantly higher in the OD group, as were waist circumference and insulin and leptin serum levels. Conversely, serum follicle stimulating hormone (FSH) levels were significantly lower. After adjustment for BMI, only serum FSH level remained significantly different between the 2 groups. Discriminant analysis suggested that FSH may have a much stronger effect on OD than BMI., Conclusion: Low serum FSH level may contribute to OD in some obese women, independently of BMI. The pathophysiological mechanism of this finding and its impact on therapeutic strategies must be clarified., (Copyright © 2019 Elsevier Masson SAS. All rights reserved.)

To examine the effect of night shift on the ovarian function, 122 teachers, 67 office workers, 377 nurses, 133 factory workers and 67 barmaids were surveyed. The incidence of irregular menstrual cycle was 13.1% in teachers, 14.9% in office workers, 24.9% in nurses, 36.8% in factory workers and 40.3% in barmaids. The incidence was significantly higher in women working at night than women working during the day. Plasma concentrations of melatonin, LH, FSH and prolactin were determined at 2200 h and 0200 h in 5 nurses working at night and in 6 nurses resting in their quarters. Plasma concentrations of melatonin and prolactin at 0200 h were significantly lower in nurses of the working group than others of the resting group, but plasma concentrations of LH and FSH did not differ between the two groups. These results indicate that night shift suppresses the ovarian function by affecting the circadian rhythm of melatonin and prolactin.

Serum steroid, gonadotropin, and alpha-subunit levels were assessed in 35 women with cycle abnormalities [11 with and 24 without polycystic ovarian disease (PCOD) according to strict clinical and biochemical criteria] and 8 regularly cycling women in the early (cycle day 3 or 4) and mid (cycle day 7 or 8) follicular phase. LH and FSH levels were estimated using two immunological techniques [RIA and immunoradiometric assay (IRMA)] and in vitro bioassays (BIO), using mouse Leydig cells and rat granulosa cells, respectively. In PCOD patients mean alpha-subunit, free androgen index [FAI; testosterone x 100/sex hormone-binding globulin (SHBG)], androstenedione, estrone, and estradiol (E2) were significantly elevated compared to levels in the early follicular phase of control cycles and non-PCOD patients. In addition, in PCOD patients mean IRMA-LH and RIA-LH levels were distinctly increased (2.8- to 3.6 fold, respectively; both comparisons, P less than 0.001) compared to control values, but in the same order of magnitude (1.3- to 1.4-fold increments) as that in non-PCOD patients. However, the median BIO-LH level in PCOD patients was 5.9-fold higher than that in non-PCOD patients and 4.0-fold higher than the BIO-LH in the early follicular phase of control women. Consequently, the median BIO/IRMA-LH ratio was 4.8-fold higher in PCOD patients compared to non-PCOD patients. In women with cycle abnormalities, individual BIO/IRMA-LH ratios correlated with BIO-LH (rs = 0.48), FAI (rs = 0.39), free estrogens (E2/SHBG ratios; rs = 0 0.47), and dehydroepiandrosterone sulfate (rs = 0.60) concentrations. Mean IRMA-, RIA-, and BIO-FSH levels and BIO/IRMA-FSH ratios were not significantly different when various groups were compared. Although RIA- and IRMA-LH levels showed good correlation (rs = 0.88), RIA-LH levels were consistently higher, resulting in distinctly higher RIA-LH/FSH ratios (mean, 4.5) compared to IRMA-LH/FSH ratios (median, 1.8) in PCOD patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Thirty-one young female athletes and 13 age-matched sedentary controls were studied throughout one menstrual cycle or over a 6 week period. Blood was sampled on 5 days per week. Episodic gonadotrophin secretion was measured in the early follicular phase and in the late luteal phase by blood sampling over a 12-h period at 15-min intervals. Eight athletes had anovulatory cycles, nine had impaired progesterone (P4) secretion during the luteal phase and 14 had normal cycles as judged from oestradiol (E2) and P4 plasma levels. Athletes with normal cycles had shorter cycles, lower E2 maxima at midcycle, and lower E2 and P4 concentrations during the luteal phase than had sedentary controls. Episodic luteinizing hormone (LH) secretion in the early follicular phase was significantly impaired in the anovulatory athletes: the average LH values over 12 h and the number of secretion episodes were significantly reduced. No significant changes were seen in follicle stimulating hormone secretion.

