PLASMA TESTOSTERONE IN KLINEFELTER'S SYNDROME: DIURNAL VARIATION AND RESPONSE TO ACTH AND DEXAMETHASONE

1975 ◽  
Vol 78 (3) ◽  
pp. 604-612 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
T. J. Benraad
Keyword(s):  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Normal Range ◽  
Short Term ◽  
Plasma Testosterone Level ◽  
Testosterone Levels ◽  
Basal Plasma ◽  
Order Of Magnitude ◽  
The Mean

ABSTRACT The mean basal plasma testosterone level in 28 patients with chromatin positive Klinefelter's syndrome was significantly lower than in 58 healthy male controls. In 12 of the patients the hormone levels were in the normal range. In both the eugonadal males and the Klinefelter patients the plasma testosterone levels spontaneously decreased throughout the day, the relative decrease in both groups being of the same order of magnitude. Short term ACTH infusion and the administration of dexamethasone did not significantly influence the plasma testosterone concentration in the Klinefelter patients. These findings do not support the view that the adrenal cortex plays a major role in contributing to the circulating plasma testosterone levels in this syndrome.

THE EFFECT OF SHORT AND LONG TERM HUMAN CHORIONIC GONADOTROPHIN (HCG) ADMINISTRATION ON PLASMA TESTOSTERONE LEVELS IN KLINEFELTER'S SYNDROME

1974 ◽  
Vol 77 (4) ◽  
pp. 753-764 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
Th. J. Benraad
Keyword(s):  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Absolute Increase ◽  
Testosterone Levels ◽  
Basal Plasma ◽  
Patient Groups ◽  
Pre Treatment ◽  
Secondary Hypogonadism

ABSTRACT The effect of acute (1500 IU/day for 3 days) and chronic HCG administration (1500 IU, 3 times weekly) on plasma testosterone levels in patients with Klinefelter's syndrome was compared with the response observed in patients with hypogonadotrophic eunuchoidism and in eugonadal male controls. Basal plasma testosterone levels in the Klinefelter patients were significantly lower than in the control subjects and significantly higher than in the patients with secondary hypogonadism. In all but one Klinefelter patient the plasma LH levels were markedly elevated even in the presence of normal testosterone levels. No significant correlation could be demonstrated between the plasma testosterone concentrations and the LH levels in the Klinefelter patients. Short term HCG administration resulted in a significant increase in the plasma testosterone levels in each of the 3 groups studied, independent of the basal value. The absolute increase in the Klinefelter patients was quantitatively comparable to that in the patients with secondary hypogonadism, but significantly lower than in the eugonadal controls. During long term HCG treatment the plasma testosterone levels definitely increased in both patient groups, but remarkably in the Klinefelter patients testosterone levels tended to decrease on continuing treatment, though in most patients testosterone levels remained higher than the pre-treatment values. The data on the effect of acute and chronic HCG administration on plasma testosterone levels in this study illustrate again that Leydig cells in Klinefelter's syndrome still retain a functional reserve, though less than in eugonadal males.

BODY PROPORTIONS AND ANDROGENICITY IN RELATION TO PLASMA TESTOSTERONE LEVELS IN KLINEFELTER'S SYNDROME

1974 ◽  
Vol 77 (2) ◽  
pp. 387-400 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
T. J. Benraad
Keyword(s):  
Upper Body ◽  
Clinical State ◽  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Body Segment ◽  
Klinefelter's Syndrome ◽  
Testosterone Levels ◽  
Arm Span ◽  
Basal Plasma ◽  
Low Testosterone

ABSTRACT Basal plasma testosterone levels (mean ± sd 290 ± 141 ng/100 ml) (range 72–684 ng/100 ml) in 25 chromatin positive patients with Klinefelter's syndrome (23 XXY, 1 XXYY, 1 XY/XXY) were significantly lower than in 25 age matched controls (mean ± sd 603 ± 169 ng/100 ml). In 11 out of the 25 Klinefelter patients however, plasma testosterone levels were in the normal range and these patients differed significantly from the patients with low testosterone levels with respect to the clinical state of androgenicity. In the group of Klinefelter patients, but not in the controls, a significant negative correlationship was found between plasma testosterone levels and each of the variables: body weight, arm span, length of the lower body segment and the ratio's lower/upper and span/upper body segment.

