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At least 55 records · Page 3Linked to original sources
PubMed1977

The LH and FSH responses to LH-releasing hormone (LH-RH) in girls with true precocious puberty treated with cyproterone acetate.

Ten girls with precocious puberty ranging in age from 7 to 10 7/12 years who were treated with oral cyproterone acetate on a long term basis, were subjected to LH-RH tests, prior to and 3 to 16 months after the institution of therapy. Cyproterone acetate was given in doses from 60 to 153 mg/m2, which proved to be clinically effective, as evidenced by the slowing down of sexual maturation. The basal levels of LH were found to be unaffected by therapy and corresponded to the pubertal stages of the individual girls. The peak increment of LH after LH-RH stimulation was markedly suppressed by the therapy. FSH secretion and its responsiveness to LH-RH was not affected by cyprotereone acetate. The basal levels of FSH were higher during therapy than before, but the peak FSH increment remained the same. An escape phenomenon in the LH peak response was evident in 2 patients upon retesting after prolonged therapy. It is possible that the antigonadotrophic action of cyproterone acetate is due to its progestational nature.

Child↗
PubMed1995

Luteinizing hormone (LH)-releasing hormone in third ventricular cerebrospinal fluid of the ewe: correlation with LH pulses and the LH surge.

Morphological evidence suggests that LHRH may be secreted into cerebrospinal fluid (CSF), but only in the rhesus monkey has CSF LHRH been found to reflect changes occurring in the LHRH neuroendocrine system. This study investigated whether LHRH is detectable in ovine CSF and, if so, whether its release profile correlates with peripheral LH profiles during pulse and surge conditions. A polyethylene catheter was threaded through a stainless steel guide cannula previously implanted into the third ventricle of an ovariectomized ewe, which enabled continuous CSF withdrawal on repeated occasions. The first experiment (n = 3) showed that peripheral LH concentrations were unaffected by CSF removal at rates of 12, 30, 50, and 100 microliters/min, and the second (n = 4) established that CSF LHRH secretion was pulsatile, with considerable variation in pulse amplitude (6.3 +/- 1.8 pg/ml; range, 1.3-18.7 pg/ml). In the third experiment (n = 6), an endogenous LH surge was induced after progesterone withdrawal and 17 beta-estradiol administration. Although CSF LHRH (15.3 +/- 1.3 h) and peripheral LH (14.8 +/- 1.0 h) surges occurred simultaneously, CSF LHRH concentrations were greater than half-maximal levels for longer (11.0 +/- 0.6 h; P < 0.005) than LH concentrations (6.0 +/- 0.4 h). This is the first study in sheep to reveal the presence of LHRH in CSF and show that it expresses dynamic and longer term changes coincident with peripheral LH fluctuations. CSF LHRH analysis also permits repeated sampling from individuals and, therefore, long term within-individual comparisons.

Animals↗
PubMed2000

Plasma endothelin and LH-RH, LH, FSH, prolactin, progesterone, 17alpha-hydroxyprogesterone, estrone, 17beta-estradiol, delta4-androstenedione, testosterone, active renin, angiotensin-II and ANP levels in blood and LH, estrone and 17beta-estradiol and pregnanediol levels in urine of normal cycling women.

