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PubMed1980

Melatonin does not suppress the pituitary luteinizing hormone response to luteinizing hormone-releasing hormone in men.

The effect of an iv melatonin infusion on the pituitary LH response to LHRH was studied in five young men. Melatonin (30 micrograms/min; total dose, 7.2 mg) was infused for a 4-h period, 2 h before and 2 h after a LRH stimulation (single iv 150-microgram dose). Each subject's control response to LRH was obtained previously. During the melatonin infusion, supraphysiological concentrations of melatonin (20 times) were documented using a specific RIA. All five subjects had a LH rise after LRH stimulation, and this response was not affected by the melatonin infusion. These results indicate that an acute constant infusion of a pharmacological amount of melatonin does not suppress LRH-induced LH release from the pituitary in men. In addition, no change in sleepiness and behavior was found.

Adult↗
PubMed1982

Evaluation of pituitary gonadotropic function in men: value of luteinizing hormone-releasing hormone response versus basal luteinizing hormone level for discrimination of diagnosis.

We examined the serum LH response to LRH in 40 normal men and 38 men with various forms of gonadal dysfunction in an attempt to determine whether the LH response to LRH was more useful than the basal LH level alone for categorizing pathophysiological subgroups of gonadal dysfunction. The subgroups studied included hypogonadotropic hypogonadism, delayed puberty, idiopathic oligospermia, and primary hypogonadism. Log transformation of all values was done in order to normalize the data. Spearman's correlation analysis showed that increased basal LH was associated with increased incremental LH responses. However, our preliminary analysis of LRH response data suggested that the changes in LH were smaller in the secondary hypogonadal and delayed puberty groups then could be accounted for by the differences in basal LH level. Accordingly, we used various statistical techniques to test whether, and under what conditions, LRH testing provides information beyond that evident from examination of basal LH values. We found that the relationship between basal LH and the LH response to LRH differs in men with and without hypothalamic-pituitary dysfunction and that this difference can be exploited to improve the discrimination of men with pituitary hypogonadism from normals.

Adolescent↗
PubMed1984

Luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in the hypothalamus of women: effects of age and reproductive status.

In the study of the effects of age and reproductive status on LHRH and TRH content in the hypothalamus of women, we found that the amount of LHRH (58 +/- 5.5 ng; mean +/- SE) in the hypothalamus of young women (16-29 yr) was significantly greater (P less than 0.001) than that (28 +/- 3.0 ng) in postmenopausal women (50-78 yr). The hypothalamic content of LHRH (18 +/- 2.4 ng) of bilaterally ovariectomized women (39-47 yr) was significantly less (P less than 0.001) than that (60 +/- 12.6 ng) in younger ovulatory women (30-39 yr) or that (56 +/- 13.5 ng) in ovulatory women of comparable age (40-49 yr). In contrast, the hypothalamic content of TRH (121.4 +/- 32.8 ng) in postmenopausal women were similar to that (122.3 +/- 12.5 ng) in young women. Although aging in women is associated with a significant reduction in the amount of LHRH in the hypothalamus, such a reduction appears to be a consequence of ovarian failure and not of aging per se.

Adolescent↗
PubMed1984

Inhibition of serum luteinizing hormone and testosterone with an inhibitory analog of luteinizing hormone-releasing hormone in adult male rhesus monkeys.

The effects of single and repeated administration of a potent LHRH inhibitory analog (antagonist) [( N-acetyl-D-p-chloro-Phe1,2,D-Trp3,D-Arg6,D-Ala10]LHRH) on serum concentrations of LH and testosterone (T) in adult rhesus monkeys were studied. In Exp 1, single sc injections of the LHRH antagonist (400 micrograms and 50 micrograms) or vehicle were administered and the temporal changes in serum LH and T were determined (n = 4 per group). Both LH and T declined markedly in all animals as soon as 30 min after the LHRH antagonist injection, reaching the nadir (80%) approximately 8 h later and remaining significantly lower than baseline levels for up to 24 h. Control animals had no marked variations in either LH or T serum levels. In Exp 2, daily sc injections of different doses of LHRH antagonist (400 micrograms, 50 micrograms, and 10 micrograms) or vehicle were administered for 7 days to four animals in each group. The animals in the control group had no significant changes in LH or T levels, whereas those treated with the lowest dose of LHRH antagonist (10 micrograms) had decreased T levels in the absence of changes in LH. The other two doses of LHRH antagonist (400 micrograms and 50 micrograms) induced, as early as 8 h after the initial injection, dramatic decreases in serum levels of both LH and T and these values remained significantly lower than control for up to 3 and 4 days after discontinuation of drug administration, respectively. We conclude from this study that LHRH inhibitory analogs are potent inhibitors of LH and T in adult rhesus monkeys. They have potential use in clinical trials for male contraception as well as in patients in whom inhibition of gonadotropin and steroid secretion is desired.

