GONADOTROPHIN-RELEASE UPON INTRAVENOUS ADMINISTRATION OF A LONG-ACTING ANALOGUE OF LUTEINIZING HORMONE-RELEASING HORMONE IN FEMALES WITH INCREASED PLASMA-ANDROGENS

1979 ◽  
Vol 91 (3) ◽  
pp. 577-590 ◽  
Author(s):  
H. Vierhapper ◽  
W. Waldhäusl ◽  
P. Nowotny

ABSTRACT D-Ser-(TBU)6-EA10-LH-RH, an analogue of luteinizing hormone-releasing hormone (LH-RH) with prolonged action evokes in normal male and female subjects a qualitatively different secretory pattern of LH, as peak levels are reached between 30 and 60 min in males and between 120 and 240 min in females. Females with increased production of adrenal androgens due to congenital adrenal hyperplasia (off substitution therapy; N = 8), idiopathic hirsutism (N = 1) and adrenocortical carcinoma (N = 2) present upon the administration of the LH-RH-analogue with a secretory pattern of LH and FSH which is qualitatively identical with that of normal female subjects, whereas the response of LH in these patients differs from that seen in normal males. Pre-treatment with dexamethasone did not induce any qualitative changes in the secretory response of LH and FSH upon the LH-RH-analogue in patients with increased endogenous production of adrenal androgens. A larger pool and/or a more pronounced de novosynthesis of LH, which apparently is not altered by increased levels of adrenal androgens, may be the cause of the more pronounced and prolonged increase of LH in female subjects following the administration of the LH-RH-analogue.

1978 ◽  
Vol 77 (3) ◽  
pp. 293-299 ◽  
Author(s):  
L. V. BECK ◽  
M. BAY ◽  
A. F. SMITH ◽  
D. KING ◽  
R. LONG

Perifusion experiments were performed to study the stimulatory effects of luteinizing hormone releasing hormone (LH-RH) on the release of LH from anterior pituitary tissue. Exposure of pituitary tissue from normal male rats to LH-RH (5 ng/ml for 5 min) induced a small release of LH; in tissue from ovariectomized rats receiving no pretreatment, the release was more than three times greater and in tissue from gonadectomized male or female rats pretreated with oestradiol benzoate and progesterone, the release was six times greater than that observed in normal rats. Further exposure of pituitary tissue from gonadectomized steroid-pretreated male and female rats to LH-RH (5 ng/ml) induced an increase in the level of LH even greater than that seen after the initial exposure (priming action of LH-RH); in tissue from ovariectomized rats receiving no pretreatment, less LH was released than after the first exposure to LH-RH and in tissue from normal male rats the response was unchanged.


1982 ◽  
Vol 92 (1) ◽  
pp. 141-146 ◽  
Author(s):  
R. L. MATTERI ◽  
G. P. MOBERG

During treatment with cortisol or ACTH, dairy heifers were given two doses of LH releasing hormone (LH-RH) spaced 1·5 h apart. Serum concentrations of cortisol and LH were monitored during each treatment. Treatment with both ACTH and cortisol raised plasma cortisol levels above the respective saline controls (P<0·001). Neither treatment affected basal LH concentrations. A slight depression in LH response was seen in the cortisol-treated animals after the first LH-RH injection, as shown by a statistically significant depression at three of the sample times. There was no significant difference between treated and control LH values after the second LH-RH administration. Treatment with ACTH resulted in significantly reduced LH values at all sample times after both injections of LH-RH.


1974 ◽  
Vol 52 (3) ◽  
pp. 754-758 ◽  
Author(s):  
S. H. Shin ◽  
C. J. Howitt

Several aqueous solvent systems were tested for their efficiency in extracting luteinizing hormone releasing hormone (LH-RH) from rat hypothalamus. Although LH-RH is a water-soluble decapeptide, neutral distilled water extracted only 10% of the LH-RH obtained using acid extraction methods. The efficiency of the acid extraction procedure suggests that in the hypothalamus the releasing hormone is bound to a relatively large molecular weight compound. Using the acidic extraction procedure, we found that hypothalamic LH-RH content is significantly lower in the castrated animal than in the normal rat.


2013 ◽  
Vol 5 (3) ◽  
pp. 173
Author(s):  
Howard Huaihan Pai ◽  
Tom Pickles ◽  
Mira Keyes ◽  
Stuart Jones ◽  
Rachel E. McDonald ◽  
...  