In order to investigate the endothelin (ET) levels and their relationship to various hormones during the menstrual cycle, we measured endothelin-1, -2 and -3 (ET-1, -2 and -3), big ET-1 and big ET-3 levels in 27 normally cycling women (mean age 27 years). Simultaneous determination of luteinizing hormone-releasing hormone (LH-RH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, progesterone, 17alpha-hydroxyprogesterone (17-OHP), estrone, 17beta-estradiol, delta4-androstenedione, testosterone, active renin, angiotensin-II (A-II) and atrial natriuretic peptide (ANP) in blood, and LH, estrone and 17beta-estradiol and pregnanediol levels in urine was made in the same 27 women. The levels of ET-2 in plasma were found to be 20% of those of ET-1. In addition, ET-1 levels were measured in the endometrium of the normal uterus. Plasma ET-1 and ET-3 levels fluctuated during the menstrual cycle, with a peak at the luteal phase, but showed only a negative relationship (p < 0.01) to each other at the menstrual phase, whereas big ET-1 and big ET-3 levels showed no significant changes. Plasma ET-1 and ET-3 levels showed no significant relationship to the big ETs. As for the relationship to other hormones, plasma ET-3 had a negative relationship (p < 0.01) to prolactin and a positive correlation (p < 0.01) with ANP during the entire menstrual cycle. Plasma ET-1 and ET-3 showed a partial positive or negative correlation to LH, FSH, prolactin and ANP levels, depending upon the cycle phase, whereas plasma ETs and big ETs were unrelated to other hormones in the blood, and LH, estrone, 17beta-estradiol and pregnanediol in the urine throughout the menstrual cycle. At each menstrual stage, plasma ET-3 levels were more significantly related to LH, FSH, prolactin and ANP than ET-1, indicating a closer relationship between ET-3 and these circulating hormones during the menstrual cycle. The ET-1 level showed no significant change in the endometrium during the menstrual cycle.

Adult↗
PubMedDate not supplied

[2 variants of the radioimmunochemical method of determination of LH-releasing factor (LH-RF). Distribution of LH-RF in various hypothalamic structures].

The authors elaborated two variants of the radioimmunochemical method of determination of the LH-releasing factor (LH-RF). Diluted antisera (AS) obtained by the immunization of rabbits with the LH-RF-ovalbumin were used in the first method; AS polymerized with isobutyl ester of chlorcarbonic acid were used in the second one. The minimal amount of the hormone determined in the I variant was 5 pg, and in the 11 one--20 to 30 pg. The method is highly specific, since the antisera gave no cross reaction with a wide set of protein-peptide hormones synthesized with the hypothalamus and the hypophysis. The presence in the samples of tissue components of the hypothalamus and of the cerebral cortex extractable with 2M CH3COOH failed to influence the precision of the test. In examining the LH-RF content in the brain structures there was revealed that in the sexually mature male rats the whole hypothalamus contained an average of 7.5 ng, the arcuate nuclei--1.5 ng and the medial eminence--2.5 ng of LH-RF; the supraoptic nuclei and the cerebral cortex contained no LH-RF determinable by the method described. Two weeks after the castration the mean content of the hormone in the whole hypothalamus decreased to 5.5 ng, in the medial eminence--to 0.6 ng, and showed no significant change in the arcuate nuclei.

Animals↗
PubMed1987

Effects of immunoneutralization of luteinizing hormone (LH)-releasing hormone on testicular prolactin and LH receptors in the golden hamster and on LH receptors in the Djungarian hamster.

In male Syrian hamsters, seasonal transitions between reproductive activity and quiescence are accompanied by major alterations in testicular binding of LH/hCG and PRL. These alterations are believed to be due to the photoperiod-induced changes in PRL secretion, but other adenohypophyseal hormones appear to be involved as well. To elucidate the role of LH and FSH in the control of testicular LH/hCG and PRL receptors, we have examined the consequences of selective suppression of gonadotropin release by immunoneutralization of endogenous LHRH. In adult Syrian hamsters, four weekly injections of LHRH antiserum produced significant reductions in plasma levels of LH, FSH, and testosterone and in the weights of the testes and the seminal vesicles; no change in plasma PRL; and a significant reduction in the total content (femtomoles per testis) of testicular LH/hCG and PRL receptors. The concentration of LH/hCG receptors (femtomoles per mg protein) was significantly increased. In adult males of another seasonally breeding species, the Djungarian hamster (Phodopus sungorus), four weekly injections of LHRH antiserum produced suppression of plasma LH and FSH, no change in plasma PRL, a reduction in the weights of the testes and the seminal vesicles, an increase in the concentration of testicular LH/hCG receptors, and a decrease in their total content. Alterations in testicular LH and PRL binding induced by treatment with LHRH antiserum in the present study were qualitatively similar to changes induced by exposure to short photoperiod or by treatment with bromocriptine. We conclude that gonadotropins normally participate in the regulation of testicular LH/hCG and PRL receptors in the Syrian hamster and LH/hCG receptors in the Djungarian hamster. Seasonal changes in the content of LH/hCG and PRL receptors in the testes appear to be due to photoperiod-induced alterations in the secretion of both PRL and gonadotropins.