THE EFFECT OF GONADOTROPHIN RELEASING HORMONE ON PITUITARY-GONADAL FUNCTION IN KLINEFELTER'S SYNDROME

1976 ◽  
Vol 83 (4) ◽  
pp. 829-838 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
R. M. Lequin ◽  
Th. J. Benraad
Keyword(s):  
Leydig Cells ◽  
Bolus Injection ◽  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Releasing Hormone ◽  
Basal Plasma ◽  
Gonadotrophin Releasing Hormone ◽  
The Mean ◽  
Lh Rh

ABSTRACT The mean basal plasma LH and FSH levels in 8 patients with Klinefelter's syndrome were respectively 5 and 15-fold higher than in 8 eugonadal males, whereas plasma testosterone concentration were half the normal value After an intravenous bolus injection of gonadotrophin releasing hormone (100 μg of LH-RH) the gonadotrophin increase in the Klinefelter patients was more marked than in the control subjects, but in both groups the plasma testosterone levels remained essentially unchanged. In contrast to the bolus injection, an 8 h infusion of LH-RH after the bolus elicited a significant plasma testosterone increase in both the eugonadal males (59%) and the Klinefelter patients (51%). These findings indicate that despite an impressive endogenous hypergonadotrophism, Leydig cells in Klinefelter's syndrome can still respond to a sustained further increase of these endogenous gonadotrophins and thus still have functional reserve.

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.

Acceleration of puberty in boys with delayed puberty by clomiphene citrate. A clinical and laboratory study

1980 ◽  
Vol 94 (1) ◽  
pp. 117-125 ◽  
Author(s):  
Zvi Dickerman ◽  
Ruth Prager-Lewin ◽  
Osnat Lahmy ◽  
Zvi Laron
Keyword(s):  
Peak Plasma ◽  
Clomiphene Citrate ◽  
Significant Rise ◽  
Delayed Puberty ◽  
Plasma Testosterone ◽  
Plasma Testosterone Level ◽  
Basal Plasma ◽  
The Mean ◽  
Group 2 ◽  
Group 1

Abstract. Clomiphene citrate was administered at a dose of 50 mg/day for 3 months to 29 boys with delayed puberty, 15 in a stage of early puberty (group 1) and 14 in stages of mid puberty (group 2). In both groups a significant acceleration in the advancement of pubertal signs was noted in the 6-month period following initiation of therapy as compared to a non-treated control group. A significant rise in the mean (± sd) basal plasma LH levels, from 1.0 ± 0.4 to 2.7 ± 2.2 mU/ml in group 1 (P < 0.05) and from 1.0 ± 0.6 to 2.2 ± 1.7 mU/ml in group 2 (P < 0.05) was observed following the treatment period with clomiphene. Concomitantly there was a rise of the mean basal plasma FSH level from 1.1 ± 0.4 to 2.0 ± 1.5 mU/ml in group 1 (P ± 0.05) and from 1.9 ± 1.6 to 3.4 ± 3.0 mU/ml in group 2 (P < 0.02). The mean LH peak response to an iv bolus of LRH (50 μg/m2 iv) rose from 8.3 ± 4.2 to 13.0 ± 5.3 mU/ml in group 1 (P < 0.05) and from 9.2 ± 5.8 to 12.6 ± 6.8 mU/ml in group 2 (NS). The mean peak plasma FSH response to LRH rose from 2.0 ± 0.6 to 5.9 ± 4.2 mU/ml in group 1 (P < 0.05) and from 4.3 ± 4.0 to 7.0 ± 6.8 mU/ml in group 2 (NS). Clomiphene therapy caused a rise of the basal plasma testosterone level from 68 ± 53 to 313 ± 270 ng/100 ml in group 1 (P < 0.01) and from 103 ± 67 to 392 ± 248 ng/100 ml in group 2 (P < 0.01). The plasma testosterone response to one hCG stimulation (5000 U im), tested in 4 boys immediately before and after the 3-month period of clomiphene administration revealed an increase in both the basal and the peak testosterone levels (P < 0.05 and P < 0.001, respectively). A standard clomiphene test consisting of the administration of 100–200 mg/day clomiphene citrate for 8 days was performed in 8 boys before initiation of clomiphene treatment for the 3-month period. In 4, including 2 boys in an early stage of puberty, there was a suppression of the basal level of gonadotrophins and their response to synthetic LRH. The other 4 boys, all of them in stages of mid-puberty, showed an increase in the basal and peak plasma gonadotrophin levels following LRH stimulation. In all 8 boys there was a significant rise of the basal plasma testosterone level. Despite the varying response to the short clomiphene test in these 8 boys, all gave a good response to the prolonged administration of clomiphene citrate. It was concluded that treatment with small doses of clomiphene citrate for a period of 3 months induces an acceleration of puberty in boys with delayed or slowlyprogressing puberty, once the stage of initiation of puberty has been passed.