Introduction: We sought to compare the rate of return of testosteronelevels and sexual function in men with prostate cancerreceiving longer acting, 3-month preparation of luteinizing hormone-releasing hormone agonist (L-LHRH-A) versus shorter acting,1-month preparation of luteinizing hormone-releasing hormoneagonist (S-LHRH-A).Methods and Materials: Men with low to intermediate risk localizedprostate cancer were randomized to either L-LHRH-A (2-3 monthduration LHRH-A) or S-LHRH-A (6-1 month duration LHRH-A) ofandrogen suppression therapy (AST) and prostate brachytherapyusing iodine-125 radioisotopes. Serum total testosterone levels andPSA were recorded every 2 months for 2 years.Results: A planned target sample size of 100 was not achieveddue to insufficient accrual. A total of 55 patients were randomizedand 46 were used for analysis. The median time to recovery oftestosterone to baseline levels (calculated from end of AST) was 8and 4 months in the L-LHRH-A and S-LHRH-A arms, respectively(p = 0.268). The median time to testosterone recovery to lower limitof reference range was 4 and 2 months respectively (p = 0.087).Interpretation: This randomized study, which failed to reachaccrual target, showed a trend towards more rapid recovery oftestosterone levels using shorter acting LHRH-A. Another randomizedstudy would be required to validate these findings. Currently,there is insufficient evidence to recommend the use of shorteracting LHRH-A as a means of providing more rapid recovery oftestosterone levels.Introduction : Nous avons voulu comparer la vitesse de retourdes taux de testostérone et de la fonction sexuelle chez des hommesatteints d’un cancer de la prostate recevant un agoniste de laLHRH à longue durée d’action pendant 3 mois ou un agoniste dela LHRH à courte durée d’action pendant 1 mois.Matériel et méthodologie : Des hommes atteints d’un cancer dela prostate localisé avec risque faible à intermédiaire ont été randomiséspour recevoir soit un agoniste de la LHRH à longue duréed’action (2 doses trimestrielles) soit un antagoniste de la LHRHà courte durée d’action (6 doses mensuelles) comme traitementantiandrogène et une brachythérapie prostatique avec des radioisotopesde l’iode 125. Les taux sériques de testostérone totale etd’APS ont été notés tous les 2 mois pendant 2 ans.Résultats : L’échantillon prévu au départ de 100 patients n’apu être obtenu en raison d’un recrutement insuffisant. Au total,55 patients ont été randomisés et 46 ont été inclus dans les analyses.L’intervalle médian de retour à des taux normaux de testostérone(calculés à partir de la fin du traitement antiandrogène) étaitde 8 et 4 mois dans les groupes sous agoniste de la LHRH à longueet à courte durée d’action, respectivement (p = 0,268). L’intervallemédian requis pour que les taux de testostérone atteignent la limiteinférieure des valeurs de référence était de 4 et 2 mois, respectivement(p = 0,087).Interprétation : Cette étude randomisée, où on n’a pas réussi àobtenir le nombre de patients voulu, a montré une tendance vers unretour plus rapide des taux de testostérone avec un traitement paragoniste de la LHRH à courte durée d’action. Une autre étude randomiséeserait nécessaire pour valider ces résultats. Actuellement,on ne dispose pas de suffisamment de données pour recommanderun agoniste de la LHRH à courte durée d’action comme moyenpour ramener les taux de testostérone plus rapidement à la normale.


1979 ◽  
Vol 81 (1) ◽  
pp. 109-118 ◽  
Author(s):  
SHUJI SASAMOTO ◽  
SHIGEO HARADA ◽  
KAZUYOSHI TAYA

When 1·0 μg luteinizing hormone releasing hormone (LH-RH) was given i.v. three times at 1 h intervals from 17.00 to 19.00 h on the day of dioestrus (day 0) to regular 4 day cyclic rats, premature ovulation was induced the next morning (day 1) with the number of ova present comparable to normal spontaneous ovulation. The next spontaneous ovulation occurred on the morning of day 5, 4 days after premature ovulation induced by LH-RH. Plasma concentrations of FSH and LH showed transient rises and falls within 1 h of administration of LH-RH; concentrations of FSH in the plasma decreased from 20.00 h on day 0 but markedly increased again from 23.00 h on day 0 to 02.00 h on day 1 and these high levels persisted until 14.00 h on day 1, with only a small increase of plasma LH during this period. The duration of increased FSH release during premature ovulation induced by LH-RH treatment was 6 h longer than the FSH surge occurring after administration of HCG on day 0. Surges of gonadotrophin were absent on the afternoon of day 1 (the expected day of pro-oestrus) and the surges characteristic of pro-oestrus occurred on the afternoon of day 4 and ovulation followed the next morning. The pituitary content of FSH did not decrease despite persisting high plasma levels of FSH during premature ovulation induced by either LH-RH or HCG on day 0. The changes in uterine weight indicated that the pattern of oestrogen secretion from the day of premature ovulation induced by LH-RH to the day of the next spontaneous ovulation was similar to that of the normal 4 day oestrous cycle. When 10 i.u. HCG were given on day 0, an increase in oestrogen secretion occurred on day 2, 1 day earlier than in the group given LH-RH on day 0. This advancement of oestrogen secretion was assumed to be responsible for the gonadotrophin surges on day 3. Similar numbers of fully developed follicles were found by 17.00 h on day 2 after premature ovulation induced by either LH-RH or HCG, suggesting that the shorter surge of FSH during premature ovulation induced by HCG had no serious consequences on the initiation of follicular maturation for the succeeding oestrous cycle in these rats. Administration of LH-RH on day 0 had no direct effect on the FSH surge during premature ovulation. Secretory changes in the ovary during ovulation may be responsible for this prolonged selective release of FSH.


Sign in / Sign up

Export Citation Format

Share Document