Animals↗
PubMed1983

Effects of LH-RH agonist or LH-RH immunoneutralization on pituitary and ovarian LH-RH receptors in female rats.

Hyperstimulation of pituitary function using daily injections of 50,500 or 5000 ng LH-RH agonist for 3 weeks or hypostimulation by immunoneutralization of endogenous LH-RH led to disrupted oestrous cycles and profound changes in ovarian morphology. Despite this, the number of pituitary and ovarian LH-RH receptors remained within the range found in normally cyclic animals. Autoradiography confirmed that specific binding was located in theca, granulosa and luteal cells. These results suggest that autoregulation of pituitary and ovarian LH-RH receptors is not of primary importance in the cyclic female rat.

Animals↗
PubMed1986

Comparison of the time courses of luteinizing hormone (LH) secretion rates during continuous stimulation by LH-releasing hormone (LH-RH) in vivo and in vitro.

The patterns of LH secretion during constant stimulation of the pituitary glands of estradiol-treated ovariectomized rats with a maximally stimulating amount of LH-RH in vivo and in vitro correspond with each other qualitatively and quantitatively. In vitro the changes with time of the LH secretion rate are somewhat retarded, especially the occurrence of desensitization.

Animals↗
PubMed1976

[Mechanism of LH release with synthetic LH-RH (author's transl)].

The purpose of this study is to examine the effect of LH-RH on LH release in the baboon. Fifteen female baboons having the normal menstrual cycle were used for this study. On hundred mug of synthetic LH-RH was injected subcutaneously in both the early follicular phase and the early luteal phase. For control purposes, 1 ml of saline was injected subcutaneously in the luteal phase. Blood samples were collected by femoral vein puncture with light anesthesia under prearranged schedule and were assayed for LH-RH, LH, estrogen and progestin. The plasma level of LH-RH reached a maximum within 4 minutes after s.c. injection of 100 mug LH-RH, decreased sharply at first, and then slowly later. Fast and slow disappearance components (t1/2 = 4.7 min., 37.1 min. respectively) were observed. In the baboon given LH-RH during the luteal phase, peaks in plasma levels of LH were observed within 30 minutes and within 90 to 150 minutes after injection. A lesser pituitary response to LH-RH for LH release occurred during the follicular phase. The first peak of LH was well-correlated with the peak of plasma LH-RH but the later elevations of LH (observed within 90 to 150 minutes after LH-RH injection) were not necessarily related to the plasma level of immunoassayable LH-RH. Elevation of plasma levels of estrogen and progestin was observed wtihin 45 minutes after LH-RH injection. In saline control, the plasma level of LH was not elevated; however, plasma levels of estrogen and progestin were increased within 45 minutes after saline injection. Later elevation of plasma LH observed between 90 and 150 minutes after LH-RH injection may be due to administered LH-RH in cooperation with elevated levels of plasma estrogen and progestin. To pursue this problem, injections of estrogen and/or progesterone were performed during the early follicular phase. Injection of 600 mug of estrodiol benzoate (EB) for 3 days caused an elevation of plasma level of LH and enhanced pituitary LH responsiveness to LH-RH for LH release; however, injection of 100 mug EB for 3 days showed less effect on LH release. Injection of 10 mg of progesterone for 3 days also caused an elevation of plasma level of LH and enhanced the pituitary responsiveness to LH-RH release. Injection of both 600 mug EB and 10 mg progesterone for 3 days did not elevate plasma level of LH and showed no significant effect of LH-RH on LH release as compared to control. These results suggest that elevated levels of circulating estrogen and progestin may determine LH release and exposure of the pituitary to LH-RH is necessary for LH release. In dose and time schedule used in this study, it is inferred that estrogen and progesterone may exert their direct effect to hypothalamus on endogenous LH-RH secretion and also may exert their effect on pituitary gonadotrophs to change the sensitivity to LH-RH, i.e. these steroid hormones may be major factors in the control of gonadotropin release in the baboon.

