Immunohistochemical and quantitative study of interstitial and intratubular leydig cells in normal men, cryptorchidism, and Klinefelter's syndrome

1991 ◽  
Vol 164 (4) ◽  
pp. 299-306 ◽  
Author(s):  
J. Regadera ◽  
J. Codesal ◽  
R. Paniagua ◽  
P. Gonzalez-Peramato ◽  
M. Nistal
Keyword(s):  
Quantitative Study ◽  
Leydig Cells ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Normal Men

Indirect evidence of chronic Leydig cell desensitization in Klinefelter's syndrome

1981 ◽  
Vol 96 (4) ◽  
pp. 552-556 ◽  
Author(s):  
Anthony G. Smals ◽  
Gerlach F. Pieters ◽  
Peter W. Kloppenborg
Keyword(s):  
Leydig Cells ◽  
Response Pattern ◽  
Indirect Evidence ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Basal Plasma ◽  
Normal Men ◽  
T Values

Abstract. The basal plasma 17α-hydroxyprogesterone (17-OHP) and testosterone (T) levels were proportionally decreased in 10 hypergonadotropic patients with Klinefelter's syndrome. The ratio 17-OHP to T was however about twice as high as in 10 eugonadal male controls, suggesting the presence of a block in the conversion of 17-hydroxylated steroids to androgens in the Klinefelter patients under basal circumstances. Administration of human chorionic gonadotrophin (hCG, 1500 IU im daily for 3 days) to the Klinefelter patients disclosed a response pattern quite different from that observed in controls. In the control subjects 17-OHP and the ratio 17-OHP/T sharply rose to maximum values at 24 h after the first injection. Thereafter both progressively fell to lowest values at 72 h, when T levels reached their maximum. In the Klinefelter patients the T response to hCG administration was greatly diminished but the 17-OHP response was similar to that in the controls. Maximum 17-OHP and 17-OHP/T values however were not achieved until 72 h after the first injection when T levels also reached their maximum. Unlike in the controls in the Klinefelter patients maximum 17-OHP and T increments and the 17-OHP and T levels 48 and 72 h after the injection were positively correlated. Together the findings of a decreased T synthesis and reserve in the presence of relative 17-OHP accumulation, further increasing after acute hCG administration in a pattern quite different from that in normal men, suggest that in Klinefelter's syndrome the Leydig cells may be chronically desensitized by the persistent endogenous hypergonadotropism.

HYDROXYSTEROID DEHYDROGENASES IN NORMAL AND ABNORMAL HUMAN TESTES

1966 ◽  
Vol 35 (3) ◽  
pp. 239-NP ◽  
Author(s):  
A. H. BAILLIE ◽  
W. S. MACK
Keyword(s):  
Similar Pattern ◽  
Leydig Cells ◽  
Seminiferous Tubules ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Colour Reaction ◽  
Adult Human ◽  
Hydroxysteroid Dehydrogenases

SUMMARY 3α-, 3β-, 11β-, 16β-, 17β- and 20β-hydroxysteroid dehydrogenases have been localized histochemically in the Leydig cells of prepubertal and adult human testes; 3α-, 16β- and 17β-hydroxysteroid dehydrogenases were present in the seminiferous tubules also. A similar pattern was found in cryptorchid testes. In addition 3β-sulphoxy steroids, including DHA sulphate, gave a good colour reaction in human Leydig cells. Testes from oestrogen-treated subjects had no histochemically demonstrable hydroxysteroid dehydrogenases and this applied also to infarcted testes. Testes from a case of Klinefelter's syndrome were found to lack 17β- and 20β-hydroxysteroid dehydrogenases in the Leydig cells. The biochemical significance of these results is discussed.

THE EFFECT OF OESTROGEN ADMINISTRATION ON PLASMA TESTOSTERONE, FSH AND LH LEVELS IN PATIENTS WITH KLINEFELTER'S SYNDROME AND NORMAL MEN

1974 ◽  
Vol 77 (4) ◽  
pp. 765-783 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
R. M. Lequin ◽  
Th. J. Benraad
Keyword(s):  
Normal Subjects ◽  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Testosterone Levels ◽  
Control Subjects ◽  
Dose Dependent Decrease ◽  
Normal Males ◽  
Normal Men ◽  
Dose Dependent

ABSTRACT In 6 eugonadal males and 6 patients with Klinefelter's syndrome the effect of increasing amounts of ethinyloestradiol (EE) (15, 30 and 150 μg daily for 7 days) on plasma levels of LH, FSH and testosterone was studied. Control levels of LH and FSH in the Klinefelter patients were significantly higher than in the normal males, whereas plasma testosterone levels were significantly lower. In 3 of the 6 Klinefelter patients plasma gonadotrophin levels were clearly elevated despite normal plasma testosterone concentrations. After EE administration a dose-dependent decrease of plasma FSH and testosterone levels was observed in both the control subjects and the Klinefelter patients, whereas the LH decrease was dose-dependent in the Klinefelter patients, but not however, in the eugonadal males. Despite significant testosterone suppression plasma LH and FSH levels in the Klinefelter patients remained supranormal when compared with the levels of the control subjects. Amounts of EE, roughly equivalent to the physiological oestrogen production (15 μg of EE daily) in men, decreased plasma LH and testosterone levels in the normal males, not however, in the Klinefelter patients. The suppression of plasma testosterone by EE in both the normal subjects and the Klinefelter patients could readily be overcome by exogenous gonadotrophin administration, favouring the concept that the EE induced testosterone decrease is predominantly gonadotrophin mediated. It is concluded that small amounts of oestrogens play a role in the pituitary-gonadal axis in normal males. Although higher doses are needed to modulate this axis in Klinefelter's syndrome, the hypothalamic-pituitary-gonadal feedback in this disorder is still operative, though at a higher setting.