Hormonal studies were attempted to specify the pathogenesis of juvenile uterine bleedings (JUB) and to optimize treatment in 104 female patients aged 10 to 17 years. It is concluded that JUB occurring during prepuberty and early puberty are not related to any derangements in the establishment of the reproductive system, apparently being a variant of this process. JUB that occur in late puberty and in the juvenile period are associated with reduced ovarian function and may be regarded as dysfunctional uterine bleedings.

Prolactin and FSH were radioimmunologically found in 16 cases of primary amenorrhoea, 73 cases of secondary amenorrhoea, 27 cases of oligomenorrhoea as well as 22 cases of eumenorrhoea and we diagnosed 36 hyperprolactinaemias, 4 tumours of the hypophysis and 4 hypergonadotropic amenorrheas. In 25 cases of post-pill-amenorrhoeas we found 12 functional hyperprolatinaemias. The prolactinomas were subjected to microsurgical therapy. Functional hyperprolactinaemia was treated with bromocryptin, especially in those cases where a child was wanted.

Thirteen women with luteal phase defects (LPD) confirmed by endometrial biopsies and 14 with histologically normal endometria were studied for early follicular and midfollicular phase follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels and for midluteal phase progesterone, estrogen, testosterone, and prolactin levels. The results showed that the women with LPD had significantly lower FSH levels and FSH/LH ratios in the early and midfollicular phases. LH levels, however, were similar in the LPD and normal women. During the midluteal phase, the LPD women showed significantly lower levels of progesterone and estrogen and normal levels of testosterone and prolactin. These findings reaffirm the prevailing concept that events surrounding follicular growth and development can indeed influence the quality of that cycle's corpus luteum. Furthermore, LPD as a result of hyperprolactinemia appears to be a different entity from that due to inadequate follicular phase FSH.

High serum follicle stimulating hormone (FSH) values are consistent with ovarian failure. We studied the progress of 67 women aged under 35 years with oligomenorrhoea or secondary amenorrhoea in whom the serum FSH value was greater than 20 U/1. Twenty-four patients remained amenorrhoeic, but 17 ovulated and six conceived, two on two occasions. Coincident mean serum luteinising hormone (LH) concentrations were significantly lower and mean total urinary oestrogen concentrations were significantly higher in patients who subsequently ovulated, but the degree of increase in FSH did not correlate well with later ovarian function. Treatment with oestrogens, clomiphene citrate, human pituitary gonadotrophin, and bromocriptine was of no benefit in inducing an ovarian response while FSH concentrations remained raised. Our results suggest that a considerable proportion of younger women with ovulatory disorders associated with FSH values in the menopausal range will spontaneously resume ovulation and some will conceive.

