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Androstenedione in the blood
Last reviewed: 23.04.2024
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DHEA - the main androgen (more precisely, their predecessor), produced by the adrenal glands. Most of DHEA is rapidly modified by the addition of sulfate, about half of DHEA is sulfated (formed by DHEAS) in the adrenal glands, and the remainder in the liver. DHEA is biologically inactive, but removing the sulfate group restores activity. DHEA is actually a prohormone, because under the action of the lyase and isomerase, this weak androgen turns into a more active androstenedione. In a small amount, androstenedione is formed in the adrenal glands by the action of the lyase on 17-GPG. Restoration of androstenedione leads to the formation of testosterone. However, in this way only a small amount of testosterone is synthesized in the body.
Androstenedione is the main precursor in the biosynthesis of androgens (testosterone) and estrogens (estrone). It is synthesized in the adrenal and sex glands.
Reference concentrations of androstenedione in serum
|
Androstenedion | ||
|
Age |
Ng / dL |
Nmol / l |
|
Blood from the umbilical cord |
30-150 |
1.0-5.2 |
|
Newborns, 1-7 days |
20-290 |
0,7-10,1 |
|
Children: | ||
|
1-12 months |
6-68 |
0.2-2.4 |
|
1-10 years |
8-50 |
0.3-1.7 |
|
10-17 years old |
8-240 |
0.3-8.4 |
|
Adults: | ||
|
Men |
75-205 |
2.6-7.2 |
|
Women |
85-275 |
3.0-9.6 |
Determination of the concentration of androstenedione (in conjunction with DHEAS) is used to diagnose and evaluate the effectiveness of treatment of hyperandrogenic conditions.
An increase in the concentration of androstenedione in the blood is most typical for patients with congenital hyperplasia of the adrenal cortex, Isenko-Cushing syndrome, ectopic ACTH secretion, testicular stromal hyperplasia or ovarian tumor. An increase in the concentration of androstenedione in the blood is possible in a number of patients with polycystic ovaries and hirsutism.
In clinical practice, the determination of serum androstenedione concentration is widely used to monitor the effectiveness of treatment with glucocorticosteroids of congenital adrenal hyperplasia (a more accurate measure than that of other androgens and 17-GPG).
Reduction of the concentration of androstenedione in the blood is found in patients with sickle-cell anemia, with adrenal and ovarian failure.
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