Animals↗
PubMed1985

Different responses of growth hormone secretion to guanfacine, bromocriptine, and thyrotropin-releasing hormone in acromegalic patients with pure growth hormone (GH)-containing and mixed GH/prolactin-containing pituitary adenomas.

There is great variability in the GH secretory responses to different stimuli in patients with acromegaly. In the present study, we compared the effects on GH secretion of two compounds (bromocriptine and TRH), which presumably act directly at the pituitary level, with the effect of the centrally acting alpha-adrenergic agonist guanfacine in 14 untreated acromegalic patients. These in vivo responses of GH release were correlated with the results of immunocytochemical studies of the pituitary adenomas. In nine patients with pure GH-containing adenomas, GH secretion was suppressed by bromocriptine by more than 50% in one patient, while TRH stimulated GH release by more than 100% in another patient. Guanfacine (2 mg, orally) did not elicit a change in circulating GH levels in any of these nine patients. In the group of five patients with mixed GH/PRL-containing adenomas, however, bromocriptine suppressed GH levels by more than 50% in all patients, and TRH stimulated GH release by more than 100% in four of them. Guanfacine stimulated GH secretion significantly in four of these five patients. Guanfacine inhibited GH secretion significantly in five other acromegalic patients who had been treated 5-10 yr previously by external pituitary irradiation. We conclude that in acromegaly, the presence of PRL within the GH-secreting pituitary adenoma makes GH secretion more sensitive to bromocriptine and TRH, while normal sensitivity to hypothalamus-mediated stimulation (alpha-adrenergic agonist) is retained to some extent. In contrast, pure GH-secreting tumors responded little or not at all to bromocriptine, TRH, or guanfacine.

Acromegaly↗
PubMed1991

Low growth hormone levels are related to increased body mass index and do not reflect impaired growth in luteinizing hormone-releasing hormone agonist-treated children with precocious puberty.

To test the hypothesis that GH deficiency might explain the low growth velocity of some LHRH agonist (LHRHa)-treated children with central precocious puberty, we measured stimulated (n = 81) and spontaneous (n = 32) GH levels during or after LHRHa treatment. GH stimulation tests in the children who were receiving LHRHa treatment were performed after 2 days of ethinyl estradiol administration. Thirty-one of 81 children (38%) who underwent GH stimulation tests had subnormal responses (less than or equal to 7 micrograms/L) to all tests administered (at least 2 stimuli), including 22 of 67 (33%) who had precocious puberty that was idiopathic or associated with hypothalamic hamartoma. Eleven of 32 children (34%) who underwent measurement of the mean nighttime spontaneous GH level had levels below the normal range for prepubertal children (less than 1.2 microgram/L). Despite the high incidence of subnormal GH levels, there appeared to be no relationship between the GH levels of these children and their growth characteristics. The height, growth velocity, bone maturation rate, predicted height, and insulin-like growth factor-I levels were not different between the children with low GH levels and the children with normal GH levels. Conversely, the GH levels were not different between the children with subnormal growth rates and the children with normal growth rates. Thus, variation in the growth rates of these LHRHa-treated children with central precocious puberty could not be explained by variation in the stimulated or spontaneous secretion of GH. In attempting to understand the high incidence of low GH levels in children with precocious puberty, we examined the relationship between GH level and body mass index (BMI). Both the stimulated (r = -0.33; P less than 0.002) and the spontaneous (r = -0.61; P less than 0.0002) GH levels were inversely related to BMI. Moreover, the children with precocious puberty as a group had significantly elevated BMI [1.2 +/- 0.1 (+/- SE) SD units] compared to normal children of the same age (P less than 0.0001). Thus, increased body mass may explain the high incidence of subnormal GH levels in these patients, and normative GH levels adjusted for body mass are needed before it can be concluded that the apparently subnormal GH levels in LHRHa-treated children with precocious puberty are in fact low.