To study the prognosis of adolescent ovulatory disturbance in patients with persistently elevated LH levels (greater than or equal to 25 mIU/ml), normal FSH levels and high LH/FSH (greater than 2.0), 17 patients aged 12-19 years were studied longitudinally for 4-9 years. These 17 patients consisted of 7 patients suffering from amenorrhea with estrogenic effect, 5 patients with functional bleeding, 3 patients with delayed menarche and 2 patients with oligomenorrhea. All of the patients showed exaggerated LH responses to 100 micrograms of LHRH administration while the FSH responses were not different from those obtained from normal women. Out of the 17 patients, 10 (58.8%) patients showed the values of testosterone and 7 (41.2%) androstenedione which were above the mean + 2SD of normal women. Consequently, the mean serum testosterone and androstenedione levels were significantly higher than those in normal women. The mean LH (36.6 +/- 8.3 mIU/ml), FSH (11.2 +/- 1.5 mIU/ml) and LH/FSH (3.3 +/- 0.8) at the age of 21.4 +/- 2.5 years were not different from the mean LH (39.9 +/- 13.3 mIU/ml), FSH (10.8 +/- 1.8 mIU/ml) and LH/FSH (3.8 +/- 1.5) at the age of 16.1 +/- 1.8 years, respectively. None of the 17 patients showed amelioration or deterioration of ovulatory disturbance during long-term observation. To further investigate the central dopamine activity, 10 mg of metoclopramide (MCP) was administered intravenously in these 17 patients. The LH and PRL responses to MCP were evaluated, and the results were compared to those obtained from 17 patients aged over 20 with PCO and from 17 normal women. The LH responses to MCP were positive in this juvenile patient group and the patients aged over 20 PCO group. However, the LH responses to MCP were negative in normal women in both the follicular and luteal phases. In contrast, the PRL responses to MCP were significantly attenuated in juvenile patients and in patients aged over 20 with PCO compared to those in normal women. Since the hormonal profiles in these 17 patients with anovulation or oligo-ovulation were very similar to those in the group aged over 20 with established PCO, it may be suggested that 1) at least part of the adult patients with PCO may have had PCO from late adolescence; 2) the majority of the patients with high LH and normal FSH levels in adolescence will suffer from ovulatory disturbance continuously; 3) in these patients, an aberration of central dopamine in control of LH and PRL may exist.

This study was designed to investigate the gonadotropin response to luteinizing hormone releasing hormone (LHRH) in patients with hyperthyroidism, as related to the presence or absence of menstrual disorders. Forty-one Japanese women with hyperthyroidism were separated into groups on the basis of the presence of a regular menstrual cycle, hypomenorrhea, or amenorrhea and further subdivided into the phase of the menstrual cycle at the time of testing. The findings in these groups were compared with those in normal subjects with respect to thyroid function, basal serum LH and FSH levels and serum LH and FSH responses to LHRH, and basal estradiol levels. Serum LH responses to LHRH were increased over normal subjects in those with hyperthyroidism regardless of the phase of the menstrual cycle and regardless of the presence or absence of menstrual disturbances. However, these augmented LH responses to LHRH were less marked in those with menstrual disorders than in those with regular menstruation. Both basal serum FSH and peak serum FSH response to LHRH were also increased in the follicular phase but not in the luteal phase of the cycle in hyperthyroid patients, regardless of menstrual function. These results suggest that high levels of circulating thyroid hormones augment the gonadotropin response to LHRH, and that increased LH and FSH secretion probably maintains the normal cyclic pituitary gonadal axis function in patients with hyperthyroidism.

Serum FSH and LH in women with luteal phase defect were measured. Their serum FSH and LH were lower than those in normal women and higher than those in women with amenorrhea. Administration of clomiphene citrate to the women with luteal phase defect were effective in 2/3 of the cases. These results are consistent with the hypothesis that a relative deficiency of FSH during the follicular phase results in diminished follicular development and subsequent inadequate corpus luteum maintenance.

Thirty-five women with menstrual abnormalities were given 100 microng of luteinizing hormone-releasing hormone (LHRH) by bolus intravenous injection in an attempt to simplify and quantitate the usefulness of this test in clinical management. Peak and total gonadotropin responses are highly correlated. Peak and total LH are significantly related to basal LH but no similar relationship could be established for follicle-stimulating hormone (FSH). There is no association between gonadotropin response and prolactin levels or body weight. Basal estradiol levels are inversely related to FSH response but not to LH response. It is concluded that the use of an intravenous 100-microng bolus of LHRH is of little use as a clinical test for the gynecologic endocrine patient.