Reference Range
Androstenedione is a C-19 (19 carbon atoms) steroid hormone found in men as well as in premenopausal women. Androstenedione originates in the gonads, with minor contribution from the adrenal glands (1.5-3 mg/day); in postmenopausal women, the adrenal gland constitutes the major source of this hormone.
Androstenedione production in the adrenal glands is under effect of the adrenocorticotropic hormone (ATCH), whereas in the gonads it is controlled by the luteinizing hormone/follicle-stimulating hormone (LH/FSH). Each laboratory has its own reference range for androstenedione, depending on the assay. The tables below show the reference ranges.
Table 1. Androstenedione Reference Ranges [1] (Open Table in a new window)
|
Conventional Units |
SI Units |
Men |
|
|
18-30 y |
50-220 ng/dL |
1.74-7.63 nmol/L |
31-50 y |
40-190 ng/dL |
1.39-6.59 nmol/L |
51-60 y |
50-220 ng/dL |
1.74-7.63 nmol/L |
Women |
|
|
Follicular |
35-250 ng/dL |
1.21-8.68 nmol/L |
Midcycle |
60-285 ng/dL |
2.08-9.89 nmol/L |
Luteal |
30-235 ng/dL |
1.04-8.15 nmol/L |
Postmenopausal |
20-75 ng/dL |
0.69-2.60 nmol/L |
Children |
|
|
1-12 mo |
6-78 ng/dL |
0.21-2.71 nmol/L |
1-4 y |
5-51 ng/dL |
0.17-1.77 nmol/L |
5-9 y |
6-115 ng/dL |
0.21-3.99 nmol/L |
10-13 y |
12-221 ng/dL |
0.42-7.67 nmol/L |
14-17 y |
22-225 ng/dL |
0.76-7.81 nmol/L |
Table 2. Tanner Stage Reference Ranges [2] (Open Table in a new window)
Tanner stage I | |
Male | 0.04-0.32 ng/mL |
Female | 0.05-0.51 ng/mL |
Tanner stage II | |
Male | 0.08-0.48 ng/mL |
Female | 0.15-1.37 ng/mL |
Tanner stage III | |
Male | 0.14-0.87 ng/mL |
Female | 0.37-2.24 ng/mL |
Tanner stage IV-V | |
Male | 0.27-1.07 ng/mL |
Female | 0.35-2.05 ng/mL |
Interpretation
Androstenedione is increased in the following:
-
Polycystic ovarian syndrome (PCOS) [3]
-
21-hydroxylase deficiency
-
17β-hydroxysteroid dehydrogenase
-
Androgen-secreting tumors of the ovary and adrenal gland
Androstenedione is decreased in the following:
-
A rare form of CAH
-
17α-hydroxylase/17,20-lyase deficiency (the enzyme is also called P450c17 or CYP17)
Collection and Panels
Collection details are as follows:
-
Patient instruction - No need for fasting
-
Specimen type - Serum
-
Collection tube - Red-top tube or Lavender-top (EDTA) tube
-
Unacceptable conditions - Grossly hemolyzed specimens or gross lipemia
-
Specimen preparation - Separate serum from cells and transfer to transport tube
-
Storage/transport temperature - Refrigerated
-
Stability - Refrigerated: 2 weeks; Frozen: 2 weeks
-
Panels: None
A new method has been developed that simultaneously measures serum testosterone, androstenedione, and DHEA in serum and plasma. [4]
Background
Description
Androstenedione is a C-19 (19 carbon atoms) steroid hormone found in men as well as in premenopausal women. Androstenedione originates in the gonads, with minor contribution from the adrenal glands (1.5-3 mg/day); in postmenopausal women, the adrenal gland constitutes the major source of this hormone. Androstenedione production in the adrenal glands is under effect of the adrenocorticotropic hormone (ATCH), whereas in the gonads it is controlled by the luteinizing hormone/follicle-stimulating hormone (LH/FSH). [5, 6, 7]
Androstenedione is a biologically inert hormone; in the peripheral tissues like skin and adipose tissue, it can be converted to estrone or testosterone.
Indications/Applications
Androstenedione can be measured in conjunction with other hormones for the following:
-
In the diagnosis and differential diagnosis of hyperandrogenism and PCOS
-
In the diagnosis and treatment monitoring of CAH
-
In the diagnosis of premature adrenarche
A study by Simons et al indicated that the reproductive features of PCOS are associated with androstenedione and total testosterone. Specifically, androstenedione levels are related to serum anti-Müllerian hormone (AMH), while total testosterone levels are linked to serum AMH and the antral follicle count. Meanwhile, serum sex hormone–binding globulin (SHBG) levels were found to be associated with the metabolic features of PCOS, suggesting “a differential underlying pathophysiology for the metabolic and reproductive features of PCOS.” [8]