Serum concentrations of gonadotrophins in hypergonadotrophic patients following stimulation by a long-acting analogue of luteinizing hormone-releasing hormone

1983 ◽  
Vol 102 (4) ◽  
pp. 610-615
Author(s):  
H. Vierhapper ◽  
W. Waldhäusl ◽  
G. Klaushofer ◽  
W. Stackl
Keyword(s):  
Luteinizing Hormone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Maximum Serum ◽  
Luteinizing Hormone Releasing Hormone ◽  
Healthy Men ◽  
Releasing Hormone ◽  
Healthy Women ◽  
Serum Lh ◽  
Long Acting

Abstract. The effect of D-Ser(TBU)6-EA10-LRH, a long-acting analogue of luteinizing hormone-releasing hormone (LRH), was studied in patients with hypergonadotrophism due to orchidectomy (n = 8) or due to Klinefelter's syndrome (n = 6). Patients orchidectomized less than 7 days prior to the administration of the compound presented with maximum concentrations of LH (63.8 ± 29.9 mIU/ml) within 60 min following iv injection of the LRH-analogue (10 μg). This behaviour of LH was qualitatively similar to that seen in healthy men. In patients orchidectomized more than 40 days prior to the administration of the LRH-analogue and in patients with Klinefelter's syndrome the occurrence of maximum serum LH-concentrations (115.0 ± 39.4 and 149.4 ± 134.5 mIU/ml, respectively) was delayed up to 240–360 min following iv LRH-analogue. This pattern of LH secretion is similar to that of healthy women. No qualitative differences in stimulated FSH-concentrations were observed between the described groups of hypergonadotrophic patients. These findings demonstrate a time-dependent increase in the 'second pool' of LH following orchidectomy. The similar behaviour of stimulated LH-release in healthy women and in male patients with long-term hypergonadotrophic hypogonadism could indicate an augmented production of endogenous LRH in these individuals as compared to healthy men, providing an explanation for the sexually related differences in the LH-response upon the administration of the LRH-analogue.

scholarly journals Randomized study evaluating testosterone recovery using short-versus long-acting luteinizing hormone releasing hormone agonists

2013 ◽  
Vol 5 (3) ◽  
pp. 173
Author(s):  
Howard Huaihan Pai ◽  
Tom Pickles ◽  
Mira Keyes ◽  
Stuart Jones ◽  
Rachel E. McDonald ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Median Time ◽  
Randomized Study ◽  
Rapid Recovery ◽  
Total Testosterone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Iodine 125 ◽  
Étude Randomisée ◽  
Long Acting

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.

scholarly journals Primary aldosteronism in Klinefelter’s syndrome: two cases

2019 ◽  
Vol 2019 ◽  
Author(s):  
Yasufumi Seki ◽  
Satoshi Morimoto ◽  
Naohiro Yoshida ◽  
Kanako Bokuda ◽  
Nobukazu Sasaki ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Primary Aldosteronism ◽  
Luteinizing Hormone Receptor ◽  
List Type ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Plasma Aldosterone Concentration ◽  
Lh Receptor ◽  
Serum Lh ◽  
Aldosterone Producing Adenoma

Summary Primary aldosteronism (PA) is more common than expected. Aberrant adrenal expression of luteinizing hormone (LH) receptor in patients with PA has been reported; however, its physiological role on the development of PA is still unknown. Herein, we report two unique cases of PA in patients with untreated Klinefelter’s syndrome, characterized as increased serum LH, suggesting a possible contribution of the syndrome to PA development. Case 1 was a 39-year-old man with obesity and hypertension since his 20s. His plasma aldosterone concentration (PAC) and renin activity (PRA) were 220 pg/mL and 0.4 ng/mL/h, respectively. He was diagnosed as having bilateral PA by confirmatory tests and adrenal venous sampling (AVS). Klinefelter’s syndrome was suspected as he showed gynecomastia and small testes, and it was confirmed on the basis of a low serum total testosterone level (57.3 ng/dL), high serum LH level (50.9 mIU/mL), and chromosome analysis. Case 2 was a 28-year-old man who had untreated Klinefelter’s syndrome diagnosed in his childhood and a 2-year history of hypertension and hypokalemia. PAC and PRA were 247 pg/mL and 0.3 ng/mL/h, respectively. He was diagnosed as having a 10 mm-sized aldosterone-producing adenoma (APA) by AVS. In the APA, immunohistochemical analysis showed co-expression of LH receptor and CYP11B2. Our cases of untreated Klinefelter’s syndrome complicated with PA suggest that increased serum LH levels and adipose tissues, caused by primary hypogonadism, could contribute to PA development. The possible complication of PA in hypertensive patients with Klinefelter’s syndrome should be carefully considered. Learning points: The pathogenesis of primary aldosteronism is still unclear. Expression of luteinizing hormone receptor has been reported in aldosterone-producing adenoma. Serum luteinizing hormone, which is increased in patients with Klinefelter’s syndrome, might contribute to the development of primary aldosteronism.