47,XXY Klinefelter's Syndrome with Low FSH and LH Levels and Absence of Leydig Cells

Andrologia ◽  
2009 ◽  
Vol 12 (5) ◽  
pp. 426-433 ◽  
Author(s):  
M. NISTAL ◽  
R. PANIAGUA ◽  
M.A. ABAURREA ◽  
L.F. PALLARDO
Keyword(s):  
Leydig Cells ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome

Ultrastructure of Leydig cells in Klinefelter’s syndrome with 48, XXYY karyotype

1978 ◽  
Vol 28 (1) ◽  
pp. 39-46
Author(s):  
Manuel Nistal ◽  
Ricardo Paniagua ◽  
Isidora López-Pajares
Keyword(s):  
Leydig Cells ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome

KLINEFELTER'S SYNDROME: EFFECTS OF OESTROGEN ON GROWTH HORMONE, PROLACTIN AND THYROTROPHIN RELEASE, AND ON THYROTROPHIN AND PROLACTIN RESPONSES TO THYROTROPHIN-RELEASING HORMONE

1979 ◽  
Vol 92 (2) ◽  
pp. 347-357 ◽  
Author(s):  
Antonino Barbarino ◽  
Laura De Marinis
Keyword(s):  
Growth Hormone ◽  
Normal Male ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Serum Growth Hormone ◽  
Oestrogen Treatment ◽  
Thyrotrophin Releasing Hormone ◽  
Trh Stimulation ◽  
Control Serum ◽  
Normal Men

ABSTRACT In 4 normal men and 8 patients with Klinefelter's syndrome the effects of oestradiol-17 β (15μg/kg daily for 8–13 days) on serum levels of pituitary hormones were investigated. Control levels of gonadotrophins in the Klinefelter patients were significantly higher than in the normal males, whereas serum testosterone (T) levels were lower. Oestradiol induced a decrease in serum gonadotrophin concentrations in both the control subjects and the Klinefelter patients, whereas a testosterone suppression was observed in the normal subjects, but not in the Klinefelter patients. Control serum growth hormone (hGH), and prolactin (hPRL) levels were of comparable magnitude in both groups and significantly increased during oestradiol administration. Serum thyrotrophin (TSH) levels were normal before and during oestrogen treatment. Basal serum oestradiol levels were within the normal male range, and were increased during treatment. Prolactin and thyrotrophin responsiveness to TRH stimulation was examined in Klinefelter patients before and during oestrogen administration. Before treatment, hPRL responses to TRH were higher than those observed in normal men. During oestrogen treatment hPRL responses to TRH were significantly increased when compared to those observed before treatment. TSH responses to TRH were normal both before and during treatment. These studies indicate that in patients with Klinefelter's syndrome pharmacological doses of oestrogen induce different effects on the hypothalamic-pituitary axis, as regards the release of gonadotrophins, prolactin, thyrotrophin, and growth hormone, similar to those observed in normal men. This fact supports the conclusion that in Klinefelter's syndrome the abnormality in the pituitary-gonadal feedback mechanism is selectively confined to the testosterone feedback control of gonadotrophin secretion. Finally, in patients with Klinefelter's syndrome, oestrogen is capable of inducing a significant increase of the hPRL response to TRH stimulation.

ADRENAL AND GONADAL CONTRIBUTION TO ANDROGEN AND OESTROGEN EXCRETION IN KLINEFELTER'S SYNDROME

1973 ◽  
Vol 72 (1) ◽  
pp. 182-190 ◽  
Author(s):  
Anders Frøland ◽  
V. Aasted Frandsen ◽  
Svend G. Johnsen
Keyword(s):  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Adrenal Androgen ◽  
Comparable Group ◽  
Correlation Studies ◽  
Androgen Synthesis ◽  
The Difference ◽  
Normal Men ◽  
Steroid Excretion ◽  
Dexamethasone Suppression

ABSTRACT Dexamethasone suppression tests were carried out in a group of 42 patients with Klinefelter's syndrome having a 47,XXY karyotype. Urinary androgen excretion obtained during suppression was considered to represent the gonadal contribution. The difference between pre-suppression values and suppression values was interpreted as the adrenal contribution to sex steroid excretion. It was shown that not only was the gonadal androgen production much lower in Klinefelter's syndrome than in a comparable group of normal men, but the adrenal androgen synthesis was also significantly reduced. Adrenal dehydroepiandrosterone as against adrenal androsterone plus etiocholanolone was positively correlated in Klinefelter's syndrome in contrast to normal men. This is taken as an indication of a qualitatively altered synthesis of adrenal sex hormones in the patient group. The oestrogen excretion was not quantitatively altered in Klinefelter's syndrome when compared with normal men. Correlation studies showed that in Klinefelter's syndrome adrenal oestrogens and adrenal DHA were uncorrelated contrary to the findings in normal men. This points towards an abnormal adrenal oestrogen synthesis in Klinefelter's syndrome.

Sign in / Sign up

Export Citation Format

Share Document