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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of fetal exposure to spironolactone (SPL), an aldosterone antagonist with weak antiandrogen and gestagen properties, upon the pituitary-gonadal axis were studied in the offspring of rats that had been treated daily from gestation day 14 to day 20 with 10 or 20 mg SPL or the solvent vehicle (for controls). At 70-80 days of age, SPL-exposed rats showed no alterations in external genitalia or in body weight. However, males displayed a dose-dependent decrease in the weights of the ventral prostate and seminal vesicles. Whereas basal and gonadotropin-releasing hormone (GnRH)-induced plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and 5 alpha-dihydrotestosterone levels were similar to controls, basal plasma and pituitary prolactin (Prl) levels were reduced (SPL-exposed 6.8 +/- 1.0 vs. controls 15.8 +/- 2.8 ng/ml and 6.1 +/- 1.2 vs. 11.6 +/- 1.8 microgram/anterior pituitary gland; mean +/- SEM). Cytosolic androgen receptors in ventral prostate were nonsignificantly decreased, but they increased after GnRH in contrast to controls. Nuclear androgen receptors were normal. Females displayed normal estrous cycles. Basal and GnRH-induced plasma FSH, Prl, estradiol, and progesterone concentrations were similar to controls, whereas plasma LH was elevated. Estrogen receptors in uterine cytosol were low and increased after GnRH. Ovaries and uteri were enlarged. The present study demonstrates that in utero exposure to SPL leads to endocrine dysfunctions that persist into adulthood. They are characterized in males by hypoprolactinemia, reduced weights of accessory sex organs, and a suggestion of functional modifications of androgen receptors. In females they are characterized by increased LH secretion, increased ovarian and uterine weights, and decreased uterine cytosol estrogen receptors, suggesting enhanced estrogenic action.
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PMID:Modifications of the gonadal function in the adult rat after fetal exposure to spironolactone. 392 11

Twenty-one post-menopausal women on no other medication were treated with a low dose (0.625 mg/day) of conjugated equine estrogen (CEE) for a mean (+/- SEM) period of 2.6 +/- 0.2 mth (range 1.75-4.75). Blood samples were collected before and at the completion of therapy, and alterations in the levels of prolactin (PRL), follicle-stimulating hormone (FSH), luteinizing hormone (LH), sex hormone-binding globulin (SHBG) and certain steroid hormones, including the free testosterone (T) index (T/SHBG) were studied. Following treatment, a significant increase in SHBG levels produced a significant decrease in the free T index (P less than 0.005). As expected, no changes were observed in the levels of PRL and steroid hormones other than estrone (E1) and estradiol-17-beta (E2). Our observations indicate that treatment of post-menopausal women with low-dose estrogen lowers the unbound T.
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PMID:The effect of estrogen treatment on plasma concentrations of steroid hormones, gonadotropins, prolactin and sex hormone-binding globulin in post-menopausal women. 392 23

Serum gonadal hormones, gonadotrophins and zinc levels were studied in thirteen men aged 29-62 yr with chronic renal failure undergoing haemodialysis. All patients had decreased libido and impotence. Serum testosterone levels in patients (18.5 +/- 1.3 (SEM) nmol/l) were significantly lower (p less than 0.05) than in the control group (24.1 +/- 2.2 (SEM) nmol/l) although salivary testosterone levels were strictly within the normal range. Mean serum 17-beta-oestradiol and luteinizing hormone levels (0.19 +/- 0.03 (SEM) nmol/l, and 57.4 +/- 13.1 (SEM) IU/l, respectively) were significantly higher (p less than 0.05 and p less than 0.005, respectively) than in the control group (0.11 +/- 0.02 (SEM) nmol/l and 14.8 +/- 1.9 (SEM) IU/l, respectively). Mean progesterone and follicle-stimulating hormone levels in patients were not significantly different from those of control subjects. Mean prolactin values in patients (1,019 +/- 285 (SEM) mIU/l) were significantly higher (p less than 0.01) than in the control group (211 +/- 24 (SEM) mIU/l). Serum prolactin levels in five patients were extremely high (above 1,200 mIU/l). There was no statistically significant difference in serum zinc levels between patients and controls. As salivary testosterone is normal, it seems that hyperprolactinaemia and raised serum 17-beta-oestradiol levels may be responsible, at least in part, for sexual dysfunction in male patients with chronic renal failure receiving haemodialysis.
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PMID:Hormonal profile and serum zinc levels in uraemic men with gonadal dysfunction undergoing haemodialysis. 393 99