SERUM LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE CONCENTRATIONS IN IMMATURE FEMALE RATS TREATED WITH MULTIPLE INJECTIONS AND VARIOUS AMOUNTS OF LUTEINIZING HORMONE RELEASING HORMONE

1975 ◽  
Vol 66 (1) ◽  
pp. 13-20 ◽  
Author(s):  
D. C. JOHNSON ◽  
R. S. MALLAMPATI
Keyword(s):  
Luteinizing Hormone ◽  
Constant Stimulus ◽  
Female Rats ◽  
Intact Female ◽  
Immature Female ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Rh

SUMMARY Release of immunoreactive LH and FSH was induced in immature intact female rats by repeated injections of synthetic luteinizing hormone releasing hormone (LH-RH). Altering the dose of LH-RH (5, 10, 20, 50 ng) and the frequency of administration (every 10, 20, 30 or 60 min) over a period of 2 h produced a variety of serum LH and FSH concentrations and ratios. When the dose was a constant 20 ng but the frequency of injections was either 20 or 30 min, a steady state in serum gonadotrophin concentrations was reached within 1 h and the level remained the same during the second hour. When given every 10 min, 20 ng LH-RH produced a much higher concentration of both LH and FSH during the second hour of stimulation. Examination of the gonadotrophin levels after each injection of LH-RH showed that the pituitary response was variable in spite of a constant stimulus.

EFFECTS OF MATING AND INJECTION OF LUTEINIZING HORMONE RELEASING HORMONE ON SERUM LUTEINIZING HORMONE AND TESTOSTERONE CONCENTRATIONS IN RABBITS

1978 ◽  
Vol 76 (3) ◽  
pp. 417-425 ◽  
Author(s):  
C. A. BLAKE ◽  
PATRICIA K. BLAKE ◽  
NANCY K. THORNEYCROFT ◽  
I. H. THORNEYCROFT
Keyword(s):  
Luteinizing Hormone ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Transient Increase ◽  
Marked Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Before And After ◽  
Lh Rh

The effects of coitus and injection of luteinizing hormone releasing hormone (LH-RH) on serum concentrations of LH, testosterone and dihydrotestosterone (17β-hydroxy-5α-androstan-3-one; DHT) were tested in male rabbits. Before experimentation, male and female rabbits were housed in individual cages in the same room. Male rabbits were then bled by cardiac puncture before and after placement with female rabbits or intravenous injection of LH-RH. Serum LH, testosterone and DHT were measured by radioimmunoassay. Sexual excitement (sniffing, chasing and mounting), with or without intromission, caused a marked rise in serum testosterone and DHT concentrations in only some of the bucks. These increases were accompanied or preceded by a small, transient increase in serum LH. In the rest of the bucks, sexual excitement with or without intromission had either no effect on serum levels of all three hormones, or only serum testosterone and DHT decreased during the collection period. Similar responses were measured in bucks which were housed in a room without does for 2–4 weeks before experimentation. Injection of 10, 30 or 100 ng or 50 μg LH-RH caused serum LH, testosterone and DHT to rise in all bucks tested, but the magnitude of the rises in serum testosterone and DHT were not related to the magnitude of the LH rise. In both mated and LH-RH-injected bucks, the rises in serum testosterone and DHT were greatest in animals with low initial testosterone and DHT values. Under the conditions of this study, the data suggest that: (1) serum testosterone and DHT rise in only some male rabbits after sexual excitement (with or without intromission), (2) the rises in serum testosterone and DHT are dependent on a small transient increase in serum LH and (3) sexual excitement is less likely to cause release of LH-RH in bucks with raised serum testosterone and DHT concentrations.

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