Animals↗
PubMed1975

Effects of estradiol-17beta on LH-RH/FSH-RH-induced, and spontaneous, LH release in prepubertal female pigs.

The effect of estrogen (E2) on pituitary response to LH-RH/FSH-RH (LH-RH) was examined in immature female pigs (gilts). Eight gilts (9-10 weeks old) received iv injections of 2.5, 5.0, 10.0, 20.0, and 40.0 mug LH-RH, beginning 4 days after placement of indwelling jugular cannulae. Blood samples were drawn at 5-min intervals following LH-RH injection and plasma LH was determined by RIA and expressed as ng R786-3/ml. Pituitary responses were expressed as the increment in LH levels above baseline (delta LH). Pretreatment LH levels were 0.45-1.25 ng/ml. Responses to LH-RH (delta LH plus or minus SE) ranged from 3.7 plus or minus 0.6 (at 5 min) to 8.4 plus or minus 1.4 ng/ml (at 20 min) for 2.5 and 40 mug doses, respectively. Three additional prepubertal gilts were cannulated and implanted with E2. After 3 days plasma estrogens rose from approximately 30 pg/ml to 289 plus or minus 34 pg/ml and the dose-response studies were repeated. Prestimulation LH concentration was consistently below 0.4 ng/ml and delta LH levels ranged from 1.4 plus or minus 0.5 (at 10 min) to 5.7 plus or minus 1.3 ng/ml (at 20 min) for the 2.5 and 40.0 mug doses, respectively. Analysis of the regression equations for delta LH on log LH-RH dose showed that the adjusted means for LH response were significantly lower (P less than 0.02) in E2 implanted animals. However, the regression coefficients were not different (P greater than 0.5). On the basis of these and other analyses, it is concluded that chronic E2 treatment depresses both basal LH secretion and pituitary responsiveness, but that pituitary sensitivity to LH-RH is not modified. Several nonimplanted females showed bursts of LH release subsequent to the LH-RH induced peak, but multiple peaks were never observed in E2 implanted gilts. An explanation was sought and 7 of the nonimplanted gilts were used to study spontaneous LH release by determining plasma LH at 10-min intervals for 20 h. During this period spontaneous episodes of LH release were observed in control animals with a mean frequency of 1.3 LH peaks/h. When 4 animals were given 5 mug E2 iv and then sampled for 12 h, episodic secretion was suppressed and the latency to the first spontaneous LH release was 9.6 plus or minus 0.8 h, significantly greater (P less than 0.02) than the latency to the first peak after saline injections (4.2 plus or minus 1.5 h) in the controls. It is suggested that "multiple" LH peaks occurring after initial LH-RH stimulation may represent the superimposition of spontaneous episodic release upon the induced response.

Animals↗
PubMed1998

Augmented frequency and mass of LH discharged per burst are accompanied by marked disorderliness of LH secretion in adolescents with polycystic ovary syndrome.