Adolescent↗
PubMed1991

The effect of long-acting analog of luteinizing hormone-releasing hormone on growth hormone secretory dynamics in children with precocious puberty.

Long-acting preparations of LHRH (LHRHa), such as leuprolide acetate, have been shown to selectively and reversibly suppress the clinical and biochemical features of central precocious puberty (CPP). The withdrawal of gonadal sex steroids results in a decline of growth velocity and a decrease in the rate of bone age maturation, with resultant improvement in predicted adult stature. The purpose of this study was to define GH secretory dynamics in children treated with leuprolide acetate. Twelve-hour nocturnal GH studies were performed in five children (four girls and one boy) with CPP before and after 6 months of treatment with leuprolide acetate. Mean GH levels, GH secretory rate, and number of GH secretory episodes were determined. Secretory profiles were analyzed using the Cluster program. Growth velocity, somatomedin-C, and dehydroepiandrosterone sulfate were measured before and after 6 months of therapy. By 6 months of therapy, there was a significant decrease in mean growth velocity from 10.5 +/- 3.3 to 6.7 +/- 1.6 cm/yr. Somatomedin-C levels remained the same at 46.90 +/- 9.51 and 52.5 +/- 12.40 nmol/L. Levels of dehydroepiandrosterone sulfate remained unchanged at 118.6 +/- 71.4 and 139.0 +/- 61.3 mumol/L at 0 and 6 months of the study. By 6 months, there was a significant decrease in mean GH levels from 13.6 +/- 5.3 to 6.4 +/- 3.4 micrograms/L (P less than 0.05). Total GH levels decreased from 1367.9 +/- 687.3 to 447.0 +/- 186.5 ng/12 h. The number of GH secretory episodes remained the same at 5.4 +/- 1.5 and 4.8 +/- 1.0/12 h at 0 and 6 months of study. Therefore, the decrease in GH that occurs during the withdrawal of gonadal sex steroids with LHRHa in children with CPP is an amplitude-modulated phenomenon, as the number of secretory peaks remains unchanged.

Antineoplastic Agents↗
PubMed1982

Biological and immunological characterization of human luteinizing hormone discharged by the stimulation of synthetic luteinizing hormone-releasing hormone (LH-RH) in normal and anovulatory women.

Plasma samples were obtained by repeated venopunctures immediately before, and at 15, 30, 60, 120 and 180 min after intravenous bolus administration of 100 micrograms synthetic LH-RH in normal and various anovulatory women. Plasma hLH levels were determined by an in vitro bioassay and a radioimmunoassay with improved reagents. The LH-RH stimulation induced an abrupt elevation of both biological and immunological hLH activities in normal and anovulatory women, although the responsiveness to LH-RH differed from case to case. Both elevated biological and immunological hLH activities decreased gradually with a half disappearance time of 122.4 +/- 27.9 min and 112.5 +/- 25.4 min, respectively (Mean +/- S.D.). A transient and significant depression in the ratio of biological to immunological hLH activities (B/I ratio) was observed at 15 min after the LH-RH administration in normal subjects. This depression is attributable to the cross-contamination of an increased amount of hLH subunits induced by LH-RH stimulation. The B/I ratios were significantly elevated throughout the investigation period in the anovulatory patients when compared with those in the normal subjects. This elevation appears to indicate the increased discharge of special type(s) of hLH subpopulations of high biological potency in the anovulatory cases.

Adult↗
PubMed1983

Qualitative and quantitative changes in plasma luteinizing hormone (LH) under stimulation by intravenous infusion of synthetic luteinizing hormone-releasing hormone (LHRH) in Japanese monkeys (Macaca fuscata) as assessed by electrofocusing.

