EVIDENCE FOR THE ADRENAL SOURCE OF ANDROGENS IN PRECOCIOUS ADRENARCHE

1976 ◽  
Vol 82 (2) ◽  
pp. 342-352 ◽  
Author(s):  
Sigrun Korth-Schutz ◽  
Lenore S. Levine ◽  
Maria I. New ◽  
Diane M. Chow

ABSTRACT In order to determine the source of androgens in precocious adrenarche, serum androgens were determined in 8 girls with precocious adrenarche and 5 agonadal children in adrenarche under conditions of adrenal and gonadal stimulation and suppression. All androgens increased with ACTH stimulation in both groups. Stimulability of serum androgens in girls with precocious adrenarche with ACTH was more consistent than in 13 prepubertal children. Human chorionic gonadotrophin administration increased serum Δ4-androstenedione, testosterone and dihydrotestosterone in the girls with precocious adrenarche but not in the agonadal children, demonstrating the failure of HCG to stimulate adrenals. Dexamethasone suppression decreased levels of all androgens in both groups, whereas Norlutin® or Ovral® produced variable changes. These studies support the adrenal origin of androgens in precocious adrenarche and the lack of ovarian contributions in this condition.

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.


1963 ◽  
Vol 43 (1) ◽  
pp. 155-160
Author(s):  
Jørgen Falck Larsen ◽  
Christian Hamburger

ABSTRACT Various modifications of the Parlow test for luteinizing hormone (ovarian ascorbic acid depletion in rats) were tried. Human chorionic gonadotrophin was used instead of hypophyseal luteinizing hormone. The precision of the method was found to be so low, however, that the test could not be used for routine clinical analysis. The low precision found in this and other laboratories is thought to be due to the strains of rats used.


1964 ◽  
Vol 45 (4) ◽  
pp. 535-559 ◽  
Author(s):  
E. Bolté ◽  
S. Mancuso ◽  
G. Eriksson ◽  
N. Wiqvist ◽  
E. Diczfalusy

ABSTRACT In 15 cases of therapeutic abortion by laparotomy the placenta was disconnected from the foetus and perfused in situ with tracer amounts of radioactive dehydroepiandrosterone (DHA), dehydroepiandrosterone sulphate (DHAS), androst-4-ene-3,17-dione (A), testosterone (T) and 17β-oestradiol (OE2). Analysis of the placentas, perfusates and urine samples revealed an extensive aromatisation of DHA, A and T; more than 70% of the radioactive material recovered was phenolic, and at least 80 % of this phenolic material was identified as oestrone (OE1), 17β-oestradiol (OE2) and oestriol (OE3), the latter being detected only in the urine. Comparative studies indicated that A and T were aromatised somewhat better than DHA and that all three unconjugated steroids were aromatised to a much greater extent than DHAS. Radioactive OE1 and OE2 were isolated and identified in the placentas and perfusates, but no OE3, epimeric oestriols, or ring D ketols could be detected in these sources, not even when human chorionic gonadotrophin (HCG) was added to the blood prior to perfusion. Lack of placental 16-hydroxylation was also apparent when OE2 was perfused. Regardless of the precursor perfused, there was three times more OE2 than OE1 in the placenta and three times more OE1 than OE2 in the perfusate. This was also the case following perfusion with OE2. The results are interpreted as suggesting the existence in the pregnant human of a placental »barrier« limiting the passage of circulating androgen. The barrier consists of a) limited ability to transfer directly DHAS and b) an enzymic mechanism resulting in the rapid and extensive aromatisation of the important androgens DHA, A and T.


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