CORRELATION OF PITUITARY AND TESTICULAR RESPONSES TO STIMULATION TESTS IN CRYPTORCHID CHILDREN

1977 ◽  
Vol 86 (3) ◽  
pp. 641-650 ◽  
Author(s):  
Dominique Gendrel ◽  
Marc Roger ◽  
Jean-Louis Chaussain ◽  
Pierre Canlorbe ◽  
Jean-Claude Job

ABSTRACT LH-RH test and HCG stimulation test were performed in 154 cryptorchid boys aged 1 month to 15 years (64 unilateral and 90 bilateral). Basal plasma LH levels and LH response to LH-RH were significantly lower from infancy to early puberty in cryptorchids compared with controls. Basal FSH levels and FSH response to LH-RH were normal. The post-HCG rise of plasma testosterone was reduced until mid-puberty. A significant positive correlation was found between post-HCG testosterone levels and pre- and post-LH-RH levels of LH. This correlation suggests that testicular maldescent and the decreased ability of Leydig cells to respond to a short course of HCG may result from an early defect or a delay of pituitary LH secretion.

1977 ◽  
Vol 85 (3) ◽  
pp. 644-649 ◽  
Author(s):  
Jean-Claude Job ◽  
Dominique Gendrel ◽  
Anne Safar ◽  
Marc Roger ◽  
Jean-Louis Chaussain

ABSTRACT Twelve male infants with undescended testes (5 bilaterally, 7 unilaterally) were studied between the ages of 1 week and 11 months. As in older pre-pubertal cryptorchid boys, a significant decrease of the LH response to LH-RH test was found, while basal plasma levels of gonadotrophins and FSH response to LH-RH were normal. Plasma testosterone levels were in the normal range, and Leydig cells responded to stimulation by HCG, the degree of this response being significantly and positively correlated to the LH peak elicited by LH-RH. It may be concluded that some early defect of the pituitary-Leydig cell axis is associated with undescended testes.


1976 ◽  
Vol 83 (4) ◽  
pp. 829-838 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
R. M. Lequin ◽  
Th. J. Benraad

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.


1971 ◽  
Vol 68 (3) ◽  
pp. 576-584 ◽  
Author(s):  
K. O. Nilsson ◽  
B. Hökfelt

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.


2000 ◽  
Vol 278 (4) ◽  
pp. E744-E751 ◽  
Author(s):  
Hisashi Kishi ◽  
Mariko Itoh ◽  
Sachiko Wada ◽  
Yoko Yukinari ◽  
Yumiko Tanaka ◽  
...  

We investigated the importance of inhibin and testosterone in the regulation of gonadotropin secretion in adult male golden hamsters ( Mesocricetus auratus). After castration, plasma concentrations of inhibin and testosterone were reduced to undetectable, whereas plasma follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were increased. After hemicastration, plasma FSH and LH increased moderately and plasma inhibin decreased to one-half its initial level. Plasma testosterone levels in hemicastrated animals decreased 3 h after hemicastration but returned to those in sham-operated animals at 6 h. Plasma LH in the castrated hamster declined comparably to intact animals with testosterone treatment; plasma FSH also decreased but still remained at levels higher than those in intact animals. After treatment with inhibin in long-term-castrated animals, plasma FSH decreased, whereas plasma LH was not altered. Intact males treated with flutamide, an anti-androgen, showed a significant increase in plasma LH but not in FSH. On the other hand, treatment with anti-inhibin serum induced a significant elevation in plasma FSH, but not in LH. Using immunohistochemistry, we showed that the inhibin α-subunit was localized to both Sertoli and Leydig cells. The present study in adult male hamsters indicates that FSH secretion is regulated mainly by inhibin, presumably from Sertoli and Leydig cells, and that LH secretion is controlled primarily by androgens produced from the Leydig cells. This situation is more similar to that of primates than of rats.


1974 ◽  
Vol 77 (4) ◽  
pp. 753-764 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
Th. J. Benraad

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.


1978 ◽  
Vol 89 (1) ◽  
pp. 126-131 ◽  
Author(s):  
G. Schaison ◽  
F. Durand ◽  
I. Mowszowicz

ABSTRACT ACTH decreases plasma testosterone levels in men. The aim of this study was to assess the part played by the glucocorticoids in this effect, and the mechanism of their action. Plasma androstenedione, testosterone, cortisol and LH were measured in 8 normal men, before and after the following tests: ACTH stimulation (2 mg im), metyrapone administration (500 mg/every 4 h/6 times) and dexamethasone suppression (8 mg/day/3 days). In addition, androstenedione and testosterone were evaluated under human chorionic gonadotrophin (5000 IU HCG/day/3 days) before and after dexamethasone suppression (8 mg/day/6 days). In all patients, ACTH decreased plasma testosterone from 5.87 ± 1.59 (sd) ng/ml to 3.06 ± 0.8 (sd) ng/ml (P < 0.001). In contrast, after metyrapone, the mean plasma testosterone was increased to 6.98 ± 1.75 (sd) ng/ml. This increase, though not statistically significant, was observed in all patients but one. Both tests resulted in a significant increase of plasma androstenedione (P < 0.01 and P < 0.001, respectively). Dexamethasone suppressed both testosterone and androstenedione levels. None of the three tests had a significant effect on the LH concentration. HCG injection increased the mean plasma testosterone to 11.46 ± 2.80 ng/ml. Dexamethasone significantly depressed (P < 0.01) the testosterone response to HCG. These data are consistent with the following conclusions: 1) The decrease of plasma testosterone levels, observed in men after ACTH administration, is not observed after metyrapone induced ACTH increase. This confirms that it is related to cortisol levels rather than to ACTH itself. 2) Glucocorticoids act directly on testicular biosynthesis since they do not induce any change in LH secretion and since dexamethasone reduces testosterone response to HCG.