The demonstration that luteinizing hormone (LH) release from the pituitary is episodic rather than constant raises fundamental questions regarding the physiologic control of pulsatile LH secretion and its possible alteration in patients with gonadal disorders. To evaluate this mode of LH secretion, quantitative means of analyzing LH pulse amplitude, frequency, shape, and area were established and utilized to study normal subjects and patients with disorders of gonadotropin secretion. Similar patterns of LH secretion were observed in normal men, in women during the follicular phase of the menstrual cycle, and in patients with hyper- and hypogonadotropism, hirsuitism, and amenorrhea (mean pulse amplitude 39-179% from nadir to peak, frequency 2.7-3.9 secretory spikes/6 h). These observations suggested that the pattern of LH secretion is similar in both normal individuals and in those with a variety of pathologic conditions. By contrast, the pattern of pulsatile secretion appeared to differ in the following conditions. LH pulses of higher amplitude (333+/-170%) and lower frequency (1.6+/-0.24 SEM/6 h) characterized the secretory patterns of women during the luteal phase of the menstrual cycle, suggesting that gonadal steroids may modulate LH pulses. LH pulses of low amplitude (26+/-2.1%) and frequency (1.3+/-0.36/6 h) were observed in women with anorexia nervosa. Either integrated LH levels or a mean LH level determined from multiple samples provided a more accurate reflection of gonadotropin secretion than the use of single LH measurements. With multiple sampling over 6 h, it was possible to reduce the 95% confidence limit of LH estimates from +/-50-90 to +/-12%. This allowed normal subjects to be distinguished from patients with low or moderately elevated LH levels in whom gonadotropin levels in single samples were often in the "normal range."Several aspects of the physiologic control of pulsatile LH secretion were studied. The concordance of follicle-stimulating hormone (FSH) with LH pulses progressively increased as LH pulse height increased (P < 0.01) suggesting possible hypothalamic mediation of gonadotropin pulses. Measurement of the "apparent half-life" of LH after secretory spikes revealed half times of 34-233 min. It is likely that this variability was attributable to at least two phenomena: (a) constant low level LH secretion that continued after certain secretory episodes but not others; (b) variable mixing of newly secreted LH into at least two pools. The alpha adrenergic-blocking agents, chlorpromazine and phentolamine, failed to block LH secretory spikes at doses sufficient to result in a 30 mm drop in systolic blood pressure in normal men.
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PMID:Episodic luteinizing hormone secretion in man. Pulse analysis, clinical interpretation, physiologic mechanisms. 472 55

In a significant proportion of patients with acromegaly, a non-specific increase in plasma growth hormone (GH) has been recognized following administration of thyrotropin-releasing hormone (TRH) or luteinizing hormone-releasing hormone (LH-RH), probably due to the lack of the specificity of the receptor in their tumor cells. In this study, the effects of corticotropin-releasing factor (CRF), a newly isolated hypothalamic hormone, in addition to TRH and LH-RH, on plasma levels of GH and the other anterior pituitary hormones were evaluated in 6 patients with acromegaly. Synthetic ovine CRF (1.0 microgram/kg), TRH (500 micrograms) or LH-RH (100 micrograms) was given as an iv bolus injection, in the morning after an overnight fast. Blood specimens were taken before and after injection at intervals up to 120 min, and plasma GH, adrenocorticotropin (ACTH), thyrotropin, prolactin, luteinizing hormone, follicle-stimulating hormone and cortisol were assayed by radioimmunoassays. A non-specific rise in plasma GH was demonstrated following injection of TRH and LH-RH, in 5 of 6 and 2 of 5 patients, respectively. In all subjects, rapid rises were observed in both plasma ACTH (34.3 +/- 6.2 pg/ml at 0 min to 79.5 +/- 9.5 pg/ml at 30 min, mean +/- SEM) and cortisol level (9.1 +/- 1.3 micrograms/dl at 0 min to 23.4 +/- 1.2 micrograms/dl at 90 min). However, plasma levels of GH and the other anterior pituitary hormones did not change significantly after CRF injection. These results indicate that CRF specifically stimulates ACTH secretion and any non-specific response of GH to CRF appears to be an infrequent phenomenon in this disorder.
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PMID:Effect of synthetic ovine corticotropin-releasing factor on growth hormone secretion in patients with acromegaly. 609 67