The aim of this study was to quantify pulsatile LH secretion, burst frequency and mass, LH half-life, and the approximate entropy (ApEn) or (dis-) orderliness of LH release in adolescents with polycystic ovary syndrome (PCOS), combining a high-precision immunofluorimetric LH assay with deconvolution techniques. We sampled LH concentration profiles every 20 min overnight in 12 girls with PCOS (mean +/- S.E.M. age 16.4+/-0.57 years, body mass index (BMI) 24.4+/-1.6 kg/m2) and 11 eumenorrheic early-follicular-phase controls (mean +/- S.E.M. age 16.5+/-0.47 years, BMI 22.2+/-1.0 kg/m2). Fasting serum levels of androstenedione, testosterone, 17-hydroxyprogesterone (17-OHP), estrone, estradiol, FSH and sex hormone-binding globulin (SHBG) were determined. Compared with euandrogenic girls, PCOS adolescents had significantly (P<0.005) elevated serum LH/FSH ratios, 17-OHP, androstenedione, esterone and testosterone levels, decreased SHBG, and similar estradiol. PCOS subjects exhibited a 3-fold higher mean serum LH concentration with almost no overlap with controls (8.8+/-1.2 and 2.8+/-0.3 IU/l respectively, P<0.001). We initially used a conventional serum hormone concentration peak analysis method (Cluster) to evaluate the characteristics of pulsatile LH release. Cluster analysis disclosed a significant increase in serum LH concentration maximal peak height, a higher LH peak frequency and a higher mean serum LH concentration in interpulse nadirs in the PCOS group. Deconvolution analysis of mechanisms underlying the foregoing showed higher frequency in the PCOS group than the controls (7.9+/-0.4 and 5.7+/-0.6 pulses/12 h respectively, P<0.05). The mass of LH released per secretory event was also significantly higher in PCOS subjects than controls (5.4+/-0.57 and 3.4+/-0.56 IU/l respectively, P<0.05). Since the pulsatile production rate is the product of the mean mass of hormone secreted per pulse and the number of pulses per day, we estimated a significantly higher mean pulsatile production rate of (endogenous) LH in the PCOS group (41+/-4.2 IU/l per day in the PCOS group vs 18+/-2.3 IU/l per day in the controls, P<0.01). The mean estimated half-life of endogenous LH disappearance was also significantly higher in patients with PCOS than in controls (110+/-8.5 and 77+/-3.7 min respectively, P<0.01). To quantify the orderliness of LH release, we used ApEn. PCOS patients had remarkably increased disorderliness (higher ApEn) of LH release (1.09+/-0.04 vs 0.77+/-0.08 in controls, P = 0.002). Mean serum LH concentration, mass of LH secreted per burst, and LH production rate in PCOS, but not in normal adolescents, correlated positively with androstenedione (P<0.02, 0.02 and 0.05 respectively). The same parameters also correlated positively with 17-OHP (P<0.05, 0.02 and 0.05 respectively). Stepwise regression analysis unmasked a negative influence of BMI in PCOS on both mass of LH secreted per burst (r = -0.77, P<0.005) and LH production rate (r = -0.70, P<+/0.01). We conclude that PCOS adolescents secrete LH molecules with amplified frequency and burst mass and with markedly disrupted orderliness. A rise in basal (non-pulsatile) LH release, more basic LH isoforms, and/or a prolongation or asymmetry of the LH secretory burst could account for the apparently prolonged LH half-life. Determining whether disorderliness of the amplified pituitary LH release process is an intrinsic abnormality in PCOS. or reflects androgen excess, may help to clarify the pathophysiology of this oligo-ovulatory syndrome in young women.

Adolescent↗
PubMed1988

Pulsatile LH-RH treatment induces a relatively low response of LH and FSH, while discontinuation enhances the response in women with amenorrhea of suprapituitary origin.

Five women with amenorrhea of suprapituitary origin were given intravenous injections of 10 micrograms LH-RH every 90 minutes for 4 days by means of a portable infusion pump. Immediately before and after this, the LH and FSH responses to a test dose of 100 micrograms LH-RH were measured. Four days after discontinuation of the treatment, so that LH and FSH could be measured, blood was sampled every 10 minutes for a period of 6 hours, during which 20 micrograms LH-RH was injected intravenously every hour. Finally, a test dose of 100 micrograms LH-RH was given. The whole procedure was repeated at least 6 weeks later, but this time hourly injections of 100 micrograms LH-RH were given 4 days after discontinuation of the pulsatile LH-RH treatment. Four days after the pulsatile LH-RH treatment was stopped, increased LH and FSH responses to LH-RH were observed. These could be reduced by 6 injections, given hourly, of either 20 or 100 micrograms LH-RH. Although the totally released amount of both LH and FSH did not differ between the two treatment regimens irrespective of the LH-RH dose used, the response of both gonadotropins to the LH-RH test dose after the hourly 100 micrograms LH-RH injections was significantly lower. This indicated that desensitization can be attributed, at least in part, to a lower responsiveness of LH and FSH to LH-RH when pulsatile LH-RH is given. Low responses during treatment with pulsatile LH-RH could not be related to higher concentrations of plasma estradiol. We conclude that women with amenorrhea of suprapituitary origin who are treated with pulsatile LH-RH have a low state of responsiveness to LH-RH, which can be caused by the presence of the LH-RH and might be attributed in part to desensitization by LH-RH. Removal of the LH-RH results in an enhancement of the responsiveness, as the pituitary gland might have recovered from this desensitization.