Using 5 adult Japanese monkeys (Macaca fuscata) of both sexes, the qualitative and quantitative changes in plasma LH caused by LHRH administration were examined before and after castration. Five hundred micrograms synthetic LHRH was infused for 2 hrs and blood samples were obtained every 15 min for 5 hrs under ketamine hydrochloride anesthesia. Plasma LH levels were determined by an in vitro bioassay using the mouse testis interstitial cell preparation. The LHRH infusion induced a biphasic release of LH in intact animals of both sexes and in castrated females but not in castrated males. The biphasic pattern of LH release was characterized by an initial acute rise followed by a plateau or a fall and the consecutive second rise after a long latent period. Aliquots of plasma samples obtained during 30-90 (corresponding to the initial rise) and 120-210 min (corresponding to the second rise) after the initiation of LHRH infusion were pooled separately (plasma pools I and II, respectively) and subjected to isoelectrofocusing (IEF) fractionation. The IEF fractionation was performed in ampholine-sucrose gradient, pH range 3.5-10, under a constant electrical power supply (3 W, 700 V) for 48 hrs at 4 degrees C. After the completion of the IEF fractionation the LH activity in each fraction was measured by the in vitro bioassay. The IEF fractionation separated plasma LH into 6 distinct species in terms of pI values. When the IEF profiles of plasma pools I and II in intact animals of both sexes were compared, the increase and the decrease in acidic to neutral LH and alkaline LH, respectively, were consistent and significant in plasma pool II. Changes of the same kind were further exaggerated when the IEF profiles in castrated animals were compared with those in non-castrated ones. The acidic LH may represent the LH species newly synthesized and not well processed. The LH species possessing pI values of 7.5-8.5 is likely to be the mature type of LH exhibiting high biological potency. The LH species migrating in the high alkaline region seems to be the LH of over-maturation.

Animals↗
PubMed1976

The ontogenesis of human foetal hormones. II. Luteinizing hormone (LH) and follicle stimulating hormone (FSH).

The content and concentrations of immunoreactive LH (LER-960) and FSH (LER-869) were determined in 79 human foetal pituitary glands from 68 days of gestation to term, and in the pituitary glands of 3 anencephalic infants, 10 infants and children 2 weeks to 7 years of age, and 4 adults. In addition, the concentration of immunoreactive serum LH, FSH, LH-HCG, and HCG was determined in 48 foetuses and 6 anencephalic infants. The mean content of LH in the pituitary glands of the female foetuses increased sharply from 88.2 +/- 44.2 ng at 10 to 14 weeks to 4983.8 +/- 1128.4 ng at 25 to 29 weeks of gestation. In the male foetuses, the mean content of pituitary LH rose from levels of 21.0 +/- 11.6 ng to peak levels of 114.5 +/- 57.1 ng at 20 to 24 weeks of gestation. The concentration of LH in the pituitary glands of the children was comparable to that of foetuses at mid-gestation. The mean content of FSH in pituitary glands of female foetuses rose from 7.4 +/- 5.2 ng at 10 to 14 weeks to 4788.6 +/- 1460.7 ng at 25 to 29 weeks of gestation. In the male foetuses the pituitary content rose from 1.8 +/- 0.7 ng at 10 to 14 weeks to 14.5 +/- 69.1 ng at 25 to 29 weeks of gestation. The differences in pituitary content of LH and FSH between the male and female foetuses were highly significant from 15 to 29 weeks of gestation. The correlation of the incremental changes in the pituitary content of LH and FSH with gestational age was significant (P less than 0.02). Immunoreactive serum FSH was detected as early as 84 days of gestation at a concentration of 11.0 ng/ml (LER-869). Serum FSH rose to peak levels (18.2 +/- 3.6 ng/ml) at 20 to 25 weeks in a range comparable to that of castrate adults. A decrease was noted by 30 to 34 weeks to levels of 1.7 +/- 0.05 ng/ml, comparable to that in cord samples at term (1.8 +/- 0.2 ng/ml). A significant negative correlation with gestational age was shown after the mid-gestational period (P less than 0.01). Immunoreactive LH, measured by a specific LH assay, was unaffected by levels of HCG present in the foetus. Immunoreactive LH was present in high concentrations by 99 days of gestation (21.5 ng/ml LER-960). Peak levels were attained by 100 to 180 days of gestation with a decrease at them to less than 1.0 ng/ml. A significant negative correlation was noted between serum LH and gestational age. Serum HCG quantified in a betaHCG radioimmunoassay decreased from the relatively high levels in foetuses at 90 to 120 days gestational age to term. The mean concentration in umbilical cord sera was 268.5 +/- 161 mIU/ml in contrast to 5400 +/- 200 mIU/ml in maternal plasma at term. ...

Anencephaly↗
PubMed1984

Effects of acute stimulation with luteinizing hormone-releasing hormone (LRH) on biologically active and immunoreactive serum luteinizing hormone (LH) in pubertal boys.

