Serum LH and FSH Response in Four-Hour Infusions of Luteinizing Hormone-Releasing Hormone in Normal Men, Sertoli Cell Only Syndrome, and Klinefelter's Syndrome

1975 ◽  
Vol 41 (5) ◽  
pp. 876-886 ◽  
Author(s):  
D. M. DE KRETSER ◽  
H. G. BURGER ◽  
R. DUMPYS
Keyword(s):  
Luteinizing Hormone ◽  
Sertoli Cell ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Normal Men

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.

HORMONAL EFFECTS OF TAMOXIFEN IN OLIGOSPERMIC MEN

1977 ◽  
Vol 73 (1) ◽  
pp. 171-178 ◽  
Author(s):  
K. J. WILLIS ◽  
D. R. LONDON ◽  
M. A. BEVIS ◽  
W. R. BUTT ◽  
S. S. LYNCH ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Hormonal Effects ◽  
Basal Serum ◽  
Serum Lh ◽  
Sperm Counts ◽  
Serum Androgens ◽  
Normal Men ◽  
Lh Rh

SUMMARY The hormonal effects of tamoxifen (10 mg daily for 6 months) have been studied in nine men with oligospermia. Basal concentrations of serum LH (1·7 ± 0·1 (s.e.m.) i.u./l) increased to a maximum of 4·1 ± 1·3 i.u./l (P < 0·001) after 6 months, and FSH rose from 4·9 ± 1·0 to a maximum of 7·7 ± 1·3 i.u./l after 4 months of treatment (P < 0·01). The response to luteinizing hormone releasing hormone (LH-RH) was studied at monthly intervals. Sums of increments of serum LH increased from 35 ± 4 to 92 ± 17 i.u./l at 4 months (P < 0·001) and of FSH from 14 ± 3·4 to 23 ± 3·5 i.u./l at 4 months (P < 0·01). Basal serum androgens rose from 25 ± 2·7 to 38 ± 2·4 nmol/l after 4 months of treatment (P < 0·05), and serum oestradiol-17β increased from 185 ± 25 to 631 ± 90 pmol/l by 6 months (P < 0·001). No significant changes occurred in sperm counts. Five normal men acted as controls: they were given tamoxifen for 1 week. No significant changes were observed in serum LH, FSH or release of these hormones following administration of LH-RH. Serum androgens and oestrogens however, increased significantly by day 4 of treatment (P < 0·05).

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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