Adult↗
PubMed1975

An in vivo assay for anti-LH-RH and anti-FSH-RH activity of inhibitory analogues of LH-RH.

A convenient and sensitive method for testing anti-LH- and FSH-releasing activities of antagonists of LH-RH was devised. The peptides to be tested were injected subcutaneously together with synthetic LH-releasing hormone (LH-RH) in immature male rats. Serum LH and FSH concentrations were measured 30 min later by radioimmunoassay. In this system, [DesHis2]-LH-RH failed to block the pituitary response to LH-RH in agreement with previous data. The administration of [DesHis2, desGly10]-LH-RH ethylamide, [Des-His2, Leu3, des Gly10]-LH-RH ethylamide, [Des-His2, D-Ala6, des-Gly10]-LH-RH ethylamide, and [DESHis2, D-Ala6]-LH-RH in doses of 200 mug/rat, and [DesHis2, Leu3, D-Ala, desGly10]-LH-RH ethylamide in doses ranging from 100-400 mug/rat caused a significant inhibition of LH-RH-induced release of LH and FSH. On the other hand, [DesHis2, desGly10]-LH-RH propylamide, and [Leu2, Leu3, D-Ala6, desGly10]-LH-RH ethylamide failed to block the response to LH-RH. Among the peptides tested, [DesHis2, d-ala6, desGly10]-LH-RH etylamide, [Leu2, Leu3, D-Ala, desGly10]-LH-RH ethylamide in doses of 200 mug and [DesHis2, Leu3, D-Ala6, desGly10]-LH-RH ethylamide in a dose of 400 mug/rat showed some intrinsic LH and FSH-releasing activities. The method described here is simple and convenient for studying the anti-LH-RH release activity of inhibitory analogues of LH-RH, and also enabled us to demonstrate for the first time an in vivo inhibition of FSH release by these analogues.

Animals↗
PubMed1999

A preponderance of basic luteinizing hormone (LH) isoforms accompanies inappropriate hypersecretion of both basal and pulsatile LH in adolescents with polycystic ovarian syndrome.