The responses of biologically active LH (BIO-LH) and immunoreactive LH (RIA-LH) to acute stimulation with LRH (0.1 mg iv) were studied in 8 pubertal boys (9-15 years, 2nd-4th Tanner's stage), and in 10 healthy adult men (20-46 years). Serum levels of BIO-LH were assessed by an in vitro bioassay method based upon testosterone production by mechanically dispersed mouse Leydig cell preparations. In pubertal boys the mean BIO-LH/RIA-LH (B/I) ratio of basally secreted LH was significantly lower than in adult men (1.2 +/- 0.2 (SEM) and 2.2 +/- 0.2 respectively, P less than 0.01). After acute administration of LRH the mean B/I ratio of circulating LH showed a significant increase from the basal value in pubertal boys (2.6 +/- 0.2, P less than 0.01 vs basal values), whereas no significant difference in LH B/I ratios were demonstrated throughout the study period in adult men (2.1 +/- 0.1, P = NS vs basal values). In agreement with this finding, the mean relative maximum response for BIO-LH (BIO-LH delta %) was higher in pubertal boys than in adult men (1702.7 +/- 500.3 and 499.6 +/- 65.4% respectively, P less than 0.05), whereas the mean RIA-LH delta % was similar in both groups (609.1 +/- 85.1 and 534.1 +/- 75.5% respectively, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Combined treatment with growth hormone and gonadotropin-releasing hormone analogues in children with isolated growth hormone deficiency.

In subjects with an isolated GH deficiency the inhibition of puberty by GnRH-analogue administration may be attempted to delay the onset, or to prolong the duration, of pubertal maturation in order to improve final height. We report our experience on the matter in 10 subjects (6M, 4F) suffering from isolated GH deficiency with a chronological age ranging from 6.5 to 10.6 years at diagnosis. After a period of 1-5.1 years of GH treatment, GnRH-analogues (long-acting D-Trp-6-GnRH) were added to GH for 12 months, when six subjects were still prepubertal and four in early puberty. During combined therapy, a regression in pubertal development was shown in three out of four children in early puberty, while serum testosterone or estradiol decreased. Height velocity decreased (from 5.23 +/- 1.49 (mean +/- SD) to 4.12 +/- 0.67 cm/year; p < 0.02), whereas height SD scores for bone age increased (from -0.75 +/- 0.42 to -0.47 +/- 0.55; p < 0.02). During the year of combined therapy, bone age increased only 0.57 +/- 0.27 years. The values for predicted height (TW2 and Bayley-Pinneau method) after combined treatment were also higher than those after treatment with GH alone (p < 0.02 and p < 0.001, respectively). Our preliminary data showed that the addition of GnRH-analogues to GH in subjects with isolated GH deficiency reduces the effect of GH on height velocity, but determines an improvement in statural prognosis, although a proper answer will not be obtained until final height has been achieved.

Body Height↗
PubMed2000

Pituitary response to luteinizing hormone-releasing hormone in women with variant luteinizing hormone.

OBJECTIVE: To assess the LH response of the pituitary gland to GnRH stimulation in healthy women with a mutant beta-subunit (Trp8 to Arg8 and Ile15 to Thr15). DESIGN: Clinical study. PATIENTS: We studied 40 healthy non-pregnant Japanese women of known zygosity for the LH beta-subunit gene (3 homozygotes for the mutant gene, 17 heterozygotes, and 20 homozygotes for the wild type). All women had normal ovulatory cycles. MEASUREMENTS: Serum LH status was determined by comparing LH immunoassays results using a monoclonal antibody recognizing only wild-type LH with those from a polyclonal antibody assay recognizing both variant and wild-type LH. The ratio of monoclonal to polyclonal immunoassay results determined the serum LH status. LH secretion in response to a GnRH stimulation test was measured. RESULTS: All women with the wild-type LH showed a normal response of LH to GnRH according to both assays. Over the time course of the response, the ratios in women with wild-type LH showed no remarkable changes. The response curves in women heterozygous for the mutant peaked 15-30min after GnRH injection; their response patterns included a statistically significant decrease in the rates of response at 15min after injection. CONCLUSIONS: There are the differences in circulatory kinetics between the two LH forms and in regulation of the two types of LHbeta genes. The maximal response of the variant LH to pituitary stimulation with GnRH appears to be greater than that of wild-type LH.

Adult↗