1974 ◽  
Vol 77 (2) ◽  
pp. 387-400 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
T. J. Benraad

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.


1985 ◽  
Vol 105 (3) ◽  
pp. 423-427 ◽  
Author(s):  
J. A. F. Tresguerres ◽  
L. F. Perez Mendez ◽  
A. Lopez-Calderon ◽  
A. I. Esquifino

ABSTRACT To study the role of testosterone on the regulation of the hypothalamic-pituitary-testicular axis, young intact male Wistar rats were given acute (24 h) or chronic (5 days) subcutaneous treatments of 500 μg testosterone propionate (TP) or vehicle alone. Plasma LH, prolactin and testosterone levels were measured both basally and after administration of LH-releasing hormone (LHRH) or human chorionic gonadotrophin (hCG) by means of specific radioimmunoassay systems using materials supplied by the NIADDK. After acute treatment with TP there was an increase in basal plasma testosterone concentrations and no modification in the hCG response when compared with vehicle-treated animals. No difference could be detected in basal plasma testosterone levels after the chronic treatment, but a significant reduction in the hCG response was observed. Both acute and chronic treatments with TP resulted in a significant decrease of basal plasma LH levels. A reduced LH response to LHRH in acutely treated rats and no response in the chronically treated rats was detected. Plasma prolactin levels showed an increase after both acute and chronic treatments. To evaluate the possible role of the increased plasma prolactin levels on the above modifications during TP treatment, another group of animals was treated with TP and bromocriptine (dopamine agonist) simultaneously to avoid the increase in plasma prolactin levels. In this situation, neither basal plasma LH levels nor the response to LHRH were altered when compared to vehicle-treated rats; a normal testosterone response to hCG stimulation was observed in spite of the high basal plasma testosterone levels. All these observations suggest that increased prolactin levels may exert a modulatory role on the negative feedback effect of testosterone both at the testicular and central levels. J. Endocr. (1985) 105, 423–427


1977 ◽  
Vol 85 (3) ◽  
pp. 456-464 ◽  
Author(s):  
Zvi Dickerman ◽  
Yehuda Bar-Haim ◽  
Ruth Prager-Lewin ◽  
Haiuta Kaufman ◽  
Zvi Laron

ABSTRACT Nineteen boys with irregular puberty (IP), defined as a discrepancy of two or more pubertal stages between the criteria for genitalia and that for pubic hair, were subjected to a standard LRH test (50 μg/m2, iv) and the response of gonadotrophins as well as the basal levels of plasma testosterone, LH and FSH were compared to those of boys with normal, regular puberty. When the results were plotted against the pubertal stage for genitalia (Pg), it was found that in the boys with IP the basal plasma testosterone levels were lower and the response of plasma LH to LRH stimulation lesser than in the controls. However, when these parameters were plotted against the pubertal stage for pubic hair (Ph) it was found, that in the boys with IP the plasma testosterone levels were significantly higher and the response of both LH and FSH stimulation greater than in the control group. It was concluded that irregular puberty in boys may be regarded as a normal variation. The delayed development of sexual hair and penile length, and retarded pubertal growth spurt and bone age maturation seen in these boys, with normal testicular development, may be explained by a temporary reduced peripheral sensitivity to androgens and a compensatory effort by the pituitary, manifested in increased secretion of LH and testosterone, relatively to their pubertal stage for pubic hair.


1978 ◽  
Vol 88 (4) ◽  
pp. 787-792 ◽  
Author(s):  
Anne Sundby ◽  
P. A. Torjesen

ABSTRACT Administration of 6000 IU HCG to 4 bulls was followed by an elevation of plasma testosterone lasting for 9–13 days. When HCG administration was repeated, the testosterone response was shortened to 4–6 days in 3 bulls due to the formation of antibodies against HCG. The appearance of HCG antibodies coincided with a sharp decrease in the plasma testosterone level, indicating that Leydig cells have to be under continuous HCG stimulation to maintain increased testosterone production. No antibody against bovine LH was detected in the plasma samples containing antibodies against HCG. In one bull the response following the second HCG injection was similar to the plasma testosterone pattern following the first. No antibodies against HCG were found in this bull. Five bulls received 750 IU HCG twice. Following the period with elevated plasma testosterone levels, subnormal levels were observed after both injections. One injection led to decreased levels without development of antibodies against HCG while the second HCG injection led to subnormal testosterone levels concomitant with measurable antibodies against HCG.


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