We recently demonstrated that adolescent girls with polycystic ovarian syndrome (PCOS) exhibit augmented LH secretion due to an increase in immunofluorometric and deconvolution-estimated LH secretory burst mass and pulse frequency. Concurrently, we inferred either a prolongation of apparent (endogenous) LH half-life or elevated basal (nonpulsatile) LH release in PCOS. The in vivo half-life of LH molecules can be affected by the oligosaccharide side-chains, which also modify in vitro bioactivity and electrostatic change. Accordingly, as a surrogate estimator of altered endogenous LH half-life and/or biopotency in PCOS, we characterized the isoelectric properties of secreted LH isoforms and determined their in vitro biological activity in adolescent girls with PCOS compared with healthy age-matched eumenorrheic controls. To this end, 12-h (overnight) serum samples from PCOS patients (n = 12) and normal adolescents (n = 10) were pooled by subject. Bioactive LH concentrations were then quantitated in a rat Leydig cell in vitro bioassay, and immunological activity was determined by immunofluorometry. The distribution of LH isoforms was evaluated by preparative chromatofocusing (pH window, 10.5 to <4.0) of samples further combined to yield three independent serum pools for each of the patient and control groups. Fasting serum concentrations of 17-hydroxyprogesterone (17-OHP), androstenedione, testosterone, estrone, estradiol, and sex hormone-binding globulin were determined as possible endocrine correlates of LH isotypes. Mean serum concentrations of immunoreactive and bioactive LH in adolescents with PCOS were 3 and 2 times higher than values in controls: immunoreactive: PCOS, 7.8+/-0.9; controls: 2.6+/-0.3 IU/L (P < 0.001); and bioactive: PCOS, 52+/-10; controls, 25+/-4.1 IU/L (P = 0.002), respectively. Bioactive LH concentrations correlated positively with 17-OHP (P = 0.022), androstenedione (P = 0.012), and testosterone (P = 0.046) concentrations in PCOS. Chromatofocusing of LH isoforms disclosed greater LH immunoreactivity at pI values greater than 8 and 7.99-7.0 in adolescents with PCOS compared with controls (P = 0.031). The percentage of basic LH isoforms was related positively to serum concentrations of 17-OHP (P = 0.032), androstenedione (P = 0.046), and testosterone (P = 0.040). In conclusion, the present isotype analysis demonstrates elevated in vitro LH bioactivity and a preponderance of basic LH isoforms in girls with PCOS. Since previously reported heterologous in vivo assays of LH kinetics point toward accelerated removal of such alkaline isotypes, our findings would favor the earlier alternative hypothesis of inappropriate hypersecretion of basal (interpulse) LH rather than prolongation of the LH half-life as the mechanism for elevated interpulse serum LH concentrations in adolescents with PCOS. In ensemble, the foregoing data thus suggest 3-fold amplification of basal LH secretion as well as both a heightened amplitude and frequency of the pulsatile mode of LH release in PCOS.

17-alpha-Hydroxyprogesterone↗
PubMed1975

[LH and FSH responses to synthetic LH-RH in various estradiol levels of anovulatory women (author's transl)].

Synthetic LH releasing hormone (LH-RH) is effective in increasing both serum LH and FSH in humans. Therefore, LH-RH is used to clarify the function of the hypothalamic pituitary ovarian axis in adult women. Variations in response to synthetic LH-RH during different phases of the menstrual cycle are known. These variations may be due to changes in the ovarian secretion of sex streoid hormones during the menstrual cycle. In the present study, effects of serum estradiol (Ed) on pituitary gonadotropin response to synthetic LH-RH were studied in 55 subjects without ovulation. Serum levels of LH, FSH and Ed were determined before and at 30 min after intramuscular administration of 100 mug LH-RH. LH and FSH levels in the serum were measured by the double antibody method of radioimmunoassay. Ed levels were determined by the radioimmunoassay method of T. Makino, using the antiserum against Ed-6-oxime-BSA donated by Dr. T. Makino and applied to the microcolumn of sephadex LH 20. Preliminary evidence about Ed levels during the normal menstrual cycle and in anovulatory women suggested that an Ed level under 30 pg/ml indicates the presence of a small amount of Ed. Therefore, 55 patients were divided into 2 groups; the low Ed group that showed low basal Ed levels (under 30 pg/ml) and the Ed normal group that showed normal basal Ed levels (over 30 pg/ml). Pituitary gonadotropin responses to synthetic LH-RH were studied in these two groups. No statistical difference was shown between the two groups studied for basal LH level and FSH level. After LH-RH injection in the Ed normal group, serum LH level was significantly higher and serum FSH level was significantly lower than that in the low Ed group. Then, in order to clarify the difference in two groups, the ratio of LH to FSH (LH/FSH) before and after administration of LH-RH was examined. The ratio in the Ed normal group was significantly higher than one in the low Ed group before and after administration of LH-RH. Moreover, the percentage increase of the ratio was significantly larger in the Ed normal group than that in the low Ed group. A positive correlation (r=0.4228, p less than 0.01) was found between LH/FSH following administration of LH-RH and circulating the Ed level. These results suggest that the response of pituitary gonadotropins to LH-RH is changed by serum Ed and that serum Ed causes a differential release of LH and FSH in response to LH-RH. The data seem to demonstrate that LH-RH and serum Ed show a complex interplay in releasing LH and FSH.

Adult↗