Hirsutism and menstrual patterns were evaluated in 32 female patients with documented diethylstilbestrol (DES) exposure in utero. Nine nonhirsute regularly menstruating and nine consecutive hirsute oligomenorrheic women with no known DES exposure served as controls. Hormone measurements included follicle-stimulating hormone, luteinizing hormone, prolactin, cortisol, testosterone, androstenedione, dehydroepiandrosterone, sex hormone-binding globulin, and estradiol. Hirsutism was present in 72% and irregular menses occurred in 50% of DES-exposed patients. The mean age of the DES-exposed group was 26.8 +/- 0.7 years (mean +/- SEM). The mean age of mildly hirsute DES-exposed patients (24.7 +/- 1.4 years) was significantly lower (p less than 0.05) than that of severely hirsute DES-exposed patients (28.8 +/- 1.1 years). Mean testosterone, androstenedione, sex hormone-binding globulin, testosterone/sex hormone-binding severely hirsute DES-exposed group but higher than in nonhirsute control subjects. Mean testosterone, androstenedione, sex hormone-binding globulin, testosterone/sex hormone-binding globulin, and luteinizing hormone levels in hirsute DES-exposed patients were similar to those in hirsute control subjects but significantly higher than those in nonhirsute control subjects. Mean DHA levels as well as the clitoral indices were comparable in all groups. Our data suggest that DES exposure in utero may result in hypothalamic-pituitary-ovarian dysfunction.
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PMID:Hirsutism and menstrual patterns in women exposed to diethylstilbestrol in utero. 621 86

Seasonal changes in the hypothalamic-hypophyseal axis were investigated using tissue from 49 light-horse mares, of mixed breeding. Hypothalamic and pituitary tissues were collected at 5 intervals throughout the years 1981 and 1982, representing midbreeding season (July, n = 10), transition out of the breeding season (October, n = 11), midanestrus (December, n = 8), transition into the breeding season (March, n = 10), and again in the following midbreeding season (July, n = 10). The hypothalamic region was dissected into preoptic area, body and median eminence. Gonadotropin-releasing hormone (GnRH) was extracted from hypothalamic samples with methanol-formic acid and quantified by radioimmunoassay. The anterior pituitary was homogenized and receptors for GnRH were quantified in a crude membrane fraction. Concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured in the resulting supernatant. Content of GnRH in each of the 3 hypothalamic areas varied with season (P less than 0.01) and was lowest during midanestrus (P less than 0.05). There was no effect of season (P greater than 0.01) on either concentration or total number of receptors for GnRH, or concentration of FSH in the anterior pituitary. Concentrations of LH in the anterior pituitary varied with season (P less than 0.001). Means (+/- SEM) for the 5 collection times were 15.5 +/- 2.7, 9.7 +/- 2.4, 2.3 +/- 0.5, 2.7 +/- 0.4 and 11.7 +/- 1.5 microgram LH/mg anterior pituitary, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seasonal variation in hypothalamic content of gonadotropin-releasing hormone (GnRH), pituitary receptors for GnRH, and pituitary content of luteinizing hormone and follicle-stimulating hormone in the mare. 632 38

Gonadotropins are released in a pulsatile fashion at a frequency of between 1 and 2 hours in the follicular phase of the menstrual cycle. Human menopausal gonadotropins are usually administered intramuscularly. We evaluated the gonadal response to intravenous human menopausal gonadotropins administered in a pulsatile fashion over nine treatment cycles in three anovulatory infertile women. Human menopausal gonadotropin pulses in doses up to 12 IU follicle-stimulating hormone at frequencies between 2 to 3 hours over 3 to 17 days resulted in ovulation in five cycles with one pregnancy being conceived. In the ovulatory cycles (5,000 to 10,000 IU of human chorionic gonadotropin was used to induce ovulation), the 17 beta-plasma estradiol level was 961 +/- 128 versus 326 +/- 95 pg/ml (mean +/- SEM) in the anovulatory cycles (p = 0.015). The dose of human menopausal gonadotropins (in ampules of Pergonal, 75 IU of follicle-stimulating hormone and 75 IU of luteinizing hormone) in the intravenous cycles needed to induce ovulation was 12.3 +/- 1.4 versus 20.4 +/- 0.9 for intramuscular cycles (n = 80 in 23 women, p = 0.008). Treatment was well tolerated and without complications. We are continuing to explore the use of this apparently more efficient mode of administering human menopausal gonadotropins to anovulatory patients resistant to other techniques of ovulation induction therapy.
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PMID:Successful induction of ovulation and conception with pulsatile intravenous administration of human menopausal gonadotropins in anovulatory infertile women resistant to clomiphene and pulsatile gonadotropin-releasing hormone therapy. 642 60