INFLUENCE OF METYRAPONE ON PLASMA CONCENTRATIONS OF TESTOSTERONE AND ANDROSTENEDIONE IN MAN

1971 ◽  
Vol 68 (3) ◽  
pp. 576-584 ◽  
Author(s):  
K. O. Nilsson ◽  
B. Hökfelt
Keyword(s):  
Body Weight ◽  
Male Patient ◽  
Gradual Increase ◽  
Plasma Concentrations ◽  
Plasma Testosterone ◽  
Testosterone Levels ◽  
Basal Plasma ◽  
Normal Males ◽  
A Minor ◽  
Secondary Hypogonadism

ABSTRACT Metyrapone was administered either orally, 750 mg every four h, in a total of six doses, or intravenously 30 mg per kg body weight as a four h infusion. In three males with normal endocrine functions, metyrapone given orally or intravenously induced a fall in plasma testosterone and an elevation of androstenedione within 2–8 h. When metyrapone was administered to a patient given dexamethasone to suppress endogenous ACTH production, the androstenedione levels did not alter whereas the testosterone levels showed a slight, transient decrease. In two normal females metyrapone administration was followed by a marked increase in plasma androstenedione whereas testosterone showed only a minor, gradual increase. In one male patient with Addison's disease the basal plasma testosterone was normal whereas the level of androstenedione was low. Following metyrapone intravenously, there was a slight suppression of plasma testosterone but no change in the androstenedione concentration. In one patient with primary hypogonadism, two with secondary hypogonadism and two with Klinefelter's syndrome the plasma testosterone was low under basal conditions and did not change following metyrapone. Basal plasma androstenedione was within the range for normal males and increased markedly following metyrapone in all the cases.

EFFECT OF ETHINYLOESTRADIOL ON PLASMA TESTOSTERONE LEVELS AND URINARY TESTOSTERONE EXCRETION IN MAN

1965 ◽  
Vol 50 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Enrico Forchielli ◽  
Govind S. Rao ◽  
Inder R. Sarda ◽  
Norman B. Gibree ◽  
Peter E. Pochi ◽  
...  
Keyword(s):  
Oral Administration ◽  
Plasma Testosterone ◽  
Testosterone Levels ◽  
The Mean ◽  
Normal Men ◽  
Daily Oral Administration

ABSTRACT The daily oral administration of one mg of ethinyloestradiol to normal men decreased the mean plasma testosterone from 0.84 ± 0.07 μg per 100 ml to 0.20 ± 0.04 in 21 trials and decreased the urinary testosterone from 63 ± 1.1 μg per day to 8 ± 0.3 in 16 trials.

SHORT-TERM EFFECTS OF COPULATION, HUMAN CHORIONIC GONADOTROPHIN INJECTION AND NON-TACTILE ASSOCIATION WITH A FEMALE ON TESTOSTERONE LEVELS IN THE MALE RAT

1974 ◽  
Vol 60 (3) ◽  
pp. 429-439 ◽  
Author(s):  
K. PURVIS ◽  
N. B. HAYNES
Keyword(s):  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Physical Contact ◽  
Male Rats ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Short Term ◽  
Testosterone Levels ◽  
Peripheral Plasma ◽  
First Contact

SUMMARY Peripheral plasma testosterone levels in the male rat were increased above control levels 5 min after the first intromission with an oestrous female, or 8–10 min after first contact with the female. The levels remained raised for at least 30 min if copulation was allowed to continue. Intravenous injection of human chorionic gonadotrophin resulted in an increased peripheral concentration of plasma testosterone after 10–15 min and an increase of testosterone content of the testis 5–10 min after injection, indicating that the rat testis has a potential to respond rapidly to gonadotrophin. The results suggested that if the testosterone surge during copulation was gonadotrophin-dependent, it was initiated before the first intromission. Indeed, plasma testosterone levels were raised in male rats 5 min after being placed in the proximity of oestrous females but not allowed physical contact.

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