The chronic administration of superactive agonists of gonadotropin releasing hormone (GnRH-A) have been reported to have a direct inhibitory effect on the sex tissues of the male rat. In an attempt to confirm or refute this statement, adult male rats were either left intact or were castrated and then treated daily for 14 days with either testosterone (T), dihydrotestosterone (DHT) or sesame oil (vehicle). Half of the intact and castrate animals also received daily injections of 200 ng of the GnRH agonist, D-Leu6, des-Gly10-GnRH ethylamide for 14 days. Twenty-four hours after completing treatment, blood levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and T were measured by radioimmunoassay and the ventral prostate gland (VP), seminal vesicle (SV) and penis were weighed. After 2 weeks of GnRH-A treatment, the plasma T level was reduced from 2506 +/- 170 (pg/ml +/- SEM) in the intact, nontreated animals to 907 +/- 69 in the intact, GnRH-A-treated group, indicating that the dosage of GnRH-A used in this study had an inhibiting effect on T secretion. No differences were observed in the VP, SV and penile weights between the castrate, GnRH-A and the castrate, nontreated groups. When exogenous T or DHT was given for 14 days to these castrated animals, the concomitant administration of GnRH-A did not appear to have any effect on the plasma T levels or the sex accessory tissue weights. These data suggest that GnRH-A itself does not appear to have a direct inhibitory or stimulatory effect on the sex tissues of the adult male rat.
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PMID:Effects of chronic D-Leu6, des-Gly10-gonadotropin releasing hormone ethylamide on male sex tissues. 642 36

This study was designed to determine whether the lack of secretion of endogenous gonadotropin-releasing hormone is the etiology of the hypogonadotropic state of pregnancy. For this purpose, five pregnant women in their first trimester received a single intravenous dose of 150 micrograms of gonadotropin-releasing hormone. Another five women in the first trimester and five women in the second trimester of pregnancy received daily intramuscular injections of 500 micrograms of gonadotropin-releasing hormone for 10 consecutive days. This was followed by a single 150 micrograms gonadotropin-releasing hormone test and then a 24-hour pulsatile infusion of gonadotropin-releasing hormone of 10 micrograms/min/6 min given every hour. Baseline plasma beta-luteinizing hormone and follicle-stimulating hormone were undetectable in all women. Mean +/- SEM plasma beta-human chorionic gonadotropin was significantly higher (p less than 0.001) in the first trimester than in the second trimester, and mean plasma estradiol and prolactin were significantly increased (p less than 0.001 and 0.05, respectively) during the second trimester of pregnancy. After the 10-day treatment with gonadotropin-releasing hormone there was a significant increase (p less than 0.05) in baseline beta-luteinizing hormone and follicle-stimulating hormone only in the first-trimester pregnant women. The single as well as the pulsatile administration of gonadotropin-releasing hormone resulted in a further significant increase in both beta-luteinizing hormone and follicle-stimulating hormone. In contradistinction, women in the second trimester of pregnancy showed a blunted response to the daily and pulsatile administration of gonadotropin-releasing hormone. Since the pituitary secretion of gonadotropin was functionally restored by the administration of exogenous gonadotropin-releasing hormone, possibly there is a lack of secretion of endogenous gonadotropin-releasing hormone during the first trimester of pregnancy. An increased negative feedback produced by increasing levels of plasma estradiol might be the cause of pituitary refractoriness to gonadotropin-releasing hormone during the second trimester of pregnancy.
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PMID:Priming with gonadotropin-releasing hormone restores gonadotropin secretion during first but not second trimester of pregnancy. 643 25


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